Full Issue Vol1 Issue2

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(ISSN22783784) VOLUME1ISSUE2 Currentlyindexedin: IndexCopernicus GenamicsJournalSeek UlrichswebGlobalSerialDictionary EditorialBoard KumarAnshul,EditorInChiefManipalCollegeofDentalSciences,India HarshRajvanshi,ExecutiveEditorI.T.SCentreforDentalStudiesandResearch,India AyeshaZaka,ExecutiveEditorHamdardMedicalandDentalCollege,Pakistan Coverartby: EbadullahShafi,DesignandGraphicsInchargeRAKCollegeofDentalSciences,UAE
Covertartillustrationshowsachipaboutthesizeofagrainofricethatstoresaperson'suniqueidentification numberlinkedtohisorherentiremedicalhistory.Thechipisimplantedinatoothwhereitcanneitherbefeltnor rejectedbythebody.
2 FOREWORD Prof.MohamedA.K.ElMassry(MBBCh.,MSc.,BDS.,Ph.D) ProfessorofOral&MaxillofacialSurgery,Alexandria,UN,Egypt. Consultant,MOHKuwait. ItisagreatpleasuretocontributetotheIDJSR,whichinfactcame outasaresultofgreateffortsofyoungDentalStudents.Iwasreally thrilledbytheideaandIhavetoadmitthatIwassurprisedbythe effortsandtheprofessionalattitudeoftheeditorialboard.Using theavailabletoolsoftechnologytobuildupsuchanetworkofambassadorsandcontributors wasanamazingandfantasticwork. Itisthespiritofthoseenthusiasticyoungmenandwomenthatwillleadourprofessioninthe futureandIamsurethatthroughyourhardworkyouwillbeabletoachievealot. Thefirstvolumecameoutwithgreatsuccessanditcontainedgoodarticlesandwasreally impressive. Theaimofourprofessionistodeliverthebestefforttoourpatientsandthiscomesthrough acquiringknowledge,developingresearchandexchangeofopinionsintopicsofmutual interest.Ibelievethroughyourjournal,siteandfacebookpageyouwillbeabletoglobalize youreffortsinaveryshorttime. Iwishyouallthebest.
INTERNATIONALDENTALJOURNALOFSTUDENTSRESEARCH|JuneSep2012|Volume1|Issue2
3 EDITORIAL KumarAnshul EditorinChief ManipalCollegeofDentalSciences,Manipal India ThreemonthsagoinMay2012,whenwereleasedthe1 issueof IDJSR,wesawadream. Adreamofrecognizingstudentswork,adreamtocreateaforumforstudentsacrosstheglobe topresenttheirresearch.Inanutshell,togiveachanceandplatformtothestudentsto publish. GettingindexedinIndexCopernicus,GenamicsJournalSeekandUlrichswebGlobalSeries DirectorywasanotherfeatwhichIDJSRachievedafterthereleaseof1stissue. 2ndissuecontainssomeamazingresearch/review/casereportarticlesfromundergraduateas wellaspostgraduatestudentsofIndia,Pakistan,China,CroatiaandCanada.Weareproudthat wearefollowingourpolicyofIDJSRasaSTUDENTONLYjournalsuccessfully. Signingoff,withthewordsofMr.RichardBranson SCREWIT,LETSDOIT
st

4 HarshRajvanshi ExecutiveEditor I.T.SCentreforDentalStudiesandResearch India
Welcome in the second issue of the journal. The editorial team is overwhelmed by the tremendous response the first issue has received from all quarters. We aredeeplytouchedbysinceregesturesofexperts,seniors,colleagues,juniors,professionals.Franklywe never anticipated that our immature effort will cultivate such a generous interest amongst all concerned, far and near, above and below, juniors and seniors. Thank you all for the belief you have showninourhumblebeginning. It is very interesting seeing a dream grow. Dream being realized. Taking shape. Evolving into reality. The second issue is coming after London Olympics. USA achieving the medal dominance from China which she lost in Beijing, a remarkable comeback. We watched with bated breath Saina Nehwal achieving the till now unachievable, M.C. Marycom, a proud mother of two, sweating it out to win, Indian Archers battling against unfamiliar hostile London winds, Virtually unknown Vijay Kumar earning glory for the nation. In the same spirit our team tried to identify themselves with the same spirit, holding our heads highwithproudresearchesofstudentsintheglobalDentalCommunity. We believe that this times selection of articles will be palatable to the hungry minds of our readers, we shallbetoohappytoreceivethefreeandfrankopinionsofourvaluedreaders.Weunderstandthatthe data being presented are for the interest of readers and it is our duty that we correct our self to the satisfactionoftheenduser,i.e.thereader. Thisissuehasbeenkeptsmallsothatthereadersareabletofinishthroughthejournalin23ofsittings. We have however restricted ourselves too much because with such a great response from our contributors,itisquiteataskwhattoincludeandwhattoleave. Wewouldrequestourreaderstoapprisewhetherincreaseinvolumeiswelcomeinfutureissues. Once again, we at the editorial desk, express our thanks and gratitude for the warm response received fromallquarters.Weshalltryourbesttobeworthyofyourbeliefinourefforts. Withbestwishes
AyeshaZaka ExecutiveEditor HamdardMedical&DentalCollege Pakistan

Afterthehugesuccessoffirstissuewearebackagainwiththesecondissueof IDJSR.Theresponsewereceivedfromfirstissuewasoverwhelmingand beyondourexpectations.Inthepreviousissuewehadrepresentationfrom fourcountries,nowinthisonewehaverepresentationfrom*five*different countries.Weplantocoverasmanycountriesaswecaninthecomingissuesandwiththerateyour articlesarepoolinginourinboxandweareveryeagertoreleasemanymoreissuesinthecoming months. Sometimesyousendyourresearchbutitgetsrejectedduetomultiplefactors,don'teverletthatstop you,its]isdoneforyourcorrection,tomakeyouthebestamongothersoutthere.Tothosewhos researchesgetpublished,don'tstopeither,workonsomethingelse,thehungerofresearchmustbe insideyouataveryearlylevel,soyoucanhaveastablecareerfromtheverybeginning. Ihopethatyou'llgothrougheacharticlewithutmostinterestandwillstrivetodoyourbitindental researchaswell.Researchiseverchanging,whatyourpredecessorshavedonemightbechangedby yousomeday,sokeepstrugglinghardandmoveforward. ThankyoutoourAmbassadorsforefficientlyspreadingawordaboutInternationalDentalJournalof StudentsResearchintheirrespectivecollegeandtoourRespectedReviewerPanelfortakingtheirtime outandgoingthrougheacharticlesocarefully. Happyreading!
6 REVIEWARTICLE
ORAL MUCOSITIS MANAGEMENT PROTOCOL BY ORAL PHYSICIAN

Dr. Suresh Ludhwani1
1Post
Graduate Student, Department of Oral Medicine and Radiology, Ahmedabad Dental College and Hospital
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Corresponding Author Dr. Suresh Ludhwani Post Graduate Student, Department of Oral Medicine and Radiology, Ahmedabad Dental College and Hospital Email: drgeminia@gmail.com
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Abstract
Oral mucositis also called stomatitis, is one of the most common and troublesome forms in individual undergoing cancer treatment. Oncology treatment does not distinguish between the malignant cells and normal epithelial cells of mucosa because of their high proliferative capacity. Thus, the mucosa becomes atrophic, and more susceptible to trauma, allowing the development of inflammation and installation of secondary infection, which aggravates the patients clinical conditions and reduce the quality of life. The clinical management of mucositis includes preventive and palliative strategies. The role of the oral physician in prevention and management of chemotherapy and radiotherapy induced mucositis is critical.
Introduction
Oral mucositis may be defined as inflammation of oral mucosa with extensive ulceration and painful irritation (1).It is considered an acute inflammation caused by the necrosis of the basal layer of the oral mucosa. The more important clinical features are erythema and/or ulceration (6), which may extend from the mouth to the rectum (2). It
can induce several life-threatening complications, such as intestinal obstruction and perforation (3), reducing the patients quality of life and leading to severe infections, which may require the interruption of the antineoplasic treatment (6). Oral and throat pain caused by the mucosa ulceration, abdominal pain, vomits and diarrhea are characteristics that compromise the patients nutritional status because of a decrease of
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food intake, leading to weight loss (5). The progression of oral lesions and its impact on general conditions of the patient may require parenteral nutrition or temporary interruption of the antineoplasic treatment (7). It is a complex biological process divided into four phases, which are interdependent and can occur due to action of cytokines on epithelium. These phases are 1. Inflammatory or vascular phase: day 0 2. Epithelial phase: days 4-5 3. Ulcerative or bacteriologic phase: days 6-12 4. Healing phase: days 12-162 proliferation and cellular differentiation occur, restoring the integrity of the mucosa (12). The anti cancer drug most commonly associated with oral mucositis include bleomycin, doxorubicin, fluorouracil and methotrexate. The cancer therapy agents vincristine and daunorubicin have a toxic effect on the mucosa [Kstler et al., 2001]. Either the use of these drugs or the cancer itself leads to neutropenia, which predisposes the mucosa to mucostitic lesions and also enables bacterial invasion of the submucosa and vascular walls, leading to bacteraemia and septicaemia [Sonis, 2004; Brown and Wingard, 2004]. The patient in the case described here initially exhibited bacteraemia, the remission of which occurred following haematological recovery associated to the use of meropenem and vancomycin. In radiotherapy, an inflammatory response is influenced by the depth and volume of radiation, total gray delivered and the number and frequency of treatments. The onset, duration and intensity vary with the individual but most often the onset starts with second week of therapy or after a dose of about 2000cGy.radiation therapy causes loss of taste by damaging the microvilli and outer surface of taste cells, the onset is rapid and progressive with ageusia or mouth blindness occurring after 3000 cGy.
Epidemiology
Mucositis has received significant attention from the physician community in the last two decades of life. It is estimated that oral mucositis affects 40% of the patients undergoing chemotherapy, 75% of the patient undergoing chemotherapy and bone marrow transplantation and more than 90% patient undergoing radiotherapy for head and neck cancer. According to chiappelli, 40% of the patient undergoing radiotherapy develop mucositis. (12)
Pathophysiology
Firstly, the chemotherapy drugs induce the death of the basal epithelial cells, which may occur by the generation of free radicals. These free radicals activate second messengers that transmit signals from receptors on the cellular surface to the inner cell environment, leading to up-regulation of pro-inflammatory cytokines, tissue injury, and cell death. The pro-inflammatory cytokines produced by macrophages, such as TNF-, amplify the mucosal injury; the production of these proinflammatory cytokines can also be stimulated by a superimposed infection of the ulcerated areas of the mucosa. Later, epithelial
Clinical Manifestation
The first symptoms reported by patients with oral mucositis are burning mouth and color changes in the mucosa, which becomes white because of insufficient keratin desquamation. Then, this epithelium is replaced by atrophic, edematous, erythematous, and friable mucosa, allowing the development of ulcerated areas with the formation of a pseudomembrane, characterized by the presence of a fibrinopurulent, yellow, and outstanding layer (6,9). The ulcerated lesions are painful and compromise the patient nutrition and oral
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hygiene, and also are considered sites for the development of local and systemic infections. In the oral mucosa, this condition involves the ventral portion of tongue, floor of the mouth and soft palate (scully et al;2004). According to the World Health Organization, oral mucositis is classified into the following grades: Grade 0 absence of mucositis; Grade I presence of painful ulcerations and erythema; Grade II presence of painful, erythema, edema or ulcerations that do not affect the patient food intake; Grade III confluent ulcerations that affect the food intake; Grade IV the patient requires parenteral nutrition (13).
Oral Hygiene Assessment

Prior to cancer therapy, the patient was submitted to an assessment of the oral cavity. Dental caries or periodontal disease associated with inadequate oral hygiene may lead to a greater risk for oral complications during the course of cytotoxic therapy. Odontogenic and gingival infections are a considerable source of bacteria, which aggravate oral mucositis lesions. These risk factors underscore the importance of an inspection of the oral environment before and during treatment that has a potentially toxic effect on the mucosa, as prior assessment allows differentiating oral mucositis from other pre-existing lesions as well as the elimination of potential sources of infection and sites of chronic irritation [StevensonMoore, 1990; Pajari et al., 1995; Brown and Wingard, 2004]. This conduct is part of the protocol for patients at the Oncology Clinic at which the present case was treated. Regarding the indices used for the assessment of mucositis, the first study employed the Daily Mucositis Index (DMI) [Tardieu et al., 1996], the gradation of which ranges from 0 to 3 and assesses different aspects in the lips, gums, oral mucosa and tongue. In the present case, the WHO scale [1979] was employed, which ranges from 0 to 4 and does not measure different aspects in the different sites analysed. Moreover, the aforementioned study assessed the lesions only on the first and last days of treatment, whereas the assessment was performed on a daily basis in the present case.
CATEGORY LIPS
RATING 1234
1 Smooth,pink,moist and intact
2 Slightly wrinkled and dry; one or more isolated reddened areas
Gingiva and oral mucosa
1234
Smooth,pink,moist and intact
Pale and slightly dry; one or two isolated lesions, blisters or reddened areas.
3 Dry and somewhat swollen, may have one or two isolated blisters; inflammatory line or demarcation Dry and somewhat swollen, generalized redness; more than two isolated lesions, blisters or reddened areas.
4 Very dry and edematous ;entire lip inflamed; generalized blisters or ulcerations Very dry and edematous; thick and engorged; entire tongue very inflamed; tip very red and demarcated with coating; multiple blisters or ulcers. Very dry and edematous; thick and engorged; entire tongue very inflamed; tip very red and demarcated with coating; multiple blisters or ulcers. Teeth covered with debris Saliva thick and ropy, viscid or mucid Severe dysfunction 16-20
Tongue
1234
Smooth,pink,moist and intact
Slightly dry; one or two isolated reddened areas; papillae prominent , particularly at base.
Dry and somewhat swollen,; generalized redness but tip and papillae are redder; one or two isolated lesions or blisters.
Teeth
1234
Clean; No debris
Saliva
1234
Thin, watery, plenty
Minimal debris; mostly between teeth Increase in amount
Oral dysfunction Score
No dysfunction 5
Mild dysfunction 6-10
Moderate debris clinging to one-half of visible enamel Saliva scanty and maybe somewhat thicker than normal Moderate dysfunction 11-15
Treatment modalities
Antioxidants Antioxidants may he particularly important since cancer treatment is an oxidative process. Radiotherapy and chemotherapy generate free radical species, which require anfioxidants to be neutralized Beta-carotene This has been proven to be useful in chemotherapy-induced mucositis. In one trial, chemotherapy patients were given 400,000 IU per day for 3 weeks and then 125,000 IU for an additional 4 weeks.
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release of the arachidonic acid cycle, which is an initiator of the inflammatory process. Corticosteroid mouthwashes These may be beneficial and are contraindicated if the patient bas a bacterial or viral infection. Triamcinolone acetonide 0.2% aqueous suspension can be used as a rinse for 1 minute twice a day and expectorated. Chamomile mouthwashes These have been used to improve mucosal healing. With controversial results. However, rinsing with 15 drops in 10 mL of warm water, three times a day, has reduced the incidence and severity of mucositis in cancer patients. Local anesthetic mouthwashes These may help to relieve pain on a temporary basis.
Vitamin E in combination with vitamin C Both act on a cellular level by protecting the cell membrane and preventing peroxidation. Glutamine A precursor of glutathione, this is very important for stress periods. It is the most abundant amino acid in the human body, and it is now considered a conditionally essential amino acid during periods of catabolism. Early studies show that glutamine has a positive effect through three mechanisms: (1) as a cellular fuel; (2) as a precursor for nucleotides needed for cell regeneration; and (3) as a source of glutathione, which is a potent antioxidant's The use of 4 grams of powdered glutamine in oral rinse in a swish and swallow suspension, twice per day, decreases the intensity and duration of the mucositis Lysofylline A protectant that reduces lipid peroxidation also decreases oxidative injury. It is presently being tested in chemoradiation trials of head and neck cancer
Analgesics
Capsaicin This is found in chili peppers and acts upon nerve endings to provide temporary pain relief. The exact mechanism of action is unknown Morphine A central nervous system analgesic, it depresses pain impulse transmission. It is effective for managing mucositis pain in cancer patients, but dry mouth is one of its adverse reactions. (13)It does not improve the health of the mucosa. Fentanyl (transdermal patch) A very potent short acting opioid, it is used primarily as an anesthetic. It is available in a sustained-release transdermal delivery system (duragesic) with a half-life of 22 hours.
Mucosal barriers
Clobetasol (0.05% ointment 1:1 with Orbase). As a topical corticosteroid, it plays a role in inflammation and immunosuppression. It is contraindicated in infection.
Mouthwashes
Benzydamine hydrochloride As an oral rinse, this has been shown to be effective, safe, and well tolerated in ameliorating the symptoms of cancer treatment induced mucositis. Rinsing then expectorating 15 mL of 0.15% solution every 2 hours will help with the painful inflammation of the mouth and throat. Benzydamine base local analgesic, antimicrobial, and antiinflammatory properties. It prevents the
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Immunomodulators
Thalidomide An immunomodulatory and antiangiogenic agent, it inhibits tumor necrosis factor-alpha (TNF-o;), which is associated with oropharyngeal ulcers. In multiple studies, the efficacy of this medication against oral and esophageal ulcers bas been demonstrated. In one trial, 92% of patients had complete healing after 4 weeks by taking 200 mg by mouth at bedtime.
Grade 2 & 3 Increase frequency of oral hygiene to every 2-3 hours Use foam oral wash if brushing is too painful Use agent to protect mucosa Apply topical agent for pain control Supplement oral intake with enteral or parental support. Provide proper analgesics and/or antibiotics if indicated Cultural suspect areas Grade 4 Continue frequent oral hygiene I.V antibiotics Laser therapy Cryotherapy
Nonpharmacologic approach
Cryotherapy This produces vasoconstriction, which reduces blood flow and diminishes the distribution of the chemotherapeutic agent to the oral mucosa. Ice swishing for 30 minutes following cancer therapy has been shown to be beneficial for these patients Low-intensity laser therapy This may improve wound healing and accelerate replication of the cells. Low-energy helium-neon (He-Ne) laser seems to be a safe, simple, atraumatic, and efficient method for the prevention and treatment of chemotherapy/radiotherapyinduced mucositis.
Conclusion
Mucositis is a common side effect of radio and/or chemotherapy anticancer treatments, but it has a complex pathophysiology and requires management strategies that have not been standardized yet. To identify patients at high risk to develop this condition is essential to reduce the costs of the anticancer treatment and to avoid its interruption after the installation of mucositis. There are many agents used for the treatment of mucositis with different mechanisms of action. However, there are no conclusive evidences on their effectiveness to establish protocols for patients undergoing radio and/or chemotherapy
Management protocol
Grade 1 Brush with soft bristled nylon brush and floss daily Rinse with salt and soda or 15% hydrogen peroxide Apply a moisturizer. Promote oral hydration and nutritional intake Remove and clean denture
References
1. Implications for evidence-based research in alternative and complementary palliative treatments. Evid Based Complement Alternat Med 2005;2:489-94. 2. Epstein JB, Schubert MM. Oral mucositis in myelosuppressive cancer therapy. Oral
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Surg Oral Med Oral Pathol Oral Radiol Endod 1999;88:273-6. 3. Gibson RJ, Bowen JM, Keef DM. Technological advances in mucositis research: new insights and new issues. Cancer Treat Rev 2008;34:476-82. 4. Rubenstein EB, Peterson DE, Schubert M, Keefe D, McGuire D, Epstein J et al. Clinical practice guidelines for the prevention and treatment of cancer therapy-induced oral and gastrointestinal mucositis. Cancer 2004;100:2026-46. 5. Volpato LE, Silva TC, Oliveira, TM, Sakai VT, Machado MA. Radiation therapy and chemotherapy-induced oral mucositis. Rev Bras Otorrinolaringol 2007;73:562-568. 6. Keefe DM, Schubert MM, Elting LS, Sonis ST, Epstein JB, Raber- Durlacher JE et al. Updated clinical practice guidelines for the prevention and treatment of mucositis. Cancer 2007;109: 820-31. 7. Arora H, Pai KM, Maiya A, Vidyasagr MS, Rajeev A. Efficacy of He- Ne Laser in the prevention and treatment of radiotherapyinduced oral mucositis in oral cancer patients. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2008;105:180 8. Lionel D, Christophe L, Marc A, Jean-Luc C. Oral mucositis induced by anticancer treatments: physiopathology and treatments. The Clin Risk Manag 2006;2:159-68. ___________End of Article__________
13 REVIEWARTICLE
IMPORTANCEOFINFORMEDCONSENTINDENTISTRY
1Dr.
Annie Mehnaz Mirza Access this Article Online SVS Institute of Dental Sciences, India
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1BDS,
Corresponding Author Dr. Annie Mehnaz Mirza E-Mail: annie.mirza24@gmail.com
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Abstract
The aim of this article is to provide fundamental information regarding consent when providing dental care. The change in attitude of patients with emphasis on being involved and informed of every aspect of care is not only apparent in adults but also when providing care for children and young adults. It is important for the dentist to be well informed of the fundamental process of consent, which exists under the law affecting both adults and minors in order to provide care within the legal framework. 2 consent are sometimes unclear in clinical work - the reasons for this are assessed and illustrated. Standards of good practice in obtaining informed consent are suggested.
Introduction
Patients informed consent is a legal regulation and a moral principle. It represents patients rights to take part in the clinical decisions concerning their treatment. In order to practice in a professionally responsible manner, dentists must assist patients to make well-informed decisions about treatment procedures. The importance of obtaining informed consent in dentistry is increasingly recognized for moral and legal arguments which are explored. Morally, patients have the right to self-determination and respect for it underpins the relationship of trust deemed so important for clinical success.3 Legally, this right is reinforced through the risk of dentists being sued for negligence if they do not adequately respect it. The practical implications of the doctrine of informed
How it is done
Dentists have a duty to explain clearly about the pros and cons of a treatment. That does not mean that he must engage in an explanation equal to the depth of three hours of dental continuing education! It does mean, however, that a dentist must inform, in laymans terms, the condition or disease present and the treatments available to the patient, whether or not the practitioner performs all of the treatments discussed. For example, a general dentist must discuss the option of implants as well as bridges and partial dentures, even if that dentist does not place or restore implants, if he plans to
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remove a tooth or two on the lower right quadrant. The patient must understand not only the importance of replacing the extracted teeth but all of the available options to do so as well. There are three essential components to valid consent: Competence: It means that the patient has sufficient ability to understand the nature of the treatment and the consequences of receiving or declining that treatment. Voluntariness: It means that the patient has fully agreed to have the treatment and there has been no coercion or undue influence to accept or decline the treatment. Information and knowledge: It means that sufficient comprehensible information is disclosed to the patient regarding the nature and consequences of the proposed and alternative treatments. All these three elements are interdependent but must be present for consent to be ethically and legally valid. procedures and prophylaxis, provided that full records are documented. 3. Written Consent: A written consent is necessary in case of extensive intervention involving risks where anesthesia or sedation is used, restorative procedures, any invasive or surgical procedures, administering of medications with known high risks etc. When the Patient disagrees As is often the case in the dental office, patients arrive in pain and simply want the pain to stop no matter what the consequences. In such cases, it is best to alleviate the pain with local anesthetic to allow a less clouded judgment and normal thought process to emerge. In the eyes of the law, a person cannot consent to anything if his or her judgment is impaired in any way. This was often meant to include drugs and alcohol, which remove the ability to make sound decisions, yet pain should also be included in this category since it too often impairs the ability to think in a rational manner. Patients have the ultimate say when it comes to treatment, but it is the practitioners duty to make sure all options for treatment are explored. In this case, a signed refusal protects the doctor by documenting the conditions found and the treatment options presented. This is called an Informed Refusal.4 A competent patient has a right to refuse medical treatment for any reason. It has been established that it does not matter if the decision is not what others would consider to be reasonable, nor does it matter if it leads to fatality as a result of the decision. What exactly is needed in the Informed Consent? It is not sufficient that a dentist simply document in the chart that he or she went over all risks of treatment and the patient understands. Specific risks must be written down, and patients must be given the opportunity to discuss with the doctor and question those issues which they do not understand. It should consist of a well formed questionnaire including but not limiting to:
Types of Informed Consent

Informed Consent is of three types: 1. Implied Consent: Implied consent refers to when a patient passively cooperates in a process without discussion or formal consent. The principles of good communication apply in these circumstances and health professionals need to provide the patient with enough information to understand the procedure and why it is being done. Implied consent does not need to be documented in the clinical record. 2. Verbal Consent: A verbal Consent is where a patient states their consent to a procedure verbally but does not sign any written form. This is adequate for routine treatment such for diagnostic
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care and consent for the child or young person should lay with his/her parents. Patients under the age of majority or adults with diminished mental capacity should have treatment consent obtained from a parent or legal guardian. The adult accompanying the pediatric patient may not be a legal guardian allowed by law to consent to medical procedures. Examples of this include a grandparent, stepparent, noncustodial parent or friend of the family. 6 Where a child requires treatment without a parent or legal guardian present: Telephone consent may be obtained. Where the child or minor is assessed as competent they may provide consent. Where a responsible adult (i.e. teacher, Grandparent) is with the child, evidence of parental consent to treatment must be sighted or parental consent obtained.
The proposed treatment plan (indicating to what extent it depends upon established versus relatively new or controversial procedures) and its cost. Likely prognosis, outcomes and benefits. Possible complications, side-effects and material risks inherent in the treatment. Possible alternative treatments and cost options. Likely consequences of no treatment. Any other aspects requested by the patient.5
This should be immediately followed by the patients signature/date, doctors signature/date and witnesss signature/date. Make sure that the patients name is legibly printed somewhere on the form since some signatures are illegible. In most cases, a consent form need be little more than one page for most dental procedures if it is organized well. When is Consent not required? In case of an emergency the treatment is a necessity and there is no written advance directive by the patient to the contrary. Treatments authorised by statute are medical treatments/interventions identified in law, including compulsory drug screening and certain procedures relating to mental health patients. Any medical treatment/intervention to be carried out or ceased as a result of a direction/order of the court. Valid informed consent by the patient is not required.
When problem arise with the child and parents with different opinions then, according to law a person with parental responsibility can always override decisions made by children. In case of an emergency, the health practitioner has a right to treat the patient without the consent.
Consent to Disclose/Release of Information

During the general consent to treatment process patients need to be made aware that their health information will be shared with the treating team within the hospital / health care facility and also to their General Practitioner (GP) as part of that treating team. And health information may also be released to third parties to ensure the provision of appropriate and continuing care. This should only occur with the specific consent of the patient without which there are
Consent for Children or minors

Obtaining consent for children is a difficult task. The primary responsibility for providing
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chances of the practitioner being sued for releasing the information.
References
1. Lewis Laska, Nashville, TN -Medical Malpractice Verdicts, Settlements and Experts. 2. Seema Lal, Consent in Dentistry, Pacific Health Dialog, Volume 10, 2003. 3. Dr. Jay Baxley, A Peer Reviewed article,Informed Consent 4. ACT - Consent to treatment, Patient safety and Quality Unit. 5. Australian Dental Association, Guidelines for good Dentistry, Consent for Care in Dentistry by Federal Council, 1999. 6. American Academy of Pediatric Dentistry- Guidelines of Informed Consent, 2005.
___________End of article____________
Conclusion
However, in dentistry, just as in medicine, unforeseen mishaps occur despite our best efforts. Therefore, it is just as important for dentists to obtain informed consent prior to every invasive and/or irreversible procedure. At first glance, most patients appear friendly and most dental procedures appear routine, but once a procedure goes wrong, an unhappy patient with a skilful attorney can become a dentists worst nightmare. A signed, written informed consent may be the only evidence that the mishap that occurred was a foreseeable risk acknowledged by the dentist and accepted by the patient. Although obtaining informed consent may at first seem awkward, cumbersome, and time-consuming, it may very well save a practitioner countless hours in the courtroom and thousands of rupees in legal fees should some mishap occur.
17 REVIEWARTICLE
MICROENDODONTICS:AGGRANDIZEMENTOFROOTCANAL TREATMENT
Sameer D Jain1 M.G.Vs K.B.H Dental College and Hospital [Mahatashtra University of Health Sciences (M.U.H.S)], Mumbai Agra Highway, Panchavati, Nashik, Maharashtra, India
1BDS,
Corresponding Author Sameer D Jain A-1 Kaustubh Park, SVP Road, Borivali-W, Mumbai-400103, Maharashtra, India Contact no. 022 28944364 +91 9892490644 +91 9029297516 Fax 022 28954657 E-Mail: sam777_25@yahoo.co.in
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Abstract
This article presents a review of the history of the dental-operating microscope and how it experienced slow acceptance. Following its introduction in 1982, it wasnt until 1997 that microscopy training became mandatory for Advanced Specialty Education Programs in Endodontics. Undoubtedly, microscopic enhanced endodontics ultimately reshaped clinical practice and created a potential for a higher standard of care.
18 Introduction
It may seem surprising that the microscope is not a high-tech instrument. It has been used in the medical field for over 50 years. According to the Zeiss Company, the microscope was first introduced to otolaryngology around 1950, and then to neurosurgery in the 1960s, and to endodontics in the early1990s (1). Dentistry, therefore, is about 40 years behind medicine in this respect. As in medicine, the incorporation of the microscope in clinical endodontics has had profound effects on the way endodontics is done and has changed the field fundamentally. For this reason, the 1998 American Dental Association accreditation requirement change states that all accredited United States postgraduate programs must teach the use of the microscope in nonsurgical and surgical endodontics (2). This was a giant step forward in the advancement of endodontics. This article outlines the key prerequisites for the use of the microscope in nonsurgical endodontic procedures. There are many microscopes on the market; the three most popular ones are presented in Fig. 1. Rubber dam placement The placement of a rubber dam prior to any endodontic procedure is an absolute requirement for sterility purposes. This technique is taught at all dental schools. In endodontics, however, the purpose is greater. Here, the rubber dam placement is necessary because direct viewing through the canal with the microscope is difficult, if not impossible. A mirror is needed to reflect the canal view that is illuminated by the focused light and magnified by the lens of the microscope. If the mirror were used for this purpose without a rubber dam, then the mirror would fog immediately from the exhalation of the patient. Thus, the powerful microscope magnification and illumination would be rendered totally useless for the necessary visualization of the chamber floor and the canal anatomy. To absorb reflected bright light and to accentuate the tooth structure, it is recommended to use blue or green rubber dams (Fig. 2).
Fig. 2: The use of a rubber dam is essential for effective microscope use Fig. 1: The three most popular microscopes in endodontics
Methods
Prerequisites for the use of the microscope in nonsurgical endodontics:
Indirect view and patient head position. As mentioned previously, it is nearly impossible to view the pulp chamber directly under the microscope. Instead, the view seen through the microscope lens is a view reflected by way of a mirror. To maximize the access and quality of the view by this indirect means, the
19
position of the patient (especially the head position) is important (Fig. 3). The optimum angle between the microscope and the mirror is 450, and the clinician should be able to obtain this angle without requiring the patient to assume an uncomfortable position. The maxillary arch is rather easy for indirect viewing. Basically, the patients head is adjusted to create a 900 between the maxillary arch and the binocular (Fig. 4). In this position, the mirror placement will be close to 450 for best viewing (3). endodontic instruments. Readjusting the mirror will necessitate refocusing of the microscope, making the entire operation timeconsuming and, at times, frustrating. This is especially true during a lengthy perforation repair. With practice, however, the correct placement of the mirror will become automatic. Some key instruments The ability to locate hidden canals is the most important and significant benefit gained from using the microscope. To do this effectively and efficiently, clinicians must use specially designed microinstruments. An explorer can pick the entrance of a canal under the microscope, but negotiating the canal with a file can be challenging because there is only a tiny space between the mirror and the tooth for a finger with a file to move around. Files specially designed by Maileffer, called microopeners, have with different sized tips and can be extremely useful (Fig. 5). These hand-held files allow the clinician to initially negotiate the canal, verifying that the catch is truly a canal. After the canal is located in this manner, clinicians can instrument the canal normally without the microscope. The use of GatesGlidden burs to enlarge the canal entrance prior to full instrumentation, however, can be easily achieved under the microscope, facilitating the subsequent steps of canal instrumentation.
Fig. 3: Patients should wear protective dark glasses and have support for the neck, such as a moldable pillow
Fig. 4: Positioning the microscope. Notice the ergonomics of the clinician and comfortable patient position
Mouth mirror placement It is always a good idea to use the best mirror for this purpose. If a rubber dam has been placed, then the mirror must be placed away from the tooth within the confines of the rubber dam. If the mirror is placed close to the tooth, then it will be difficult to use other
Fig. 5: Micro-openers by Maillefer are ideal instruments for exploration of hidden canals at high magnification
20
It has been found that nearly an astounding 50% of all molars (maxillary and mandibular) have a fourth canal, more than 30% of all premolars have a third canal, and close to 25% of all anterior teeth have two canals. What was considered a rare exception in the past has become a routine finding when using the microscope. Considering this as the benefit of using the microscope for endodontic procedures is obvious. There are teeth where the canal bifurcates at 3 to 5 mm into the canal and in the maxillary second molar, where the MB and DB are in very close proximity of each other; the microscope is an invaluable tool in clearly detecting the bifurcation and the two separate canals (4). Management of calcified canals With normal vision or low-power loupes, calcified canal in the pulp chamber is not detectable. When the calcified canal is looked at through the microscope at high magnification, however, the difference in the color and texture between the calcified canal and the remaining dentin can be easily seen. Careful probing and use of ultrasonics with CPR or Buc tips (Obtura/Spartan, Fenton, Missouri) will allow clinicians to detect and negotiate the calcified canal easily (Fig. 7). Sometimes in these cases, the ultrasonic preparation of the canal or canals has to go as far as a couple of millimeters short of the apex. Again, the microscope allows the clinician to detect and prepare conservatively, and not to gouge the healthy dentin structures (Fig. 8). Perforation repair Perforation does occasionally occur no matter how carefully the tooth is accessed for endodontic therapy. When a perforation occurs, the microscope is the key instrument to identify and evaluate the damaged site.
For what procedures is the microscope really essential? Some enthusiasts claim that the microscope must be used for all steps of nonsurgical endodontic procedures. This may a noble idea, but in reality, it is not needed or desired. A clinician must consider the benefit/risk ratio when using the microscope. The following procedures are those that benefit from the use of the microscope. Diagnosis The microscope is an excellent instrument to detect microfractures that cannot be seen by the naked eye or by loupes. Under 16_ to 24_ magnification and focused light, any micro fracture can be easily detected (Fig. 6). Methylene blue staining of the microfracture area assists this effort greatly. A persistently painful tooth after endodontic therapy may be due to an untreated missing canal (eg, MB2 in a maxillary molar). Re-examination of the chamber at high magnification under the microscope may locate the missing canal (see the article by Kim elsewhere in this issue [Fig. 5]). Locating hidden canals The most important utility of the microscope in nonsurgical endodontics is locating hidden canals. The canal anatomy is extremely complex. All endodontic textbooks have information on molar teeth with three canals, premolars with two canals, and anterior teeth with one canal. Often, dental anatomy is not that predictable.
Fig. 6: Microfracture detected under the microscope (A) and the same tooth after extraction (B) Arrows identify the fracture line.
21
Retrieval of broken files With the more frequent use of nickel-titanium rotary files in general dentistry, the incidence of file separation within the canals has increased. When the file is broken at the apex, the microscope cannot be of help. If the file breaks within the coronal half of the canal, however, then the microscope is essential to guide the clinician to retrieve the broken files. In this manner, the broken file can be removed while minimizing the damage to the surrounding dentin. Final examination of the canal preparation It takes a simple step to see whether a canal is completely cleaned. Under the microscope, a small amount of sodium hypochlorite, a popular irrigation solution, is deposited into the canal and observed carefully at high magnification. If there are bubbles coming from the prepared canal, then there is still remnant pulp tissue in the canal. In short, the canal needs more cleaning.
Fig. 7: Buc tips (Obtura/Spartan) are ideal ultrasonic instruments for cleaning the pulp chamber and floor for clear viewing of the canals.
Discussion & Conclusion

Cost versus patient benefit Many of the practitioners who perform endodontic procedures and do not yet own a dental microscope are still evaluating the benefits of its use. Practicality is the key concern. How does one recoup the cost of the capital expenditure and the cost and time associated with training? Are the clinical benefits worth the expenditure of time and money? To address the critical cost and efficiency issue, clinicians should take an intensive training course at the very beginning to make them comfortable with handling the microscope and with working underneath it. Clinicians should also become totally committed to using the microscope in each of their treatment cases, not just selected ones. This practice is the fastest route toward proficiency and the best way to maximize the return on investment. In addition to clinical benefits associated with the use of the microscope in endodontics, after the initial learning
Fig. 8: Access preparation and management of calcified canals at a high magnification under the microscope (A F)
The results of a careful inspection will be the basis for which the preparation of the perforation repair will be made. Briefly, the microscopic procedure is to place a matrix precisely, just outside of the perforation site (i.e. just exterior of the root substance). The matrix can be calcium sulfate or resorbable collagen. After the matrix is placed, mineral trioxide aggregate is packed against the matrix. This procedure requires delicate and careful handling of the materials so as not to extrude, overfill, or underfill. The microscope is essential for this procedure.
22
curve, endodontic procedures can be done in less time because of the greater visibility of the root canal anatomy. Procedural errors can be greatly reduced (5), if not eliminated, and complicated cases become less so under the microscope. Another benefit of the microscope is the flexibility with documentation. Compared with intraoral video cameras, microdental images can be captured on computer or digital camera. The information can then be shared with referring dentists or patients and the images are, of course, also required information for the patient record. 3. Branson BG, Bray KK, GadburyAmyot C, et al. Effect of magnification lenses on student operator posture. J Dent Educ. 2004;68:384-389. Valachi B. Vision quest: finding your best working distance when using loupes. Dental Practice Report. 2006;4:49-50. 4. Spear FM. One clinicians journey through the use of magnification in dentistry. Advanced Esthetics and Interdisciplinary Dentistry. 2006; 2:30-32. 5. Cuomo GM. Posture-directed vs. image-directed dentistry: ergonomic and economic advantages through dental microscope use. http://www. heryschein.com/usen/dental/services/ce hp/HomeStudy.aspx. Published April 27, 2006. Accessed November 14, 2008.
References
1. Syngcuk Kim. Modern Endodontic Practice: Instrumentsand Techniques, Dent Clin N Am 2004; 48: 19. 2. Syngcuk Kim, Seungho Baek. The microscope and endodontics. Dent Clin N Am 2004; 48: 1118.
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of
article_______
23 CASEREPORT
ENDODONTIC THERAPY IN A 3ROOTED MANDIBULAR SECONDMOLAR:ACASEREPORT

Dr. Saurabh S. Chandra1, Dr. Supriya Chandra 2, Dr. Nilofer Hussain3, Dr. Anurag Ahuja4 MDS, Assistant Professor, Dept. Of Conservative Dentistry & Endodontics, School Of Dental Sciences, Sharda University, Greater Noida, India
1
Corresponding Author Dr. Saurabh S. Chandra MDS, Assistant Professor, Dept. Of Conservative Dentistry & Endodontics, School Of Dental Sciences, Sharda University, Greater Noida, India Email: saurabhchandra@yahoo.com Access this Article Online
MDS, Senior Lecturer, Dept. Of Periodontology, Sree Bankey Bihari Dental College, Ghaziabad, India
2
www.idjsr.com
Intern, School of Dental Sciences, Sharda University, Greater Noida, India

3
School of Dental Sciences, Sharda University, Greater Noida, India
4 Intern,
Quick Response Code
Abstract
A rare case of a three-rooted mandibular permanent second molar in a 21-year-old male patient is reported. After clinical and radiographic examination, four separate root canal orifices were detected. A mesial shift radiograph confirmed the presence of an additional disto-lingual root. The tooth was treated by orthograde endodontic treatment in two visits. The case report underlines the importance of complete knowledge about root canal morphology and possible variations that exist in mandibular molars; coupled with full clinical and radiographic examination, in order to increase the ability of clinicians to treat root canal aberrancies. Aim: Clinicians should be aware of these unusual root morphologies in the mandibular second molars. The initial diagnosis of a third root before root canal treatment is important to facilitate the endodontic procedure, and to avoid missed canals. Keywords: Dental Anomalies, Mandibular molars, Radix Entomolaris, Three rooted mandibularmolar
24
Introduction
Orthograde endodontic treatment comprises of meticulous cleaning & shaping, disinfection of the entire root canal space followed by a three dimensional obturation. Root canals may be left untreated during endodontic therapy if the clinician fails to identify their presence, particularly in teeth with anatomical variations or extra root canals.1,2 Comprehensive knowledge of the presence of unusual root canal anatomy and morphology is important for successful dental practice and for identifying features of anthropological significance. It is commonly acknowledged that both deciduous and permanent mandibular molars display several anatomical variations. The majority of mandibular second molars are two-rooted with two mesial and one distal canal.3 However, the number of roots and root canals may vary. An additional third root, first mentioned in the literature by Carabelli, is called the Radix Entomolaris (RE).4 This supernumerary root is located distolingually in mandibular molars, mainly first molars. An additional root at the mesiobuccal side is called the radix paramolaris (RP).1,4-6 The identification and external morphology of these root complexes, containing a lingual or buccal supernumerary root, are described by Carlsen and Alexandersen.6 This supernumerary root (RE) has a frequency of less than 4% in Caucasians, 2.8% in African populations, whereas in populations with Mongoloid traits (Chinese, Indians and Eskimos) this macrostructure occurs with a frequency between 5% and 30%.1,2,6 In these populations, RE is considered to be a normal morphological variant and can be seen as an Asiatic trait.1 The aim of this paper is to report a mandibular second molar featuring
with three roots, which is a rare clinical entity.
Case Report
A 21-year-old southeast-Asian male patient reported to the Department of Conservative Dentistry and Endodontics, Ragas Dental college & Hospital, Chennai with the chief complaint of spontaneous dull pain in the lower right region for the preceding few months. His medical history was noncontributory. An intraoral clinical examination revealed a deep carious lesion in the right mandibular second molar (tooth #31) with tenderness on percussion. Radiographic and sensitivity tests were performed that led to a diagnosis of irreversible pulpitis with apical periodontitis, necessitating endodontic treatment (Fig. 1). The tooth was anesthetized using 2% lignocaine with 1:100,000 adrenalin (Lignox; Indoco Remedies, Mumbai, India) and isolated under rubber dam (Hygenic Dental Dam, Coltne Whaledent, Germany). Caries was excavated, and an adequate endodontic access cavity was made using an Endo Access bur (Dentsply Maillefer, Ballaigues, Switzerland). The chamber was flushed with 3% sodium hypochlorite (Dentpro, Chandigarh, India) to remove the debris. Observation via a conventional access cavity revealed the presence of 3 canal orifices, 2 mesial and 1 distal. The dentinal map on the floor of the chamber was traced and explored using a DG 16 endodontic explorer (Hu-Friedy, Chicago, IL) following which the pulp tissue was extirpated using barbed broaches (Dentsply Maillefer, Tulsa, OK). On inspection with 2.5 magnification prismatic loupes (Seiler, St. Louis, MO), a dark line was observed between the distal canal orifice and the distolingual corner of the pulp chamber floor. At this corner overlying dentin was removed with a diamond bur with
25
a noncutting tip (Diamendo, Dentsply Maillefer) and a second distal canal orifice was detected (Fig.2). Canal patency was established using a #10 K file (Mani, Tochigi, Japan). The canal length was determined electronically using an electronic apex locator (Root ZX II; J. Morita, Tokyo, Japan) and subsequently verified with an intraoral periapical radiograph. Root canal instrumentation was performed with ProTaper Ni-Ti rotary files (Dentsply Maillefer, Tulsa, OK) using a crown-down technique. During preparation, EDTA (Glyde File Prep, Dentsply Maillefer, Tulsa, OK) was used as a lubricant and the root canals were disinfected with 3% sodium hypochlorite solution (Dentpro, Chandigarh, India). The canals were finally rinsed with saline (Marck Biosciences, Gujrat, India), dried with sterile absorbent paper points (Dentsply Maillefer), and an intra canal medicament of calcium hydroxide was place. Initially, the distolingual root canal was thought to be a second canal in one distal root. Radiographically the outlines of the distal root(s) were unclear; however, the unusual location of the orifice far to the distolingual indicated a supernumerary root, and the presence of an RE was confirmed on the postoperative radiograph. The patient was recalled after a week and the canals were obturated with cold laterally condensed guttapercha (Dentsply Maillefer) using AH Plus resin sealer (Dentsply Maillefer). A postoperative radiograph (Fig. 3) was taken; the opening cavity was sealed with posterior composite (Solare, GC Fuji, Japan) and the patient was scheduled for a permanent coronal restoration. supernumerary root can be found on the first, second and third mandibular molar, occurring least frequently on the second molar.1 There are various case reports of mandibular first molars featuring an RE. On the contrary, RE in the mandibular second molars has been seldom reported. Poorni et al. reported a case of mandibular second molar featuring an RE confirmed using spiral CT.7 The RE is located distolingually, with its coronal third completely or partially fixed to the distal root. The dimensions of the RE can vary from a short conical extension to a mature root with normal length and root canal.1 In most cases the pulpal extension is radiographically visible. In general, the RE is smaller than the distobuccal and mesial roots and can be separate from, or partially fused with, the other roots. A classification by Carlsen and Alexandersen describes four different types of RE according to the location of the cervical part of the RE: types A, B, C and AC.6 Types A and B refer to a distally located cervical part of the RE with two normal and one normal distal root components, respectively. Type C refers to a mesially located cervical part, while type AC refers to a central location, between the distal and mesial root components. This classification allows for the identification of separate and nonseparate RE. The etiology behind the formation of the RE is still unclear.1 In dysmorphic, supernumerary roots, its formation could be related to external factors during odontogenesis, or to penetrance of an atavistic gene or polygenetic system (atavism is the reappearance of a trait after several generations of absence). In eumorphic roots, racial genetic factors influence the more profound expression of a particular gene that results in the more pronounced phenotypic manifestation.5,6 Curzon suggested that the three-rooted molar trait has a high degree of genetic penetrance as its dominance was reflected in the fact that
Discussion
Anatomical variations of mandibular molars are documented in the literature. Nonetheless, variations of the anatomy of the root canal system in molars are not appreciated by a great number of general practitioners. A
26
the prevalence of the trait was similar in both pure Eskimo and Eskimo/ Caucasian mixes. position and the other taken either 30 mesially or distally. This buccal object rule has also been called Clarks rule, the same lingual, opposite buccal (SLOB rule) and Waltons projection. It is imperative that a comprehensive pre-operative radiographic evaluation is done prior to initiation of endodontic therapy.
The location of the orifice of the root canal of an RE has implications for the opening cavity. The orifice of the RE is located disto- to mesiolingually from the main canal or canals in the distal root.1 An extension of the triangular opening cavity to the (disto) lingual results in a more rectangular or trapezoidal outline form. If the RE canal entrance is not clearly visible after removal of the pulp chamber roof, a more thorough inspection of the pulp chamber floor and wall, especially in the distolingual region, is necessary. Visual aids such as a surgical loupes, or dental microscope can be useful. A dark line on the pulp chamber floor can indicate the precise location of the RE canal orifice. The distal and lingual pulp chamber wall can be explored with an angled probe to reveal overlying dentin or pulp roof remnants masking the root canal entrance. The calcification, which is often situated above the orifice of the RE, has to be removed for a better view and access to the RE. An initial relocation of the orifice to the lingual is indicated to achieve straightline access. 8 These anatomic variations in distal root anatomy may be identified through careful reading of angled radiographs. Slowley has demonstrated how difficult it is to detect extra roots, let alone extra canals.9 On the contrary, completing a thorough radiographic study of the involved tooth with exposure from three different horizontal projections, the standard buccal-to-lingual projection, 20 from the mesial, and 20 from the distal reveals the basic information regarding the anatomy of the tooth in order to perform endodontic treatment.8,9 However, using the buccal object rule with two radiographs with different horizontal angulations may suffice to determine the position of a lingual root. One of these radiographs is taken in the orthoradial
Conclusion
Knowledge of both normal and abnormal anatomy of the mandibular molars dictates the parameters for execution of root canal therapy and can directly affect the probability of success. Therefore, practitioners must be familiar with all molar abnormalities, as well as their prevalence.
References
1. Calberson FL, De Moor RJ, Deroose CA. The radix entomolaris and paramolaris: clinical approach in endodontics. J Endod 2007;33:5863. 2. De Moor RJ, Deroose CA, Calberson FL. The radix entomolaris in mandibular first molars: an endodontic challenge. Int Endod J 2004;37:789 99. 3. Skidmore AE, Bjorndal AM. Root canal morphology of the human mandibular first molar. Oral Surg Oral Med Oral Pathol 1971;32:778-784 4. Carabelli G. Systematisches Handbuch der Zahnheilkunde. 2nd ed. Vienna: Braumller and Seidel 1844; 114. 5. Bolk L. Bemerkungen ber Wuzelvariationen am menschlichen unteren Molaren. Zeitschrift fr Morphologie Anthropologie 1915;17:60510. 6. Carlsen O, Alexandersen V. Radix entomolaris: identification and
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7. morphology. Scan J Dent Res. 1990;98:16373. 8. Poorni S, Senthilkumar A, Indira R. Radix entomolaris in mandibular molars confirmed using spiral CT: a case report. Endond Prac Today 2010;4 9. Ingle JI, Heithersay GS, Hartwell GR et al. Endodontic diagnostic procedures. In: Ingle JI, Bakland LF, eds. Endodontics, 5th edn. Hamilton, London, UK: BC Decker Inc., 2002;20358. 10. Slowley RR. Radiographic aids in the detection of extra root canals. Oral Surgery, Oral Medicine and Oral Pathology 1974;37, 76272.
Legends Fig. 1 Pre-operative radiograph Fig. 2 View of Pulp chamber Fig. 3 Post operative radiograph
Fig. 1
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Fig. 2
Fig. 3 _____________End of article______________
29 ORIGINALARTICLE
SEMEVALUATIONOFEFFECTOF37%PHOSPHORICACIDGEL, 24%EDTAGELAND10%MALEICACIDGELONTHEENAMEL ANDDENTINFOR15AND60SECONDS:ANINVITROSTUDY

Narendra Parihar1, Manish Pilania 2
1BDS,
Jodhpur Dental Hospital, Jodhpur
College
General
2. Manish Pilania G-43, Shastri Nagar, Jodhpur Contact no. (+91)9461055068 Email: manishpilania3@gmail.com
2Intern,
Department of Conservative Dentistry and Endodontics, Jodhpur Dental College General Hospital, Jodhpur, Rajasthan, India
www.idjsr.com
Corresponding Authors 1. Narendra Parehar Khanda Falsa, Jalori Gate, Jodhpur. Contact no. (+91)9799108142 Email: narenparihar.np@gmail.com
Quick Response Code
Abstract
Background: The purpose of this study was to investigate the relationship between etching of enamel and dentin with different acids: 37% phosphoric acid, 10% maleic acid and 24% EDTA, at different etch durations of 15 and 60 seconds; so as to analyze the surface characteristics of etched enamel, diameter of the dentinal tubules and the depth of demineralization in the tubules under scanning electron microscope (SEM). Method: Thirty freshly extracted maxillary and mandibular premolars, indicated for orthodontic extraction were selected from patients in the age group of 14 to 21 years. The teeth were randomly divided into 3 groups of 10 teeth each and were etched with 37% phosphoric acid, 24% EDTA gel and 10% maleic acid gel respectively for 15 and 60 seconds. The samples were then split along their long axes, dehydrated and sputtered with palladium gold. The sputtered specimens were examined under scanning electron microscope. Results: Acid etching causes various types of etching patterns in enamel indicating preferential dissolution of the enamel prisms. With 37% phosphoric acid, type 2 etching pattern is seen; with 10% maleic acid, type 1 etching pattern is predominant and etching with 24% EDTA leads to type 4 etching pattern. In dentin, etchants widen the dentinal tubule orifices due to demineralization of peritubular dentin and this demineralization extends deep into the dentinal tubules for varying depths depending upon the type of acid used and time of its application. No statistically significant difference exists in the widening of the dentinal tubule orifices between the group I (37% phosphoric acid) and group III (10% maleic acid) specimens. Conclusion: It can be suggested that 15 seconds etching with a milder acid like 10% maleic acid instead of 37% phosphoric acid is sufficient to obtain adequate bond strength because there is no significant difference within the observational parameters, except for the depth of demineralization in tubules. Additional depth is unnecessary because the adhesive systems cannot penetrate completely into the dentinal tubules, leading to nanoleakage.
30 Introduction
An ideal restorative material would be the one which chemically bonds to the tooth and has strength comparable to that of the tooth structure. In 1955, Buonocore instituted the use of 85% phosphoric acid solution to cause selective decalcification of tooth structure. This produced microporosities in the enamel, increased the surface area, as well as enhanced wettability of the surface providing an intimate contact between tooth and restoration thereby changing the retention form from mechanical to micromechanical. In 1979, Fusayama introduced and popularized the concept of etching of dentin.3 Stronger acids like phosphoric acid not only decalcify the enamel and dentin surfaces but also demineralize in depth to a greater extent. The increased depth of demineralization is not essentially required because the adhesive systems are not able to penetrate till the complete depth, leading to nanoleakage and incessant degradation.6 Dentin being a vital tissue and containing more organic content than enamel, requires use of milder acids (10% maleic acid and 24% EDTA) so as to prevent damage to micromorphological structure and preserve the integrity of the collagenous mass as they do not denature it.2
Materials and Methods

Thirty intact, caries free maxillary and mandibular premolars extracted due to orthodontic reasons were used. These were extracted in the Department of Orthodontics, Jodhpur Dental College General Hospital, Jodhpur, from patients in the age group of 14 to 21 years. After extraction, the teeth were thoroughly cleaned using pumice slurry, and the roots were sheared off from the crown at the labial cementoenamel junction with a diamond abrasives coated safe sided disc. The teeth were then stored in normal saline at 4C. At the start of the study, the buccal surfaces of the premolars were ground wet on 320 grit and 600 grit silicon carbide paper till the dentin was exposed to create a flat surface on the enamel and dentin. The samples were then sectioned in the middle along their long axis through the lingual surface with a diamond abrasive coated safe sided disc 1 1.5 mm short of the buccal flat surface. The samples were rinsed thoroughly in normal saline to clear off any debris. The following materials were used for etching of the specimens:* * The group I, II and III were further divided into two
subgroups of 5 teeth each. Ia Ib IIa IIb IIIa IIIb

5 specimens to be etched with 37% phosphoric acid gel for 15 seconds. 5 specimen to be etched with 37% phosphoric acid gel for 60 seconds. 5 specimens to be etched with 24% EDTA gel for 15 seconds. 5 specimens to be etched with 24% EDTA gel for 60 seconds. 5 specimens to be etched with 10% maleic acid gel for 15 seconds. 5 specimens to be etched with 10% maleic acid gel for 60 seconds.
37% phosphoric acid gel. 24% Ethylenediamine (EDTA) gel. 10% maleic acid gel. tetracetic acid
The etchant gels were applied on the flat buccal surfaces with the help of a brush, the gel was rinsed off from the teeth with 10ml distilled water for 20 seconds. The specimens were then sectioned into two halves with a sharp chisel and mallet by placing the chisel into the groove which had been prepared along the long axis of the samples. The sectioned specimens were utilized for analyzing the depth of demineralization in dentin by the etchants.
The prepared samples were randomly divided into three groups:Group I, Group II and Group III.
31
Photograph 1: Armamentarium used for the study
Photograph 2: Materials used in the study
The samples were transferred to small bottles containing graded concentrations of ethyl alcohol (60% to100%). The samples remained in each alcohol concentration for two hours. The dehydrated samples were removed from 100% ethyl alcohol and were mounted on aluminium stubs and placed in vacuum chamber to desiccate them completely.
Samples were viewed under scanning electron microscope (LEO) at various magnifications. The magnifications selected were:For enamel For dentin -
x 3,000 x 2,000
32
Photograph 3: Scanning Electron Microscope
The parameters to be observed were:*
The etching patterns on enamel surface.

categorized according to Galil & Wrights classification4: The etching patterns were
2 pattern together with regions in which the pattern of etching could not be related to prism morphology.
Type 4 Pitted enamel surface. Type 5

Flat smooth surface of enamel without microirregularities.
Type 1
Preferential dissolution prism cores resulting honeycomb appearance
of the in a
Type 2 Etch pattern showing preferential

dissolution of the prism peripheries giving a cobblestone appearance leaving prism cores relatively unaffected.
* *
Diameter of the widened dentinal tubules Depth of demineralization in the dentinal tubules.
The diameter of the tubules and the depth of demineralization were measured in m ()
Type 3
A more random etch pattern, areas of which corresponded to type 1 and
33 Statistical Analysis
Using the standard deviation, the student t-test was applied The probability value (p value) was kept constant at 5% significance STATISTICAL ANALYSIS FOR THE WIDTH OF LOSS OF ENAMEL PRISM CORE / PERIPHERY Intragroup comparison Mean Standard Deviation Standard Error T-value Status p<0.05

significant
p> 0.05
insignificant
I II III Ia Ib IIa IIb IIIa IIIb 0.39 0.54 0.00 0.00 3.30 4.29 0.0554 0.2040 0.00 0.00 0.9758 1.5614 0.0248 0.0912 1.65 -0.4364 0.6983 1.195
Insignificant
Insignificant
STATISTICAL ANALYSIS FOR DIAMETER OF THE OPENED DENTINAL TUBULES Intragroup comparison Mean Standard Deviation Standard Error T-value Status p<0.05
significant
p> 0.05
insignificant
I II III Ia Ib IIa IIb IIIa IIIb 2.99 3.87 1.94 2.68 2.93 3.33 0.8450 1.3881 0.3837 0.2663 0.4168 0.3671 0.3779 0.6208 0.1716 0.1191 0.1864 0.1642 1.208 3.543 1.626
Insignificant Significant Insignificant
STATISTICAL ANALYSIS FOR DEPTH OF DEMINERALIZATION IN THE TUBULES Intragroup comparison Standard Deviation Standard Error T-value Status p<0.05
Mean
significant
p> 0.05
insignificant
I II III Ia Ib IIa IIb IIIa IIIb 8.87 11.48 0.00 3.92 7.09 8.83 1.0405 2.0587 0.00 0.8050 0.5575 1.5382 0.4653 0.9207 0.3600 0.2493 0.6879 2.532 10.894 2.375
Significant Significant Significant
34 Results
All etchants changed the micromorphological appearance of enamel and dentin surfaces. Etching of enamel with 37% phosphoric acid gel resulted in a 'cobblestone' appearance of the etched surfaces due to preferential dissolution of the peripheries of enamel prisms (photographs no. 4 and 5). This type of etching is classified as type 2 etching pattern.4 On dentinal surface, phosphoric acid gel removed the smear layer and caused widening of the dentinal tubules (photograph no. 6). The widening of the tubule orifices occurs due to demineralization of peritubular dentin. The demineralization extends into the depth of tubules giving a 'funneled' effect (photographs no. 8 and 9). The dentinal surfaces treated for 15 and 60 seconds showed particulate residue. This surface residue is possibly silica which is used to thicken the etching gel (photographs no. 6 and 7). ETCHING OF ENAMEL WITH 37% PHOSPHORIC ACID Effect of 37% Phosphoric Acid Gel on Prepared Specimens for 15 Seconds. Sample No. Width of loss of enamel prisms periphery 0.33 0.34 0.44 0.38 0.45 0.39 Diameter of opened dentinal tubules 2.56 2.9 4.3 2.03 3.15 2.99 Table: 1 Depth of demineralization in tubules (Type 2 Etching Pattern)
1. 2. 3. 4. 5. Mean
7.67 8.58 10.43 9.26 8.4 8.86
Photograph 4: Etching Time-15 Seconds

Effect of 37% Phosphoric Acid Gel on Prepared Specimens for 60 Seconds. Sample No. Width of loss of enamel prisms periphery 0.44 0.36 0.50 0.89 0.53 0.54 Diameter of opened dentinal tubules 2.67 3.90 6.22 3.16 3.38 3.87 Table: 2 Depth of demineralization in tubules
1. 2. 3. 4. 5. Mean
9.64 9.31 11.96 14.34 12.15 11.48
Photograph 5: Etching Time- 60 Seconds
35
ETCHING OF DENTIN WITH 37% PHOSPHORIC ACID (Widened Dentinal Tubule Orifices) (Particulate Residue on Surface) ETCHING OF DENTIN WITH 37% PHOSPHORIC ACID GEL (Depth of Demineralization in Tubules)
Photograph 6: Etching Time- 15 Seconds Photograph 8: Etching time - 15 seconds
Photograph 7: Etching Time- 60Seconds
Photograph 9: Etching time - 60 seconds
Effect of 24% EDTA gel on enamel after 15 and 60 seconds etching was comparatively insufficient. The surface micromorphology depicted pitted enamel surface which falls into the category of type 4 etching pattern (photographs no. 10 and 11). The dentinal surfaces after 15 seconds and 60 seconds etching were smooth and debris free. The dentinal micrmorphology showed presence of peritubular dentin around the tubule openings in both the subgroups etched with EDTA, indicating its partial
or selective demineralization (photographs no. 12 and 13). However no discernible depth of demineralization was observed in the specimens.
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Effect Of 24% EDTA Gel for 15 Seconds Application on Prepared Specimens. Sample No. Width of loss of enamel prisms core / periphery 0.00 0.00 0.00 0.00 0.00 0.00 Diameter of opened dentinal tubules Depth of demineralization in tubules
1. 2. 3. 4. 5. Mean
1.73 2.54 1.52 2.01 1.88 1.94 Table : 3
0.00 0.00 0.00 0.00 0.00 0.00
Effect Of 24% EDTA Gel for 60 Seconds Application on Prepared Specimens Sample No. Width of loss of enamel prisms core / periphery 0.00 0.00 0.00 0.00 0.00 0.00 Diameter of opened dentinal tubules Depth of demineralization in tubules
ETCHING OF DENTIN WITH 24% EDTA GEL (Open Dentinal Tubules)
1. 2. 3. 4. 5. Mean
2.76 2.59 2.29 3.02 2.72 2.67 Table : 4
3.7 5.14 3.85 2.9 4.02 3.92
ETCHING OF ENAMEL WITH 24% EDTA GEL (Type 4 Etching Pattern)
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ETCHING OF DENTIN WITH 24% EDTA GEL (Depth of Demineralization in Tubules)

With 10% maleic acid gel, preferential loss of the prism cores was evident. The surface topography of the etched enamel resembled that of a 'honeycomb' (photographs no. 16 and 17) and is categorized as type 1 etching pattern (according to Galil and Wright's Classification). This study also showed that acid etching with 10% maleic acid for 15 and 60 seconds removed the smear layer and widened the dentinal tubule orifices. The surface morphology was that of a smooth, debris free surface (photographs no. 18 and 19)
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EFFECT OF 10% MALEIC ACID GEL APPLIED FOR 15 SECONDS ON PREPARED SPECIMENS. Sample No. Width of loss of enamel prisms core. 3.56 3.67 2.19 4.61 2.49 3.30 Diameter of opened dentinal tubules 2.62 3.41 2.57 3.35 2.68 2.93 Table: 5 Depth of demineralization in tubules ETCHING OF ENAMEL WITH 10 % MALEIC ACID GEL (Type 1 Etching Pattern)
1. 2. 3. 4. 5. Mean
7.32 6.78 7.04 7.90 6.43 7.09
EFFECT OF 10% MALEIC ACID GEL APPLIED FOR 60 SECONDS ON PREPARED SPECIMENS Sample No. Width of loss of enamel rods periphery 2.45 5.2 4.76 6.13 2.9 4.29 Diameter of opened dentinal tubules 3.52 2.99 3.8 2.93 3.41 3.33 Table: 6 Depth of demineralization in tubules
1. 2. 3. 4. 5. Mean
6.91 11.02 8.02 9.4 8.81 8.83
ETCHING OF DENTIN WITH 10 % MALEIC ACID GEL (Widened Dentinal Tubule Orifices)

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Photograph 19: Etching time - 60 seconds Photograph 21: Etching time - 60 seconds
ETCHING OF DENTIN WITH 10% MALEIC ACID GEL (Depth of Demineralization in Tubules)

bonding to dentin remarkably problematic. The higher organic content of dentin predisposes it to Discussion denaturation and weakening of the collagenous mass. Phosphoric acid gel is a strong acid with pH = The objective of etching enamel is to create 1 and dissociation constant, pKa = 2.1. Maleic acid microporosities for resin penetration. Dentinal gel is an organic acid with higher molecular weight, etching removes the smear layer and smear plugs pH = 2.9 and dissociation constant pKa = 1.8. EDTA along with demineralization of the surface. It also is a powerful organic chelating agent. It is odorless, exposes both intertubular and peritubular collagen.5 crystalline white powder with pKa = 6.1 and neutral Etching of dentin is comparatively a complex pH. The results of the study indicate that in group phenomenon. This can be attributed to the I, in which the prepared surfaces of the specimens heterogenous structure of dentin and the dentinal were etched with 37% phosphoric acid for 15 and 60 fluid flow in an outward direction that make reliable seconds had no significant difference on the etching INTERNATIONALDENTALJOURNALOFSTUDENTSRESEARCH|JuneSep2012|Volume1|Issue2
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effect and subsequent bond strength values on enamel. On etching of enamel with 10% maleic acid for 15 seconds etching time, the dissolution of the prism cores was lesser, amounting to 3.3 and with 60 seconds etching time, there was greater dissolution of the prism cores (4.29). However, there was no significant difference (p>0.05) in the width of loss of prism core when the teeth were etched for 15 and 60 seconds.24% EDTA etchant gave relatively smooth appearance on enamel and did not alter the intact enamel surface significantly with non-uniform shallow pittings being visible. Photomicrographs of the dentinal surfaces treated with 37% phosphoric acid gel showed that the tubule orifices were open. With 24% EDTA gel, the mean diameter of the tubule orifices was 1.94 and 2.67 with 15 seconds and 60 seconds etching respectively. There was no significant difference (p>0.05) in widening of the tubuli when the etching time was extended from 15 seconds to 60 seconds. Etching with 10% maleic acid gel showed enhanced widening of the dentinal tubules. The mean diameter of opened tubules was 2.93 when the specimens were etched for 15 seconds and 3.33 with 60 seconds etching time. No statistically significant difference (p>0.05) was observed. The dentinal surface appeared smooth and free of debris in contrast to the samples etched with 37% phosphoric acid which showed evidence of particulate residue (Silica dioxide) on surface. Intergroup comparison of different acids showed that there exists no significant difference in tubule diameter whether the teeth were etched with 37% phosphoric acid gel or 10% maleic acid gel (p>0.05). However, significant variation exists when the tabulated results were compared between phosphoric acid and EDTA, and maleic acid & EDTA (p<0.05) with EDTA showing less widening of the tubule orifices as compared to the effect of the other two acids. Maximum penetration of the acid into the tubules was seen with 37% phosphoric acid. Phosphoric acid not only dissolves the mineral phase of dentin but also results in denaturation of the collagenous matrix1, 2 which may interfere with hybrid layer. For better retention of the restorative materials, the number of resin tags into dentin is more important than the depth of the tags. The depth of demineralized dentin to the extent of 11.96, 12.15 and 14.34 in group etched with 37% phosphoric acid for 60 seconds is not desirable. Moreover, the adhesive resins may not be able to infiltrate demineralized dentin completely till the depth of demineralization. The incomplete penetration of the demineralized collagen network could result in a delicate zone inside the hybrid layer and, between the hybrid layer and the unaltered dentin that could be susceptible to continuous degradation and a pathway for nanoleakage causing failure of the restoration.6 Further, as the resin penetrates deeper into dentin, the more difficult it will be for them to polymerize if they rely on light activation. In addition, dentinal fluid may interfere with polymerization of the resin comparison between 37% tags.7Intergroup phosphoric acid, 24% EDTA and 10% maleic acid shows comparable results of phosphoric acid and maleic acid apart from the depth of demineralized dentin which is significantly higher (p<0.05) for the 37% phosphoric acid gel group. Considering that 10% maleic acid gel provides clinically acceptable depth of demineralized dentin, 7.09 (15 seconds) and 8.83 (60 seconds etch time) it can be inferred that milder acid like 10% maleic acid can replace stronger, more destructive, 37% phosphoric acid for etching of teeth so as to enhance retention of the adhesive restorations.Although acid etching is more than 57 years old, answers to some of the basic questions concerning it are still being sought.
Conclusion
With this study we conclude that:1. Acid etching causes various types of etching patterns in enamel indicating preferential dissolution of the enamel prisms. With 37% phosphoric acid, type 2 etching pattern is seen; with 10% maleic acid, type 1 etching pattern is predominant and etching with 24% EDTA leads to type 4 etching pattern. In dentin, etchants widen the dentinal tubule orifices due to demineralization of peritubular dentin and this demineralization extends deep into the dentinal tubules for varying depths depending upon the type of acid used and time of its application. No statistically significant difference exists in the widening of the dentinal tubule orifices between the group I (37% phosphoric acid) and group III (10% maleic acid) specimens.
2.
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37% phosphoric acid causes maximum demineralization in the tubules with mean depth of demineralization being more pronounced in 60 seconds subgroup (11.48). 10% maleic acid also causes demineralization in tubules but the mean depth is significantly less (8.83) than that seen with 37% phosphoric acid. With 24% EDTA etching for 15 seconds, no discernible demineralization is seen in tubules and for 60 seconds. 3. Milder acids like 10% maleic acid can be effectively used for etching of teeth instead of 37% phosphoric acid.
References
1. Blomlof JPS et al. Acid conditioning combined with single component and two component dentin bonding agents. Q.I. 2001; 32: 711 715. Blomlof JPS, Cederlund AL, Blomlof LB et al. A new concept for etching in restorative dentistry. Int J Perio Rest Dent 1999; 19: 31 35. Fusayama T, Nakamura M et al. Non pressure adhesion of a new adhesive restorative resin. J Dent Res 1979; 58 (4) : 1364 1370. Galil KA and Wright GZ. Acid etching patterns on buccal surfaces of permanent teeth. Paediatric Dent 1979; 1: 230-234. Matos AB, Palma RG et al. Effects of acid etching on dentin surface : SEM morphological study. Braz Dent J 1997; 8(1) : 35 41. Perdigao J, Lopes M. The effect of etching time on dentin demineralization. Q.I. 2001; 32 : 19 Sidhu GK. The effect of acid etched dentin on marginal seal. Q.I. 1994; 25 : 797 800.
of article___________
2.
3.
However, a larger sample size is required before deriving any definite conclusions. Acknowledgement We place on records our deep gratitude towards our mentor, an eminent academician, Dr. (Mrs.) Sumita Kaswan, MDS, Professor, Department of Conservative Dentistry & Endodontics, Jodhpur Dental College General Hospital, Jodhpur, who prudently provided us the impetus for the present study. Photomicrograph Courtesy- Scanning Electron Microscopy Department, AIIMS. 4.
5.
6.
7.
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42 ORIGINALARTICLE
AMSA(ANTERIORMIDDLESUPERIORALVEOLAR):ALTERNATE TOMULTIPLEINFILTRATIONSINMAXILLARYANAESTHESIA
Dr Amit Sangle1 Dr. Ritika Tambuwala2 Dr. Ritika Agrawal3
1 MDS, Professor and Guide, Department of Oral and Maxillofacial Surgery, M.A. Rangoonwala College of Dental Sciences and Research Centre. 2MDS,
Corresponding Author Dr. Ritika Agrawal Address: M.A. Rangoonwala College Of Dental Sciences And Research Centre, Hidayatullah Road, Azam Campus, Camp, Pune- 1 Tel No: 02026452288, 02026452040 Contact number: 09604646209 E-Mail: drritika22@yahoo.in ritikaagrawal1386@gmail.com Access this Article Online
Professor and HOD, Department of Oral and Maxillofacial Surgery, M.A. Rangoonwala College of Dental Sciences and Research Centre.
Graduate Student, Department of Oral and Maxillofacial Surgery, M.A. Rangoonwala College of Dental Sciences and Research Centre.
3 Post
Abstract
Quick Response Code
This article describes an alternate technique of anaesthesia of single injection for the maxillary arch, pulpal anaesthesia from the central incisor to the second premolar without requiring collateral anesthesia of the face and muscles of facial expression. The importance of this review was to bring about awareness among the general clinician who have to use multiple injection for any treatment to be performed in the maxillary arch. The non compliance of the treatment on the maxillary arch is usually due to these factors. Hence introducing this technique can help patient compliance as well ease for the clinician. Also the duration of treatment is reduced. In our study we have introduced a modification of administration of injection using a disposable syringe and needle instead of computer controlled local anaesthetic delivery system (CCLAD); which makes this technique a very useful technique for various multiple extractions, anterior maxillary cysts and other procedures like flap surgeries for dentists as well as oral surgeons. Keywords: Pulpal Anaesthesia, Disposable Syringe and Needle, Single Injection
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Introduction
Maxillary mucogingival or flap surgery usually requires up to five injections to obtain anesthesia of the hard and soft tissues. Posterior superior alveolar, middle superior alveolar, and anterior superior alveolar block injections are used to anesthetize buccal tissues whereas greater palatine and nasopalatine blocks are used for palatal anesthesia. Although this series of injections effectively anesthetizes maxillary tissues, it may also inadvertently affect facial structures such as the upper lip, lateral aspect of the nose, and lower eyelid [1,2]. The palatal soft tissue anesthesia is achieved without numbness to the lips and face or interference with the muscles of facial expression. A bilateral AMSA injection supposedly anesthetizes 10 maxillary teeth extending from the second premolar on one side to the second premolar on the opposite side [3].The AMSA injection derives its name from the injections ability to supposedly anesthetize both the anterior and middle superior alveolar nerves [4]. The middle superior alveolar (MSA) and anterior superior alveolar (ASA) nerves branch from the infraorbital nerve before they exit from the infraorbital foramen. This technique anterior middle superior alveolar block was first reported by FREIDMAN & HOCHMAN in 1997[5] with the development of CCLAD system; it provides pulpal anaesthesia to multiple teeth from a single injection site.
mesiobuccal root of the first molar. The anterior superior alveolar nerve provides pulpal innervation to the central and lateral incisors and canines [5]. The plexus where both nerves join is the target site for the AMSA injection [6].
Figure 1
Method
Inclusion Criteria In our study we used AMSA on patients requiring multiple maxillary extractions and/ or anterior maxillary cysts, unilateral or bilateral as per the requirements. Anatomy (Figure1 and 2) a) The middle superior alveolar (MSA) and anterior superior alveolar (ASA) nerves branch from the infraorbital nerve before they exit from the infraorbital foramen. The middle superior alveolar nerve is thought to innervate the maxillary premolars and plays some role in pulpal innervation of the
Figure 2
Clinical Case Presentation Patient aged 55/male was advised extraction with 11,12,13,14 and 15 due to grade 3 mobility and gingival recession
Modification
We used of a 27 guage disposable syringe and needle (Fig 3) instead of CCLAD system (Fig 4) .0.6 to 0.9 ml Lignocaine hydrochloride in
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the conc of 1:100000 dilution of vasodepressor was used as the local anaesthetic agent. site at a methodic rate of 0.5 ml per minute [3]. Slow deposition of the anesthetic agent, the bound nature of the palatal tissue promotes diffusion of the anesthetic agent through the palatal bone via numerous nutrient canals [3]. A successful AMSA injection typically blanches the palatal tissue in a unilateral fashion that does not cross the midline [21]. Anesthesia of structures typically innervated by the greater palatine nerve, nasopalatine nerve, anterior superior alveolar nerve and middle superior alveolar nerve is achieved [22, 23].
Figure 3
Figure 5:
point of insertion of the needle.
Figure 4
Technique a) Malamed [1, 4] described the injection site to be on the hard palate about halfway along an imaginary line connecting the mid-palatal suture to the free gingival margin. Another description of the injection site is that it is located on the hard palate at the intersection of a vertical line bisecting the premolars and a horizontal line halfway between the midpalatine raphe and the crest of the free gingival margin [20].(fig 5) b) To avoid patient discomfort due to the tightly bound nature of the palatal tissue, the anesthetic agent should be injected into the
c) Within 2 minutes of this block ,pulpal anesthesia anesthetizing from central incisor to 2nd premolar along with the pulpal anesthesia, palatal tissues from the midpalatal region to the free gingiva of the same region are also considerably anaesthetized. d) The duration of anaesthesia is about 60 minutes to 90 minutes. The needle during injection is oriented at a bevel of 45 degree with constant and controlled pressure. e) The classical blanching of the palatal tissues is seen in AMSA block clinically indicating proper point of insertion and anaesthesia of the associated tissues along
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with the other clinical subjective signs. (Figure 6)
Figure 6: Blanching of the tissues on the anaesthetized side is shown.
Results
1. Most of the patients reacted well to the technique. Adequate anaesthesia for an accepted duration is achieved and it reducesthe cumulative reduction of the number of injections reducing patient discomfort.
2. In certain patients short lived central incisor anaesthesia was observed 3. In some other patients an additional buccal vestibular infiltration was required.
Discussion
Advantages 1. The ability of the AMSA injection to cover large maxillary surgical fields provides multiple benefits because it reduces the cumulative number of necessary injections.
2. The elimination of repetitive transmucosal punctures, the elimination of multiple injections reduces the total amount of delivered vasoconstrictor and may prove useful for cardiovascular-compromised patients requiring maxillary anesthesia. 3. For maxillary anterior esthetic procedures, the AMSAs maintenance of upper lip function allows for continuous evaluation of gingival contours unimpeded by the lip drooping that
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typically occurs with traditional anesthetic techniques. 4. Maxillay mucogingival procedures, the AMSAs palatal delivery of a full carpule of anesthetic with vasoconstrictor provides outstanding hemostasis and reduces the need for multiple re-injections to attain hemostatic control during graft harvest if indicated. 5. As we used a modified technique to the original one using CCLAD system, cost factor was decreased making it an affordable technique. Disadvantages 1) The long administration time: Some patients may find it disconcerting to have an injection last 4 minutes, and attempts to speed up the AMSA injection may lead to increased patient discomfort at the injection site. 2) The reduction of cumulative anesthetic vasoconstrictor may also prove to be problematic for certain surgical procedures. 3) The reduction in vasoconstrictor proves beneficial for cardiovascular- compromised patients, it may lead to less than desirable hemostatic control. 4) The AMSA eliminates the need for multiple injections, less vasoconstrictor enters the buccal tissues and a subsequent decline in hemostasis may obscure portions of the surgical field. 5) Several cases of short-lived anesthesia in the maxillary central incisor is observed.
Conclusion
This technique has the advantage to anaesthetize multiple teeth with a single injection covering large surgical area in the maxillary region; thus can be used in day-today practice by oral surgeons and general dentists.
References
[1] Malamed SF. Handbook of Local Anesthesia, 5th ed. St. Louis: Mosby; 2004;213-216. [2] Gomolka KA. The AMSA block: Local anesthesia without collateral numbness. CDS Rev 2000;93:34. [3] Friedman MJ, Hochman MN. Using AMSA and P-ASA nerve blocks for esthetic restorative dentistry. Gen Dent 2001;49:506511. [4] Malamed SF. Handbook of local anesthesia. 4th ed. St. Louis: Mosby; 1997; p. 149, 150, 160. [5] Friedman M, Hochman M. A 21st century computerized injection system for local pain control. Compendium 1997;18:995-1003. [6] Friedman M, Hochman M. The AMSA injection: a new concept for local anesthesia of maxillary teeth using a computer-controlled Quintessence Inter injection system. 1998;29:297-303. [7] Blanton PC, Roda RS, The anatomy of local anesthesia. J Cal Dent Assoc 1995;23(4):5569.
[8] Donaldson D, James-Perdok L, et al, A comparison of Ultracaine, DS (articaine Hcl) and Citanest, Forte (prilocaine Hcl) in maxillary infiltration and mandibular nerve block. J Can Dent Assoc 1987;1:38-42. [9] Gibson RS, Allen K, et al, The Wand vs. traditional injection: a comparison of pain related behaviors. Pediatric Dent 2000;22(6):458-62. [10] Saloum FS, Baumgartner JC, et al, A clinical comparison of pain perception to the Wand and a traditional syringe. Oral Surg Oral Med Oral Pathol 2000; 89(6):691-5. [11] Goodell GG, Gallagher FJ, Nicoll BK, Comparison of a controlled injection pressure system with a conventional technique. Oral Surg Oral Med Oral Pathol 2000;90(1):88-94. [12] Carter RB, Keen EN, The intramandibular course of the inferior alveolar nerve. J Anat 1971;108:433-40. [13] Rood JP, The nerve supply of the mandibular incisor region. Br Dent J 1977;143:227-30. [14] Frommer J, Mele FA, Monroe CW, The possible role of the mylohyoid nerve in mandibular posterior tooth innervation. J Am Dent Assoc 1972;85(1):113-7.
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[15] Madeira MC, Percinoto C, Silva MGM, Clinical significance of supplementary innervation of the lower incisor teeth: a dissection study of the mylohyoid nerve. O Surg O Med O Pathol 1978;46:608-14. [16] Sutton RN, The practical significance of mandibular accessory foramina. Aust Dent J 1974;19:167-73. [17] Haveman CW, Tebo HG, Posterior accessory foramina of the human mandible. J Prosthet Dent 1978;35:462-8. [18] Wilson S, Johns P, Fuller PM, The inferior alveolar and mylohyoid nerves: an anatomic study and relationship to local anesthesia of the anterior mandibular teeth. J Am Dent Assoc 1984;108:350-2. [19] Chapnick L, Nerve supply to the mandibular dentition: a review. J Can Dent Assoc 46:446-8, 1980. [20] Holtzclaw D, Toscano N. Alternative anesthetic technique for maxillary J Periodontol periodontal surgery. 2008;79:1769-1772. [21] Lee S, Reader A, Nusstein J, Beck M, Weaver J. Anesthetic efficacy of the anterior middle superior alveolar (AMSA) injection. Anesth Prog 2004;51:80-89. [22] Perry DA, Loomer PM. Maximizing pain control: The AMSA injection can provide anesthesia with fewer injections and less pain. Dimens Dent Hyg 2003;1: 28-33. [23] Nusstein J, Lee S, Reader A, Beck M, Weaver J. Injection pain and postinjection pain of the anterior middle superior alveolar injection administered with the Wand or conventional syringe. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2004;98:124131. [24] Holtzclaw D, Toscano N. Alternative anesthetic technique for maxillary periodontal surgery. J Periodontol 2008;79:1769-1772. [25] Allen KD, Kotil D, Larzelere RE, Hutfless S, Beiraghi S. Comparison of a computerized anesthesia device with a traditional syringe in preschool children. Pediatr Dent. 2002;24:31520. __________End of arti cle_____
48 REVIEWARTICLE
ENDOTHELIALCELLBASEDENGINEERINGOFCAPILLARIESLIKE NETWORKINATISSUEENGINEEREDSKINSUBSTITUTE
Dr. Mohammad Ahmad Javaid1
1BDS,
Faculty Canada
MSc Dental Sciences Candidate, of Dentistry, McGill University
Corresponding Author Dr. Mohammad Ahmad Javaid Faculty of Dentistry 3640 University Street, Room B/15 Montreal, QC H3A 0C7 Canada Telephone: 438 401 8150 Email: mohammad.javaid2@mail.mcgill.ca
Quick Response Code
Abstract
Treatment of patients with burns, surgeries and accidents involving extensive skin replacement has long been a challenge for reconstructive surgery. Classical approaches like cadaver skin or xenografts have failed to provide a permanent solution to this ever increasing problem. Different tissue engineering techniques have been tried in the past but, clinically none has lived up to the early promise that in vitro studies showed mostly, due to limited vascular supply leading to cell death when grafts comprising of epidermis and dermis were used in deep wounds. More recently scientists have developed a new approach using endothelial cells for construction of pre vascularised tissue engineered skin grafts constituting epidermis and dermis. In this mini review we look at a few experiments and animal studies which have been conducted so far and have yielded promising results, both in vitro and in vivo. This new approach involving endothelial cells for engineering of capillary like network in tissue engineered skin substitute is the way forward and can potentially provide a solution to this problem which scientists and surgeons have been trying to address for the last half century.
Acknowledgment
I am immensely grateful to my supervisor, Dr. Mari Kaartinen, Associate Professor at Faculty of Dentistry and Medicine McGill University and Director Biomedical Sciences, Faculty of Dentistry and Faculty of Medicine at McGill University for her continuous support, encouragement, guidance and advice. I would also like to extend my gratitude to Dr. Satya Prakash, Professor of Biomedical Engineering Department at McGill University for his guidance in writing this mini review.
49 Introduction
Treatment of burn victims or patients with surgeries involving extensive skin removal is a complex procedure. The classic therapeutic options which have been tried like cadaver skin or xenografts have proved to be temporary solution[1, 2] [3]. In recent times tissue engineered skin has offered a therapeutic alternative [4-6]. Although human epidermis has already been developed in large quantities from skin biopsy by using techniques developed in tissue engineering [7, 8] [9]but if dermis is destroyed due to trauma, replacement by epidermis alone does not lead to optimal healing [3, 8]. In such instances, a bilayered tissue engineered substitute is sought [10]. Drawbacks for replacement of skin wounds with epidermal substitutes alone are many and include high sensitivity of mechanical damage and variable percentage of graft take which may be attributed to absence of underlying dermis. With engineered constructs consisting of both epidermis and dermis, many of these drawbacks will be potentially overcome [3, 11] Researchers have tried to transplant skin substitutes with increasing thickness to accommodate for increased tissue loss in different clinical scenarios. Although there have not been many such transplantation experiments but, there have been studies which, show unfavourable results which may be due to insufficient vascularisation in dermis which in turn leads to deleterious effects on epidermis survival as this layer is dependent on diffusion of nutrients from dermis[4, 12, 13]. In most of the cases the graft failure is due to inadequacy of vascularisation which leads to hypo perfusion and ischemic injury [4, 9, 1416]. The graft cells are dependent on diffusion of nutrients and oxygen from underlying wound which is generally insufficient for sustained survival of graft [9]. Cell located within 100-200 micro meter of a vessel can derive nutrients via diffusion [17-21]. As the distance increases, diffusion alone cannot sustain cells and so cell death increases. Inosculation has been explained as the anastomoses or connection of capillaries present in graft with vessels in the hosts wounds [4, 22, 23]. In some studies it was demonstrated when human skin was grafted onto mouse, initial vascularisation was due to anastomoses between severed ends of human capillaries with mouse micro vasculature[16, 19]. Later mice endothelial cells replaced the human endothelial cells. This demonstrated that grafts with intrinsic blood supply may have a better long term prognosis and survival. Hence it was proposed that methods should be sought to replace skin with grafts containing intrinsic microvasculature [13]. This observation found the basis of idea to develop a tissue engineered skin substitute with intrinsic vascular component [4]. Many approaches are currently being investigated to increase vascularisation in tissue engineered skin substitutes to promote inosculation and hence survival of the transplanted engineered skin substitute [19] One approach is to incorporate growth factors into scaffold biomaterial. [24]. A different approach is to pre-encapsulate the growth factors in microspheres which are then transferred to the scaffold leading to steady and sustained released of growth factor [25]. This has been proven by studies like [26]who demonstrated that various biodegradable polymers can be developed and used for transplantation of isolated or encapsulated cells which would allow to form an engineered tissue with intrinsic vasculature [26]. Many studies have been carried out to promote vascularisation in engineered tissues through use of growth factors including Vascular Endothelial Growth Factor [5, 6, 27-30], Fibroblast Growth Factor [29] and Transforming Growth Factors [31]. But it has been shown in previous studies that systemic delivery can cause unwanted tissue growth and subcutaneous injections yield a very
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limited promotion in neovascularisation [26]. Another approach is utilization of stem cells for creation of tissue engineered vascular grafts [24, 32, 33]. Studies involving genetic modification of cells have also been carried out. For instance study by [34]. In this study it was demonstrated that over expression of platelet derived growth factor A in tissue engineered skin substitutes by genetically modified keratinocytes and fibroblasts was not statistically significant compared to unmodified keratinocytes and fibroblast. It was also observed that Tissue Engineered Skin substitute was devoid of intrinsic micro vasculature and this limitation can hypothetically be overcome by over expression of certain cytokines [35]. Lastly a different approach is to engineer micro vessels in vitro in scaffold using endothelial cells. After transplantation, the endothelial cells form blood vessels which develop interconnections with host blood vessels leading to adequate perfusion of the graft. However one issue needs to be addressed which is homogenous distribution of endothelial cells and resulting blood vessels [24]. This issue has been addressed in a few studies like [26].Their paper hypothesizes that endothelial cells if seeded in tissue engineered scaffold would form capillary like tubular structures which can form the basis of intrinsic graft microvasculature which would increase the long term survival of graft by anastomoses between graft and host micro vasculature [26].Human endothelial cells have also been shown in previous studies to spontaneously sprout capillary like structures and form microvasculature when co cultured with fibroblasts and seeded on tissue engineered skin substitutes in vitro. For instance in a study by [36] conditions for HUVEC (Human Umbilical Vein Endothelial Cells) to form capillary like tubular structures with in a 3D scaffold were demonstrated which would allow HUVEC to form in vitro capillary like tubular structures within tissue engineered scaffold which can then be transplanted onto graft site on host. In this mini review, we look at different studies which used endothelial cells in different models to increase the development of microvasculature in the engineered skin substitutes so as to promote inosculation and hence survival of the tissue engineered skin substitute.
In Vitro Experiment, First of its Kind In a study by [4], the objective was to develop Endothlialized Skin Equivalent (ESE) in which capillary like structures could be reproduced in vitro. For this purpose Human Keratinocytes and Dermal Fibroblasts were isolated. As it has been shown by [37]] that human dermal fibroblasts and keratinocytes produce a more well organised tissue engineered construct in comparison to bovine cells which results in the production of auto or self produced tissue engineered skin construct which would increase the tendency for take of the graft. Human Umbilical Vein Endothelial Cells (HUVECs) were taken as endothelial cells. Three dermal equivalents were produced with seeding fibroblasts on top of biopolymer in one; HEVEC on biopolymer in second and endothelial-fibroblast dermal equivalent was prepared seeding both fibroblasts and HUVEC on biopolymer in third. Keratinocytes were seeded in all three dermal equivalents [4]. It was observed that HUVEC when cultured alone although expressed on the biopolymer scaffold but mostly showed features attributed to dying cells and produced very limited extracellular matrix. On the other hand fibroblast cultured alone attached to the biopolymer scaffold, proliferated and laid down extracellular matrix in appreciable amount. In equivalents with both cells, proliferation of fibroblasts with deposition of extracellular matrix was observed in which HUVEC migrated and formed new capillary like tubular structures. The capillary like tubular structures observed in
51
Endothelialized Dermis Equivalent (EDE) and Endothelialized Skin Equivalent (ESE) was not observed in case of absence of HUVEC. Taking in vitro results to in vivo experiments In another study by Tremblay et al. HUVEC seeded in dermis were used to develop microvasculature with in engineered skin substitute and transplanted onto mice to take the in vitro technique developed by [4]to in vivo stage. This was compared with dermis without HUVEC. Two different tissues were prepared. One the standard reconstructed dermis without endothelial cells and second reconstructed dermis with human umbilical vein endothelial cells (HUVEC). Adult male athymic mice were selected for graft transplantation. Excisions were made and deep wounds were created in three groups of mice. In one group human skin was transplanted, in other reconstructed skin without endothelial cells and in third endothlialized reconstructed skin was transplanted. Four mice in all three groups were sacrificed at day 4, 7 and 14 postgrafting for analysis. [16] Capillary like Structures (CLS) were observed under epidermis in ERS before placement of graft while no such structures was observed in RS. Also red blood cells were detected in capillaries on fourth day after placement of skin graft. These red cells came from mice as no red cells were observed in capillaries of human skin before transplantation. In ERS, after four days, blood containing vessels were seen underneath the epidermis. These vessels were identified via double staining which showed that vessels beneath epidermis contained human Endothelial Cells (ECs). It was also shown that mouse EC were only present in the lower compartment of graft and not in epidermis as seen with RS. At 14 days after graft placement, a colocalization between human and mouse endothelial cells was seen in the graft through use of confocal microscopy. Presence of red blood cells in their lumen was a clear evidence of inosculation between graft capillary like structures and mouse capillaries. Lastly total number of capillaries human and mouse were evaluated per tissue section for each type of grafts i.e. Human Skin, Reconstructed Skin without endothelial cells and Endothelialized Reconstructed Skin. There was a twofold decrease in number of human capillaries in Human Skin graft. This could be attributed to degeneration of supernumerary vessels that did not anastomose with the mouse capillaries. This type of decrease was not observed in Endothelialized Reconstructed Skin, in fact a statistically significant increase in number of mouse capillaries was observed in ERS [[16] In another study by Laschke et al., microvascular network was formed in the PLGA scaffold by placing the scaffold onto flank of donor mice. After 20 days when blood vessels had grown into the scaffold, forming a network of micro vasculature within the scaffold, the engineered scaffold was excised and transplanted onto the recipient mice. The results showed that preformed microvessels within tissue engineered skin substitute developed interconnections with host micro vasculature which resulted in accelerated vascularisation of cells in the graft compared to avascular grafts [25] In 2010, a study was carried out by Gibot et al in which two substitutes were prepared. Endothelialized Reconstructed Skin (ERS) and RS (Reconstructed Skin) serving as control. The dermal layer in these models comprised of three layers of fibroblasts with inferior two plated with Human Umbilical Vein Endothelial Cells (HUVECs) in ERS and without HUVEC in RS. Graft site were prepared on athymic mice by removal of back skin and then tissue engineered skin was grafted onto the mice. [19] After 30 days of in vitro culture, the Endothelialized Reconstucted Skin showed well developed and fully differentiated human
52
epidermis. In this model, human endothelial cells formed Capillary like Structures which has also been shown in previous studies. The lumens of micro vessels were well defined. Reconstructed skin endothelialized with either Human Umbilical Vein Endothelial Cells (HUVEC) demonstrated an organised network of Capillary like Structures (CLS) with a branching morphology. The Endothelialized Reconstructed Skin developed its own intrinsic microvasculature where as Reconstructed Skin which was considered a negative control did not show development of such microvasculature. All the grafts showed a complete take at day. Both grafts, RS and ERS adhered completely with underlying hosts tissues at day but more vascularisation was observed in ERS compared to RS. It was also revealed that the human endothelial lined vessels transported mice red blood cells which demonstrated that functional anastomoses was established between graft microvasculature and hosts capillaries at. The human vessels formed were homogenously distributed in superficial and deeper layers ensuring complete perfusion of the entire graft [19]. diffusion, followed by inosculation and finally by neovascularisation. Composite skin substitutes without intrinsic blood supply cannot vascularise as the natural split thickness graft. Diffusion is responsible for supply of nutrients to the epidermis which is not sufficient to ensure the permanent implantation of grafted skin substitute until process of neovascularisation takes over. In study carried out by [4]which was the first study of its kind the aim was to develop capillary like network within the skin substitute in vitro, which may prove to be a cornerstone in tissue engineered skin substitutes [4] The aim of the Black ET AL study was to develop in vitro endothlialized tissue engineered skin substitute which would demonstrate vascular like tube formation developed from human cells without the use of specific growth factors or carcinogenic agent like PMA. Their results were very promising and formed the basis of further trial of endothelial cells for formation of blood vessels within the Tissue Engineered Skin Substitute which could be tried in vivo. The results of [4] study strongly suggest that HUVEC can organise and give rise to network of capillary-like structures when cocultured with dermal fibroblasts and keratinocytes. On the other hand these structures do not develop when each cell type is cultured independently. The results showed strong evidence that fibroblasts when present in conjunction with endothelial cells in a 3D culture medium lay down the extracellular matrix in which capillary like structures formed [4] The study Black et al formed the basis of taking in vitro results to in vivo experiments carried out by Tremblay et al in which it was hypothesized that a reconstructed skin containing capillary like structures would promote faster vascularisation by anastomoses between graft vessels and hosts capillaries as had been shown by
Discussion
One of the main obstacles in wide spread use of Reconstructed Skin for wound coverage is delayed vascularisation due to thickness of dermis. But this thick dermis is important because it protects the reconstructed epidermis against mechanical, chemical and bacterial accumulations and also results in better healing. This however delays the complete vascularisation of the graft which ultimately culminates in necrosis of epidermis [16] It took years to fully understand and appreciate the phenomenon of neovascularisation which is a key step in increasing take of graft and keeping it viable. It has been shown in previous studies that split thickness skin graft survives by
53
transplantation of full thickness human skin on wounds in previous studies. In this study it was demonstrated that Human Umbilical Vein Endothelial Cells when added to the Reconstructed Skin accelerated the process of vascularisation as compared to conventional Reconstructed Skin. Human capillaries filled with red blood cells were observed near the epidermis. These findings were in coherence with the previous work done by other groups of researchers. Same results were observed with ERS. Human capillaries containing mouse red blood cells were observed beneath epidermis after 4 days of graft placement and no mouse blood vessel was observed in the area in that time. The filling of human capillary with mouse blood pointed to the fact that there were anastomoses or inosculations between the human and mouse vasculature. It was also observed that blood circulation establishment beneath epidermis was faster in ERS compared to RS and was as fast as seen in Human Skin. The results showed that initial vascularisation observed at 4 days was due to inosculation of human capillary like structures with mouse vessels. Mouse capillaries extended by process of neovascularisation were not detected beneath epidermis of ERS until day 14. According to authors of study this was the first study which demonstrated inosculation process between human capillaries reconstructed in vitro through tissue engineering with wound bed vasculature [16] The latest study in this regard using Endothelial Cells was carried out Gibot et al which was again based on the initial work done by Black et al. In this study, the aim was to develop an easy to handle ERS model, which could demonstrate in vitro formation of capillary like network by co culture of fibroblasts, endothelial cells (HUVEC) without use of external growth factors. This model could also be completely autologuos for future clinical applications. In this model, cell secreted extra cellular matrix and there was also cell-cell and cell-extracellular matrix interaction which created a physiological micro environment allowing endothelial cells to express capillary like structures. Also the thickness of model could be compared with human skin slit thickness graft generally used in clinical arena which is categorized as thin (130-300), intermediate (300-460) or thick (460-760) micro meter. The human microvasculature created in vitro anastamosed with host capillaries and became functional in less than 96 hours. Mouse red blood cells were found in lumen of human endothelial capillaries which demonstrated efficacious blood circulation. These anastomoses could only be established if hosts micro vessels grow in the graft and then establish inosculation with graft vessels. Complete replacement of graft vasculature endothelial cells by host cells is key for skin graft revascularization and long term survival and acceptance of graft. In this study the graft was remodelled completely with hosts endothelial cells. [19]
Conclusion
From use of Split thickness skin grafts, to grafts from cadavers and xenografts, the science of development of perfect Tissue Engineered Skin Substitute has come a long way. With in vitro development of microvasculature in Tissue Engineered Skin, the first steps towards perfect skin substitutes were taken. Although many studies have been conducted but it is safe to say that Tissue Engineering of Skin and its application in clinical practise is the beginning of a long journey. Now with improvement in cell culture techniques and advancement in knowledge, epidermis and dermis are being prepared separately from small biopsies taken from the recipient, in vitro. This is just the beginning, with final
54
aim of generating a full transplantable replica of skin with adnexa and vasculature [38].
11.
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Nat Biotechnol, 2005. 23(7): p. 879-84. INTERNATIONALDENTALJOURNALOFSTUDENTSRESEARCH|JuneSep2012|Volume1|Issue2
56 REVIEWARTICLE
BENIGNFIBROOSSEOUSLESIONSOFJAWSAREVIEW
Rashi Bahl1, Sumeet Sandhu 2, Mohita Gupta3
1Reader,
Corresponding Author Mohita Gupta (BDS) Address: 302, Green Avenue, Punjab. PIN 143001 Contact number: 08146182200 E-Mail: mgupta910@gmail.com Access this Article Online
Department of Oral and Maxillofacial Surgery, Genesis Institute Of Dental Sciences & Research, Ferozepur, Punjab, India & Head, Department of Oral and Maxillofacial Surgery, Sri Guru Ramdas Institute of Dental Sciences & Research, Amritsar, Punjab, India
Amritsar,
2Prof.
www.idjsr.com
Institute of Dental Sciences and Research, Ferozepur, Punjab, India
3Genesis
Quick Response Code
Abstract
Benign Fibro-osseous Lesions is a group of lesions in which normal bone is replaced initially by fibrous connective tissue and over a period of time, the lesion is infiltrated by osteoid and cementoid tissue. This is a benign and idiopathic process. Fibro-osseous lesions of the maxillofacial bones comprise a diverse group of pathologic conditions that include developmental lesions, reactive or dysplastic diseases, and neoplasms. The concept of fibro-osseous lesions has evolved over the last several decades and now includes two major entities: fibrous dysplasia and ossifying fibroma. The less common lesions include florid osseous dysplasia, periapical dysplasia, focal sclerosing osteomyelitis, proliferative periostitis of Garre, and osteitis deformans. It represents a diverse group of pathological conditions that includes developmental lesions, reactive or dysplastic diseases, and neoplasms. Owing to substantial overlap of the histopathologic findings, sub classification of Benign Fibro-osseous Lesions may be problematic. Despi te the advances i n the u nde r st and ing of the se co ndi tion s , fibr o-o sseo u s l es ion s c on tin ue t o p re sent problems in classifi cation, di agno si s, an d ma nage men t due to mul ti ple hi sto logi cal a nd r a d i o g r a p hi c si mil a ri tie s . The objective of this article is to review the most current clinic pathologic, radiographic, and molecular studies of Benign Fibro-osseous Lesions to aid the surgical pathologist in the recognition and diagnosis of this diverse group of maxillofacial lesions.
57 Introduction
The fi bro -o s seou s les ion s rep re sen t a l arge group of di so rde rs that may have c o m mo n c ha ra c teri s ti c s i ncl udi ng cli ni cal , r adiog rap hi c and mi cro scopic fe at ure s. Alt hough mo st a re of unk now n e tiolog y, some are be lieved to be neo pl asti c an d ot hers a re rela ted to met abo lic i mbal an ces. I t is no t un u su al to s ee the se le sio ns p re sen tin g wi th a ran ge of radiographic appearance s, ca using conside rable di agnosti c co nfusio n 1 . Benign fibro-o sseo u s lesion i s a well k now n , de script ive te rm t h at en co mp asse s a wi de ran ge of c ond itio n s, t he diag nose s of w hi ch may be challeng ing . In part, the c ha llenge a ri se s be ca u se the h istop at hologi ca l appe aran ce s of all fi bro-o sseous le sions are very simil ar, if no t ide ntical , maki ng cl ini cal d iag nosi s dif fic ul t ba sed on mi cro scopic feature s alone. The max illofaci al fibro-osseous le sions are the le sio ns that are diffe rent (ex cept fibrous dysplasia) to t ho se fou nd in t he res t of t he skele ton . Charles Waldron wrote In absence of goo d cli nic al a nd rad iologi c i nformation a pa thologi st can o nly st ate th at a given biop sy is con si s ten t wi th f ibr o osseo us le sion s . Wi th adequate clini cal & radiologi c i nfor mation , mo st le sion s c an be a ssig ned wi th rea son able cert ain ty i nto one of the seve ral catego rie s 2 owi ng to the ir si mil ar hi stology. Radiog raphically , fi bro-o sseo u s le sio ns vary co nside rably from a si mple radiolucent le sio n to mixed radiolucent/ radiopaque or radio paque le sio n . The se c an be well defi ned or ill -defi ned ble ndi ng i mpe rceptibly i nto the su r rou ndi ng bone . The re may o r may no t b e e x pan si o n o f bone , wit h o r wit ho ut di spl ace men t o f too th . Histologi cally, the f ibro-o s seous le sio ns mai nly consi st of two c o m p o ne nts - h a r d t i s sue a n d sof t t is s ue compo nen t . The tre atmen t of fi bro-o s seous le sions varie s depending on the nature of the le sion. It may v a r y f r o m s i mpl e s urgi cal excision o r curettage in cemento ossifyi ng fi bro ma to a su rgical ex ci sion and rese ction of the involve d jaw i n cases of juvenile o ssif ying fi bro ma, o steo geni c s ar co ma and c ho nd ro s a r co ma .
Classification
Charles A Waldron i n 1985 classifie d fi bro osseous le sions i nto main groups on t he ba si s of cli ni cal beh avio r, histopathology and radiographi c fi ndi ng s :
1 ) Fib rou s Dy sp la sia 2 ) R e a c tiv e ( dy sp l a st i c) l e sio n s a ri si ng in t he tooth bearing a re a : Pe ria pi c al c e ment o osseous dysplasia Focal cemento o sseous dysplasia Florid ce mento o sseous d y s pl a si a 3 ) Fibro o sseous neoplasms Ce mentifying fibroma Ossifying fibro ma Ce men to o s sifyi ng fi bro ma
58 FIBROUS DYSPLASIA
It i s one of the mo st pe rplexing d ise ase s o f o s seou s tis s ue s & h as been de scribed a s a lesion of un kno wn e tiology, uncertai n pathogenesi s and d iverse h istop at holog y. It is a conge nital, metaboli c, no n-fami lial d i s tu rb an ce tha t p ro d uce s 2 .5% o f al l bo ny tu mor s a nd o v e r 7 % o f a l l no n mal ign an t t umo rs of bo ne 3 . I t i s a be nign fibro o sseous le sion c ha ra c teriz e d by f o rma ti o n o f f i bro u s c on nec tive t i ssue wi th in t he spon gio sa of the affecte d bo ne and ofte n by the painle ss ex pansio n of that bone to c a u se d e f o r mi t y 4 . The re is the repl ace men t of n o rmal bony archi tecture wi th fibrous and o s teoid tissue 5 . It m ay al so con tai n i s l an d s o f cal cifie d t issue , t he appe aran ce of whi ch i s depe nde nt on the age of the le sio n . The re i s p rolife ra tion o f fi bro blast li ke cell s that have feature s of o steoblasts in so me areas and tho se E tiolo gy and Pathoge ne si s Fib rou s dy sp la sia is po stulat ed to o cc ur a s a r e su l t o f a l a c k o f s t re s s alignme nt and insuffi cient mine rali zation re sults i n substantial lo ss of me chani cal strength, le ading t o the develo pme nt of p ain , de fo rmity , and pathologi c f racture s 6 .Ma rie e t al s ho we d t ha t a n ac tiv a ti ng mutation of G s in o steoblasti c cell s of patients wi th McCune-Al bri ght sy nd rome and mono stoti c d i sea se lead s to c o n st i t utiv e a ct i v a tio n of adenylate c y c l a se , i n c re a sed c e l l p ro l i f e ra ti o n , a nd i n appr o p ria te cell dif fere ntiation, resul ting i n overproduction of a d i so rg ani ze d f i b ro t i c b o ne m at ri x i n po lyo sto tic an d mono stoti c fi bro us d y s pl a si a 6 , 3 . Preg na nc y ha s bee n i mp lic ate d in ex ace rb atio n of fi bro us of cho nd rob la st s i n o the rs. It o cc ur s be cause of maturation a rre st of bone f o r ma ti o n a t t he stage o f wo v e n / f i b re bo ne 6 . The re sul tan t fib ro o s seou s t is s ue i s poo rly fo rmed , el as ti c a nd structurally inadequate . It can i mpai r c osme ti c & st ru ct ur al fu nc tio n of bo ne le ading to o steol yti c le sio n s, f ra ct ure s, & deforma tion s . I t may i nvolve one or more bo nes of the crani al o r extra cranial skeleton. It has two basic clinical fo rms: mono stoti c a nd polyo sto ti c 4 . It may a l so be a s so cia te d wi th e ndo c ri ne d ysfun c tion , ab nor ma l pig me nt at ion , a nd pre cocio us pu bert y in g irl s 7 . It wa s fi rst repo rte d by Von Re ckli ng hausen in 1891. Fibrous d yspla si a i s def ined a s a di sea se of bo ne , cha ra c teri zed by lo cali zed areas, usually in a unil ate ral d istr ibu tion sho wing a ma tu ra tio n a r rest of bo ne fo rma tion at the stage of wo ven bone 8 . d yspla si a pe rh ap s becau se of est roge n receptors in the fibrous tissue 3 . Cl ini c al Fe ature s I t oc cu r s mo st co mmonl y i n se cond o r t hi rd de cade of li fe 9 . The ave ra ge age of o cc u rren ce i s t en ye ar s. S ome st udie s r evea led no ge nder 1 0 predilection .M ale to female ra tio in s o me st u d i e s i s 2 :1 . So me st u d i e s a l so sho w that sex predile ctio n i s almo st equal . A mong the jaw bone s, max illa i s mo re co mmonl y affected than the mandi ble. The mo st common sign is painless ex pan sio n o f the affe cte d area a nd de formi ty of the affected si te . The fo ra mi na of cr ani al ne rve s, may be encroached upon p rod uc ing ne rve p a l si e s , t h e d i s figure ment may be
59
extre me justifyi ng the term leontiasis ossea . Diff u se polyo sto ti c le sio ns i n l arge weigh t- bea ring bone s a re p rone to lea d to bo wing de formi ties that increase wi th age and skele tal g rowth. Unlike defo rmities in p atie nt s wi th mono stoti c d ise ase , de formi ties in patie nts wi th po lyo sto tic di sea se may con tin ue to progre ss af ter skeletal ma tu ri ty 1 0 . Oral Manife stations P ai n o r p ar ae st hesi a i s a n u nu s ual complaint. Di splacement of the teeth wi th resultant ma locclusion and i nte rfe renc e wi th no r mal er up tion p at ter n s may o c cu r . I n chil dren tee th i n t he affec te d pa rt may fail to e ru pt. De nti nal dy sp la sia i s a di sorder t hat o cc ur s in pa tie nt s wi th inhe ri ted fibrous d y s p l a si a . Patho logically, fi bro u s ti ssue th at is fi r m, rub ber y, a nd g ri tty 7 . Histologi cally, f ib rou s dy sp la sia consi sts of varying amounts o f s pi ndle cell bu nd les a nd t rabe cul ae of i mma tu re wove n bone . The fi bro us tissue in fibrous dysplasi a i s well v as cu la ri ze d a nd o f ten sho w nu me rou s small vessels in the centre and large pe ri phe ral si n u so i ds 7 . Th ree si te specific patterns of hi stop at holog y have been i dentified. C h ine se wri ting t ype ; scle roti c/p aget oid type; a n d sc lero ti c / h ype rcel lul ar type . R adio graph i c Pict ure The le sions o f fi bro u s d y s p l a s i a a r e usuall y poo rly circumscribe d , wi th the le sio ns de monstrating a blending m a rgi n an d a re r ad i o pa que ( g rou nd gl a ss appe aran ce) a lt hough ea rly le sio ns ma y be l arge l y r adio l uce nt. A cco rdi ng t o Aki nto ye , i t ca n prese nt a s a spe c tr u m of fou r p at ter ns in a p ano ra mi c r ad i o g r ap h : g ro u nd g l a ss ( condensed/granul ar) , radiol uce nt (l yti c) , mixe d radioluce nt/radiopaque ( mixe d den si ty) a nd radiop aq ue ( s clero ti c) . Vari atio ns in the co rti cal t hi ck ne ss a re ca u sed by slo w r e so rp tio n o f t he en do ste al su rf ace , c ommo nly refe r red to a s "en do ste al scalloping ." The per io stea l su rf ace remains smooth 1 0 . T h ree v arie ti e s o f a ppea ra n ce s a re seen o n C T scan: gro und glass pattern, ho moge neously dense p at te r n , an d cy s ti c v arie ty 6 . Magnetic r eso na nce i magin g i n a ddi tio n c an he lp di sti nguish f i bro u s d y s p l a si a f ro m men ingio ma , osteo ma , or mu co cele an d def ine t he extent of sof t tissue invol veme nt, parti cularly if c e n tr a l ner v o u s sy ste m st r uc tur es a re i mp inge d on 7 . Single pho ton e mi s sion computed tomo graphy has been repo rted to be more sensitive i n dete cti ng the are as i nvolved in case s of f ibrous 6 d y s pl a si a . A slight elevatio n of serum a l kal i ne pho s pha ta se ma y be s e e n i n so me ca ses bu t may no t alwa ys be rai sed. Calci u m, p ho sp ha te and vario u s othe r hormone s are seen in no r mal ran ge 4 .
I) Polyostotic Fibrous Dysplasia

Invol vement of two o r more bone s i s calle d as polyo sto ti c fi bro us d y s pl a si a . T wo app are nt type s o f po lyo sto tic f ib rou s d y spl a sia a re de scribed :
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o steoi d le sio n. trabeculae i nhe rent in the
a ) J a f f e L i ch te n stei n sy nd rom e b ) M c C u ne Alb ri ght syn d ro me I t mo st com m o nl y o cc u r s i n c hi l d ho o d . Medi an age of o n set of sy mptoms i s 81 0 y e a r s , wi th mo s t o cc ur ri ng be f o re the age of ten 1 1 . The dise ase a ppa re ntly h as a di st in ct tenden cy to o cc ur i n w o me n w i t h a m a l e : f e mal e r a tio o f 1 :3 1 1 . Lo ng bo ne s of ex tre mi ty are mo st of ten affecte d in follo wing o rde r of fre que ncy : fe mu r , ti bia , h u me r u s & r adi u s . N e x t i n o rde r o f f req uen cy a re bone s of t he sk ull ( crani al vau lt & jaw bo ne s) 1 1 .
T he typ i ca l mi c ro sc o p i c f i n d i ng s o f fi bro u s dy sp la sia sho w i r reg ula rly shaped trabeculae of i mma ture bo ne i n a ce llular, loo sely arranged fi bro u s s t ro ma . The bo ny tr abe cu lae a re not c on nec ted to e ac h ot he r 1 2 . Stellate o steo blasts are seen parti cularly in a c tive le sio ns an d a ppea r t o arise f ro m fib rob la st s .
II) Monostotic Fibrous Dysplasia

It is more common than the po lyo sto tic type . It mo st commonl y o ccurs a t t he age of 20 to 30 yea r s with some case s be co min g do rma nt by t he t hi rd de ca de a nd ho rmo nal c ha nge s l ike in p re gna nc y r e a ctiv at i n g a dor ma nt l e sio n 7 . It can a lso o c cu r i n inf anc y 5 , o cc u rs wi th appare ntly equal predilection for male s and fe male s. Ri bs and craniof acia l bo ne s are mo st commonl y affected 7 . O t her b one s a ffe cted i ncl ude , cla vicle , t ibia , fe mu r et c. The p atie nt m a y be a sy mp to ma ti c a nd le sio n dis co vere d in cide nta lly or p atie nt ma y pre se nt wit h a p ainle s s swell ing caused by a slow growi ng le sio n causing expansio n of the jaw a nd p ro du ci ng a no n ten de r f aci al a sy m me try 1 3 . In children the teeth may f ail to erupt 1 3 . Fibrous dysplasia of the maxill a is an e spe cial ly serious fo r m of the di sea se si nce it h a s a m a rke d p re d i l e c ti o n f o r o cc ur re n ce i n chil dre n . Seve re malocclusion and bulgi ng of the canine fo ssa or extre me p ro mine n ce of the zygo mati c p ro ces s , producing a marked f aci al deformity, a re typ ic al se qul ae of t his di sea se in max illa. Seru m al kali ne pho s pha ta se an d u ri na ry h y d ro x y po l i ne are examples of
Cl ini c al Pre se ntati on A l imp , pa in i n leg a nd fr ac tu re i s the initi al sy mp tom. It pursue s a p ro tr a c te d c l i ni ca l c o u r se c ha ra c teriz e d by pai n , def o r mi t y & a t e nde nc y t o p at ho l o g i cal f ra ctu re o f t he af fect ed bo nes 1 1 . Le g length d isc repa ncy i s ve ry commo n a s a resul t o f i nvolve ment of the uppe r po rtion of the femu r 1 2 . Fre que nt ly i dentified de for mi tie s i nc lude cox a v ar a, the s he phe rd ' s c rook defo rmity , bo wing of the ti bia etc 1 0 . The o bje ctive fe ature s seen i n roentge nograms o f bo ne s affecte d by polyo stoti c fi bro us d yspla si a in cl ude : b roa deni ng or ex pan sio n of bone , th in ning o f c or tex, c ha ra c teristi c ra refied & a ppa ren tly t r abe cula ted ap pearan ce , second ary de formi ties of affe cte d bo ne s 1 1 . Pre mature se cretion of pituitary folli cle stimul ating ho rmone has been r e p o r te d as well as mode ra tely ele vate d b a sal me tabol ic rate. Most surgical ti s sue i s obt ai ned b y c u ret ta ge . The s pe ci me n h a s a distinct gritty feeling refle c ti ng the
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u sef ul ma rke r s and a re u sed to moni to r respo nse i n t he no n su rgi ca l t re at men t of di sea se ra the r th an fo r d i ag nosi s 1 3 . A ground glass or o range pee l appearance i s see n when there are areas of co ndensatio n i nte r spe rsed w ith are as of radiolucency. The le sio n causes reso rptio n of roots of erupted t e e t h 1 3 .I t m ay sho w fo cu s o f g rit ty t is s ue in the bone 5 . The t ra becul ae may be devoi d of o steo blastic ri mming , the reby a ppea ri ng t o be f o r me d by f i b ro b l a sti c o s seous me tapl asia 1 3 . S y nd ro me s A sso cia te d wi th Fi bro u s D y spl a sia M cCune-Albrig ht syndro me is an endocri nopathy o c curri ng mainly i n gi rl s, co nsi sti ng of t he t ria d of p re co ci o u s p u ber ty , po l y o sto tic fi bro u s d yspla si a a nd ch ara c teri stic c u taneo u s p ig men ta tion . Th e c u taneo u s le sion s ar e fla t pig men ted macule s, of ten re ferred to as "caf au l ait " spot s Ma za braud sy nd rome i s the r a re combin at ion of fibrous dysplasia and soft- ti s sue myxo ma s. There are three mode s of treatment i .e . ob se rva tion , medi ca l the rap y & s u rgi cal t re at me n t . C o r ti so ne ha s bee n re por te d to p rod uce so me relief i n pai n of bo ne le sion s. Impo rtant line of me di cal treatment is with b ispho sp hon ate s w hi ch i nh ibit o steo cla stic ac tivi ty 6 . Young patients r e cei v i ng p a mid ro n ate s ho u l d be moni to red w it h se ria l radio gra ph s to che ck fo r a transie nt mi ne ralization de fect , wh ich pre sen t s a s in crea sed g ro w th pla te t hi ck ne s s , t hi c ken i ng o f corti ces and/o r o ssifi cation of radiolucent are a s 1 0 .
Surgical Treatment
A cco rdi ng to El Dee b M, t he t re at men t of choi ce is su rgi ca l , de pending upo n the si ze of the l esion a s a s cer ta i ned by t he r adio g ra phi c p i c tu re an d by b i o p sy . In the o steol yti c t ype radi cal cu re tt age i s i ndi ca ted , w he re a s in t he m o re ma tu re , soli d type su rgi cal shav ing a nd re con tou ri ng i s in di ca ted . Fibrous d y s pl a si a i s t re ate d b y cu ret tage an d p ac ki n g wi th ca ncello us chip g raf ts, by subpe rio steal excision and c an ce l l o u s b o ne g r aft , by extrape rioste al exci sion and can cello u s bone g raf t, co rt ica l graf t o r bo th. In ma xillof aci al are a , a co mmon pro cedure i s to del ay surge ry until bo ne g rowth cea se s an d to con tou r the b ulge d por tio n o f the bo ne fo r an e st he ti c ap pea ra nce . I n c ase o f v i su al d i s tu rb an ce cau se d by co mp ressi o n o f op ti c ne rve , i mmed iate s urge ry i s nee ded 5 . A cco rdi ng t o Edge rt on the su rgi cal tec h niq ues used a re : 1 ) Si mple bo ne co ntou ri ng 2) Rese ction and acryli c i mpl ant 3) Re sectio n, replantation re model ing and
Re cu rre n ce of fibrous dysplasia follo win g cu re tt age i s mo re common in c hi l d re n th an i n a du lt s . Thi s re move , resha pe , an d repl ant te chn ique h as excelle nt bone heali ng, good po s tope ra tive co ntou r s , and no c lin ic al evi den ce of re cu rre nce of bone enlarge ment. Mal ignant t r an sfo rma tion of fi bro u s dy sp la sia o cc ur s v e ry i nf re q uen tl y , w i th r epo rte d p rev alen ce s ra ngi ng f rom 0 .4% to 4% wi th ave rage incide nce be ing 1% 1 0 . The mo st commo n
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mali gna nt t u mo rs we re o steo sa r coma , fi bro sarcoma, a nd chon dro s ar coma . Pe ria pi cal Ce me nto O s seo u s D y spl a sia a l so k no wn as cementoma , osseous dysplasia a nd periapical cemental dysplasia. The first compre hensive clini cal, radiographi c , a nd hi st opa tholo gi c st udy w as r e po rte d by Sta f ne i n 193 3 . B l um i n 1 930 and Tho ma in 193 7a nd 194 4 de fine d i ts h i sto pa tholog y . PCD i s not a tr ue ne o p l a s m b ut a dys pl as ti c conditio n in whi ch multi ple fo cal a rea s of bo ne an d ma rrow are repl ace d by cellular connective tissue le sio ns wi th li mi ted g row th po ten tia l. The le sion attains a f ixed si ze and l ate r un der goe s a ma tu ra tion p ro cess t ha t c ul mi na tes in t he for mat ion of mul ti ple dense cal cifie d intrao sseous no dule s 1 2 . P C D i s a n a sy m pt o m ati c le sio n of ten di scove red o n r ou tine radiographi c examination .Multi ple le sio ns a re ofte n pre sen t . B u cc al a nd l i ngu al e x p an si o n o f the co rti ce s i s of ten absent. The age of occurre nce has bee n v ari ably repo rted by va rio us au tho r s f ro m 3 r d to 5 t h de ca de wi th a ra nge of 1 4-8 2 ye ars and mea n of 42 .5 yea r s wi th ca se s r a rely o cc u rr ing befo re 20 ye ars of age 1 2 . Mandible ( 6 8 .15 %) 5 i s more commonl y affe cted than 1 4 max illa .The lesio n princi pally i nvolve s the api cal a rea of one o r more vital mandibul ar teeth, p ar ti cul arly t he i nci so rs . F emale to male ratio has been vari ably repo rted be twee n10:1 to 14 :1 . Mo st le sion s a re l e s s t han 0 .5 c m i n si ze . M a x i mu m si ze ra rely excee d s 1.5 cm. Pe ri api cal ceme nto -osseous dysplasia has bee n c la s si cally de sc ri bed a s p rog re ssing t h roug h 3 r a d i o g r a p hi c sta g e s . 1) Osteoloytic stage 2) Ceme ntoblasti c stage . 3 ) The thi rd o r mat u re stage INTERNATIONALDENTALJOURNALOFSTUDENTSRESEARCH|JuneSep2012|Volume1|Issue2
Diffferential Diagnosis
O the r e ntit ies wh ic h ma y be con fu sed wi th fi brou s dy splasia are ossifying fi bro ma, c eme nto o s seu s dys pl as ia , Page t s di sea se , c eme nto ma , c he ru bi sm , h y per pa ra th y roi di s m , c h roni c sc lero si ng o steo myeli ti s, o steo geni c s a r coma e tc . Le sion s th at may suggest fibrous dysplasi a incl ude simple bone cy sts, nono ssifyi ng fi bro mas, o steo fib rou s dy sp la sia , a da ma nti no ma , low-grade i nt ra med ull ary o s teo sa rco ma , and P a g e t d i sea se 1 0 .
CEMENTO-OSSEOUS DYSPLASIA (COD)

Ce mento-osseous dysplasia i s the mo st co mmon f ibro-o sseous le sion o ccurri ng i n the tooth be ari ng areas of the jaws. COD i s a group of no n neo plastic proce sse s usually confine d t o the too th be ar ing a rea s of the ja ws o r e den tulo us alveol ar p ro ce s ses 1 4 . Ma ny te rms h ave been u se d to refe r to ceme nt-osseus dyspla si a : Peri api cal ceme nt-osseous dysplasia (PCD), Flo rid o sseus dy splasia ( FOD) , Flori d c eme nto osseu s dy sp la sia ( FLCOD ) , Focal cemento osseus dysplasia ( FCO D) . Ro binso n a tt ri bu te d the ca u se as i n ju red bone rea ct s in an a bno rmal w ay to low- gr ade o r c h roni c in ju ry by reso rb ing fo rmed bone trabe cul ae and r epl aci ng i t wit h c ell ula r f ib rou s connective tissue , in which i mmature bo ne an d a ceme nt um-li ke subst an ce a re de posit ed .
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to 6th u s ual l y o cc u r s b e twe e n 3 r d de ca de s, fe ma le: male ra tio bei ng 8 : 1to 1 0: 1 . Mandible is more commo nly the site of occurrence wi th around 77% of le sions bei ng in mandi ble ; particularly too th be ari ng areas of po ste rio r ma ndi ble , and 1123% o f lesions occurri ng in max illa. The si ze ra nge va ries fro m 0 .2 -1 1 c m wi th ave rage of 1 .8 cm 2 . Re gardless of st age , a n impo rt an t d iag nosti c fe ature i s it s clo se a sso ci atio n wit h t he pe ri apex or previous ex tr ac tion si te . Focal ce mento-o s seous dyspl asia te nds t o be well de marca ted wit h or wi tho ut c or ti cat ion. The re is no bowi ng of i nfer ior ma ndi bul ar bo rde r . A t t he time of s u rgi cal explo ra tion , t he su rgeon usually fi nd s gr it ty he mo r rha gi c mate ria l. The se gro s s fi ndi ng s con t ra st sha rp ly wi th t ho se of ce me nto-o ssifyi ng fibro mas, which s h are m an y f e a tu re s hi sto l o g i cal l y . The la tte r neopla sms ten d to enucleate i n o ne piece and are ofte n w hite , gl ist eni ng an d ho moge neou s on cut surface . Radiology was of central i mpo r tan ce to the det ec tion of a t lea st 64% of f o cal c e me nt - o s se o u s dysplasi as fo und i n cide ntally to radiography 1 5 . On the basi s of histopathologic study 3 progressi ve stage s can be i dentified: The early (o steo lytic) , the inte rme diary ( fibroo sseous) , the late (Osteoscle rotic) . Be cau se fo cal ce men to-o s seous dysplasi a ge nerally ex hibi ts l ittle or no ten denc y to e nla rge eve n a fte r partial removal of the le sion, these l e sio ns do no t requ i re a ny t re a tme n t .
Differential diagnosis
R adio lu cen t s tage Apical periodo ntal o r a rad i c ul a r cy st g r anuloma
Pr imo rd ial odo ntoge ni c c ys t Ea rly ph a se fi bro ma of o s sif yin g
Chro nic o steomyelitis( if 4 to 6 a nte rio r tee th a re i nvolve d)
Mi xed stage an d radio paq ue stage O do n to ma Chro nic o steomyelitis Ossify ing fi bro ma Osteoblasto ma
Treatment
Only pe riodic obse rvation i s necessary d uring whi ch o ne wou ld ex pect t o see t he radiog ra phi c ch ange s a ssociate d wi th mat ur a tion of the lesion .
Focal Cemento-Osseous Dysplasia

T hi s c on di tion d e rive s histoge neti call y f rom ele me nts of the pe rio don tal l igamen t . O ther e tiologi cal theo rie s consi der it to be a rea ctive le si o n an d i t i s mo re co mmon i n wo men 2 . Cl ini c al Fe ature s FCOD is al mo st in va riab ly an asympto mati c di scove red le sion o n a radiographic examination an d o c cu rs i n per iapi ca l are as of tee th wi th v ita l p ulp s o r i n r egio ns o f ex tr ac tio ns . The conditio n rarely pro duce s expansion o f t he bone . La rge r le sio ns may ho weve r c au se sl igh t jaw enl arge me nt . FCOD
Florid Cemento-Osseous Dysplasia

Ce mento-osseous dysplasia has a pattern of expre ssion that i s often mul tifo cal a n d co mmonl y a ffe ct s all
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quadrants of the max illa and mandi ble . Thi s multifocal e xpre s sion i s kno wn as f lori d ce mento-o s seous dysplasi a. It is cl inically the mo st extensive fo rm of ce mento-o sseous d y s pl a si a a nd he nce t he ter m f l o ri d. Mel ro se et al initi ally repo rte d FLCOD as florid osseous dysplasia. T he di sea se a ppea r s t o ha v e a f a mi l i al d is tr ibu tion ; i t i s more co mmon in wo me n 2 . The di sor de r i s s t ri ctl y lo cali ze d to the too th bearing areas a nd not a s so cia te d wi th any o the r skeletal deformity. When the le sio ns a re la rge , ja w expa n sion ma y be no ted , p ar ti cu l a rl y o f t he m a ndi bl e le ading sometime s to facial defo rmity, sy mp to ms su c h as du ll p ain, discharging sin use s o r seq ue str a tion s. O c ca sio n al l y , pat i e nt s wit ho ut si g n s of infe ction compl ain of an i nte rmittent, dull , achi ng sensation in the ma ndibular molar area. All Tee th h av e no rma l spo nt ane o u s p ai n a nd a re vi tal . It is see n mo re co mmonly in fe ma les 2 . They ha ve st ri king ten den cy t owa rd s b ila tera l, often quite sy mmet ri ca l, lo cat ion , a nd i t i s not u nu s ual to f i n d e x ten si v e l e sio ns i n a ll fou r qu ad ra nt s, p arti cul arly t he po sterio r region ( mol ar-pre molar region) . The y affe ct onl y the alveolar p ro ces se s a nd see m t o be in depe nde nt of tee th. Le sio ns have been f ound more c ommonl y i n ma nd ible an d so meti me s i n t he maxil la . Radiog raphically , a wi de spe c trum is seen. R adiographs usuall y di splay d i f f u se d i s tr i bu tio n of l o b ul a r , i rre gul arl y sh ape d r a diopa ci ties t h roug hout t he alveol ar p rocess. The lo bular densi tie s are of ten enme shed i n poo rly de fine d area s of decrea sed radiodensity, of ten havi ng a groundg l a ss a ppea ra nce . The l e sio n s a ppea r as multiple sclero ti c masse s, lo cated i n two o r more quadrants usually in t he too th be ari ng a rea s . Bio psy i s no t ne ce ssa ry . Manage ment of FLCOD i s of ten d iffi cul t an d not ve ry sat isfa cto ry . In t he a sy mp to ma tic p atie nt , it is p rob ably wi se to kee p the p a tien t u nde r o b se rva ti o n wi tho ut su rgi ca l i nte rvention be cause the radiologi c fe at ure s are diag no st ic. Ma nage men t of the sympto matic patient is mo re d iffi cul t . Se que st r atio n of t he c eme nt u m-li ke ma ss e s wil l o cc ur slowl y and he ali ng will follow thi s . S au ce ri za tio n o r su rgi cal ex ci sio n of t he scle ro tic ma sse s is of ten not su c cessf ul a nd may ma ke ma tte r s wo rse 1 2 . D iffe re ntia l Di ag no si s The se in cl ude c h roni c d iffu se sclero si ng o s teomyeli ti s, Page ts dise ase of bo ne , the o steomas of G ar dne r s sy nd rome , G iga nt ifor m c eme nto ma , o s teogene si s i mpe rfe ct a a nd pol y o st o ti c f i b ro u s dy spl a si a. Malig nant Po tential Deve lopment of ma lig nant spindle cell t u mor ha s b e e n rep o r te d i n a p a tie nt wi th FLCO D b ut i t is a r are o cc ur re n ce.
Hereditary Cemnto Dysplasia/Gigantiform Cementoma
Osseous
In 1953, Ag azzi & Bello ni repo rted a conditio n that was clini cally and r ad iogr ap hi call y simil ar to flor id ceme nto -osseous dysplasia but was i nhe rite d a s an au to so mal domin ant trait. They proposed the name Gi g an ti f o rm c e men to ma . This c ond itio n is r are . The g nat hi c
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enlarge ment i n mo st patients resul ts i n sig nifi ca nt fa cia l de for mi ty , a s well as i mpactio n, ma lpo sition and malo cclusion of the i nvolved de nt itio n . I f not trea ted the o sseo u s enlarge ment eventually cease s during t he 5 t h de ca de 1 2 . Usual ly develop d ur i ng 1 s t de ca de of l ife a nd by adole sce nt typi cal obvio u s le sions are no ted a nd followe d by a rap id an d expansi ve growth p at te rn . It de mo nstrates mul tifo cal invo lve ment of both ma xilla and mandi ble 1 2 . The i niti al fe atu re s re se mb le t ho se seen in ceme nto -osseous dysplasia, appe aring as mul tiple radiol ucencie s, in the pe ri api cal region s. Wi th pro gressio n , the affe cted site s expand to repl ace mu ch of the nor ma l bone w ith in t he i nv o l v e d q ua dr an t a nd dev e l o p a m i x e d rad i o l u ce n t a n d rad i o pa que p at ter n . Wi th f ur the r ma tu ra tion , the le sio n be co me s p redomin an tly radioopaque but of te n maintain a thin radiolucent ri m. Extensive resectio n of t he altered bone an d re con stru ctio n of the faci al skeleton and asso ciated soft ti ssue is re comme nded ca n produce acceptable f unctional and ae sthe tic re sul t 1 2 . D iffe re ntia l Di ag no si s O steiti s defo r man s o r Page t s d ise a se of bone , ch ron ic scle rosing o steo mye lit is , S cele roti c cemen tal ma sse s , ch ro nic p rod uc tive o stei ti s , osseous dysplasia, mu lti ple enosto se s. v ari able a mo un ts of mine ra li zed m a ter i a l r e se mbl i ng b o ne a nd /o r c e me nt u m . M o n tg o mer y w a s f i r st to c o i n the te r m o s si f y i ng f i bro m a t i s s ue wit hi n w hi ch t he bone i s fo rmed 1 7 . I t accou nts fo r on ly 0 .1% of t he bo ny l e sio ns . Os s i f y i ng f i b ro ma be l o n g s to t he poo rly def ined g roup of fi broosseous lesions involving the jaws and craniof acia l bone s t ha t resul t in repl ace ment of the bo ne by fibro us tissue and subsequent 1 8 , 1 9 mine rali zation . The c au se o f the o s sifyi ng fi bro ma re mai n s un kno wn . OF usual ly o ccurs be tween the 3 r d a nd 4 t h de ca de of life with the a vera ge age be ing 30 yrs 1 2 .M arked predile ctio n fo r o ccurrence is repo rted to be seen in fe ma les wi th fe male to male r atio v ary i ng f ro m 1 .5 6 :1 t o 5 :1 . Goaz and White repo rted that when OF occurs in the ma xilla, i t i s most commo nly lo cated i n the canine fo ssae and zy gomati c arch. It may g row to comple tely fil l the ma xillary sinus. It can effe ct bo th maxill a and mandible but the prefe rre d si te of occurrence is r epo rte d to be mandi ble va ryin g fro m 70%- 89% of cases and max illa i n 11%26% with af fini ty fo r premolar & molar area. The max illary le sio n s we re fo und to be more ag gre ssive . O s sif y i ng F i b ro mas a re a ss o c i ate d wi th a slowly progressi ng enlarge ment of the affected bo ne . Le sion i s asymptomati c until the growth produce s a no table swel ling and mild deformi ty an d fa ci al a sy mme try. Di sp la cemen t of tee th i s a n ea rly cli ni cal fe at u re . When ra pid g row th doe s oc c ur , the sy mptoms a re r ela ted to t he le sion si te a nd may i ncl ude painle ss chee k swe lling , u nil ate ral p rop to sis, di plopia and
OSSIFYING FIBROMA (OF)

O s sify ing fib ro ma is a be nign odo nto genic t umo r of me sen ch y mal o rigi n . O F beh ave s li ke a be nig n bone neo pla sm 1 6 . The t u mo r is de mar c ated and occasionally encapsul ated le sion c on si st ing of fi bro us t issue co nta ini ng
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epi stax is. De at h i s a ra re o ccu r ren ce s e co nd ary t o i n t ra cr an i al e x ten si o n . The se le sion s may o cc as iona lly h ave ill -defi ned border, if rel ative ly rapid g row th o c cu r s . A s the le sio n ma tu re s , m i x e d rad i o l u ce n t a n d rad i o pa que a ppea ra n ce may be se e n . The c ha ra c teris ti c f e a tu re s o f O F i n r a d i o g r a p hs a re e x p a n si o n a nd l e sio n margi nation, demarcation, or . c o r ti ca t i o n Co rti cal e xpansion is pre sent, of ten with an eg gshell- thi n c o rte x . La rge o s sifyi ng fib roma s of ma ndi ble ofte n de monst ra te a c ha ra c teris ti c d o w nw a rd b o wi ng o f i nfe rio r cor te x of man di ble . O n s u rgi ca l e xplo rat ion , the tu mo r i s fo und to be re lat ively hy pova scul ar and well de marcated f rom the su r roun din g ti ssue , permi tti ng r ela tively e asy sepa ra tion f ro m the surrounding bone . Some lesions will h ave a def ini te c ap s ule. Thi s de mar ca tion f ro m t he s u rr ou nding t is s ue i s a n i mpor t an t featu re i n distinguishing OF fro m FD . The va sc ul ar sp ace s re se mble arteriole s o r capillarie s di spl ayi ng a c on tin uou s e ndo theli al l ayer w it h p l u mp e ndo the l i al c e l l s p ro tr ud i ng i nto the capillary lumen .The calcif ied c ompone nt c on si s t s of ro unde d o r lo bulated basophili c ceme ntum-li ke masse s, trabeculae of o steoid or bo ne o r co mbi na tion s of bo th , t he m a jo ri ty of bony t r abeculae in ce men too ssifyi ng fi bro ma are thi n , single , and sep ar ate wi th o steo bla stic ri mmi ng . Tre at me nt of o ss ifyi ng fi bro ma i nvolve s the co mple te re mov al of le sio n by cu ret tage, en ucleatio n , o r exci sion. Co mple te exci sio n of the t u mor ha s be co me a ne ce s sit y s in ce it i s no to rious fo r re cu rr en ce 2 0 .
Juvenile Ossifying Fibroma

Juvenile ( agg ressive) o s sifyi ng fi bro ma was used in 2 n d edition of WHO classifi cation of odontogeni c t u mor of ch ild ren to de sc ri be a le sio n a ffec tin g the jaw s unde r the a ge of 15 ye ars.
De fin it ion The second edi tion of the WHO classifi cation of o dontoge nic tumo rs de fine s juve nile ( agg re ssive) ossifyi ng fi bro ma as a n actively g rowi ng le sion c on si st ing of cell ric h fib ro us ti ssue c on tai ning b a nd s of c ell ula r o steoi d wi tho ut o st eobla sti c r i mming toge the r wi th tr abec ul ae o f mo re ty pic al bo ne . Gi an t ce ll s may al so be pre se nt. Cl assifi catio n I t i s the t er m use d t o de s cribe two d istin c t hi sto pa thologi c va ri an t s of o s sifyi ng fi bro ma of t he c ra niof aci al skele ton psammo matoid juvenile o s sifyi ng fi bro ma t r abe cula r ju veni le o s sifyi ng fi bro ma 1 6 . J uv e n i l e a ct i v e o s sif y i ng f i bro ma a ffec t s p redo mi na ntly pa tie nt s i n t he fi r st two de cade s of life , t he mea n age of o cc u rren ce be ing 3 to 2 3 yr s 1 6 . No si gnif icant sexual pre dilectio n i s seen i n any of the two fo rms 1 2 . Psammo ma toid juve nile ossifying fi bro ma o ccurs overwhel mingly i n the sino na sa l a nd o rbit al bo ne s of the skull, whereas trabe cular juvenile o s sifyi ng fi bro ma i s p redo mi nan tly a g na thi c l e s i o n a f f e c ti ng the j a w s , w i t h a predilectio n fo r maxilla. In the mandi ble , the tumor occurs more commo nly in the ramus than i n the
67
bo dy of ma ndi ble 1 2 . The JOF is ofte n cha ra c terized by a p rog re ssive and so meti me s rapid expansio n of the affected area. T he cli ni cal di ag nos ti c c ha ra c teris ti c s s ug g e sti v e o f J OF a re t he pa tie n t s a g e , r ap i d i nc re a se i n le sio n si ze an d ab se nce of pa in , p are s the sia a nd b ru i t . When the o rbi tal bone s and pa ra na sal sin u se s a re i nvolve d , t he p at ien ts ma y de velop propto si s, exophthal mos, and bulbar displace ment 1 2 , 1 6 Rarely , i nt ra cr ania l e x ten si o n ha s re su l te d i n meni ngi ti s 1 2 , 1 6 . The le sio n ex hi bit s a p ri ma ry r ad i o l u ce nt q uali ty with varying amounts of inte rnal radiopaci ty ,refle cting degree of mine rali zation. So me lesions contai n n u me ro u s u n i f o r m, r o und , o f te n l a m i na ted s t r uc tu re s d e s cr i b e d a s o s sic les or psa mmoma like bo die s . Foci o f mul tinucleated g iant cell s may also be present.
References
1 ) M M u pp a rap u e t a l : Fo ca l ce men to - o s se o u s dy spl a sia. Den to maxi l l o f a cial Ra diology 2 005 :34 :3 9- 43 2 ) S ak u ma T, K a wa sa ki T : Co nc u rre nt cemen tifyi ng a nd o s sifyi ng fi broma s of th e mandi ble : Repo rt of a case . J Oral maxillofac Surg; 1998; 56: 778-82 3) A ra ki M , H a sh i moto K , Ma t sumo to K , E ji ma K , Kaw a shi ma S,M at s u moto N , e t al . R adiographi c patte rns of fi bro-o s seous le sio ns in t he ja ws -co mp ari so n wi th hi stopathologi cal image . Dent Radiol 2 00 5 ; 45: 9 71 04 . (I n J apa ne se) . 4) 5) M A r ak i e t al . Fi bro osseous le sions usi ng bi nary i mage s. J Dentomaxillofacial C ho ng V F H , . K hoo J B K . Fibrous Dy splasia Involvi ng the Base o f the Skul l .
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6 ) D i c ap rio MR , En ne ki ng WF .Fib rou s dy sp la sia : pat hop hysiology , Evaluation and Treatment. Journal of Bone and Joint Surgery. 2005; 87:1848-1864 7 ) R i c a l d e P , H o r s w e l l B B : C ra ni o f a ci al F i b ro u s Dy sp l a sia o f t he F ro nt o - O rbi tal Regio n : A c a se serie s a nd l ite rat u re rev iew . J Oral Maxillofac Surg 2001; 59, 157-
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9 ) Khadilkar VV , Khadil kar A V : Or al Bi sp ho spho na te s in Po lyo sto tic Fi brou s Dy spla sia . Indian Pediatrics 2003; 40: 894-896 1 0) Go nclave s M , Pi spico R : Cli nical , Radiographic, Bio che mical and histolo gical fi ndi ng s of Flo rid Ce mento-osseous Dysplasia and Repo rt o f a C a se. Braz Dent J 2 005 ; 16( 3) :2 47- 250 1 1) Po poff SN, Marks SC : The regulation of skeletal mo deling and remodel ing in t he ja ws. Oral and Maxillofacial Clinics of North America 1997; 9 (4): 563-580.
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1 3) Fro del JL, Funk G . Ma nge men t o f Agg re s sive Midf ace a nd O rbi ta l Fi bro us Dy spla sia . Arch Facial Plast surg .2000; 2:187-195 1 4) N A Al s ufy an i a nd EW N L a m: Cemento-o sseous duslpasia of ja w bone s. J
Dentomaxillofacial Radiology 2011; 40:141-146 1 5) DS Mc Donald-Jankonaski. Foc a l c e ment o s se o us d y sp la sia :a sy stematic review . Dentomaxillofacial Radiology 20 08;3 7 :35 0-3 60
1 6) Y L iu et al : O s sif y i ng Fib ro ma s of jaw bo nes .
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804-809
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69 CASEREPORT
INTENSIVECAREUNITSSTAFFSKNOWLEDGEANDORAL HYGIENEPRACTICEINCROATIANHOSPITALS
Emina Kabil1, Maja Miladinovi2, Matej Par3
1Undergraduate
Corresponding Author Emina Kabil Undergraduate Student, Year 4, School Of Dental Medicine, University of Zagreb, Zagreb, Croatia E-Mail: ekabil@sfzg.hr Access this Article Online
Student, Year 4, School Of Dental Medicine, University of Zagreb, Zagreb, Croatia Student, Year 4, School Of Dental Medicine, University of Zagreb, Zagreb, Croatia Private Dental Practice, Dankoveka 9/I Zagreb, Croatia
2Undergraduate
3DMD,
Quick Response Code

Abstract
Aim: Intensive Care Unit (ICU) patients require thorough oral care. Inadequate oral care may predispose ICU patients to severe nosocomial infection, Ventilator Associated Pneumonia (VAP). On the other hand, appropriate oral hygiene in ICUs can potentially reduce morbidity from VAP and therefore shorten hospital stay and reduce ICU mortality. Aim of this study was to assess the awareness of this problem and oral hygiene practice of ICU medical staff. Material and Methods: The study was conducted among 249 members of ICU nursing staff from 14 Croatian hospitals. A written survey comprising questions divided into two groups: staff knowledge and oral hygiene practice was used. Results: 94.7% of respondents declared they were familiar with the VAP. Only 32.6% of respondents know the right cause of VAP. 44, 9% reported having an oral care protocol in their hospital. Tongue brushing was reported by 42.2% nurses, and the most frequently used oral hygiene agent is gauze soaked in paraffin oil (75.1%). Most of the nursing staff was aware of the importance of oral care practice in ICU and they allege lack of time (47.1%), lack of staff (39.6%) and the lack of resources (36.6%) as limiting factors in the implementation of adequate oral hygiene. Only 60.6 % wanted additional education and training. Conclusion: This study indicates a relatively low level of knowledge and great diversity of oral hygiene practices in Croatian ICUs. In order to improve oral hygiene in ICUs, a standardized written protocol should be introduced. Encouraging staff education and providing ICU nurses with sufficient resources is needed in order to improve oral hygiene enforcement in ICUs
[Type text]
.
Introduction
Intensive Care Unit (ICU) patients require 24hour care and monitoring. Oral hygiene in critically ill patients is often neglected or inadequately performed by quickly swabbing patients' mouths [1]. Possible reasons for this practice are staff's attitude that other aspects of nursing care are more important than adequate oral care [1, 2, and 3], lacking awareness of thorough oral hygiene importance [4] and lack of standardized evidence-based protocol [1, 4, 5, 6, 7, and 8]. Oral flora of critically ill adults differs from that of healthy adults and contains bacteria that may cause pneumonia [1]. Inadequate oral care may predispose ICU patients to severe nosocomial infection, known as Ventilator Associated Pneumonia (VAP). VAP is defined as nosocomial pneumonia that develops in a patient who has been intubated for more than 48 hours [9]. Endotracheal intubation not only compromises the natural barrier between the oropharynx and trachea but also facilitates the entry of bacteria into the lower parts of respiratory tract [10]. Studies have shown that most cases of VAP were caused by bacteria that colonize the oral cavity and dental plaque [10, 11, and 12]. Furthermore, endotracheal tube may become colonized by bacteria. Intubation disables physiological cleaning of upper respiratory tract by coughing, compromises mucociliary transport and increases the secretion of mucilage. [13] All of these factors additionally facilitate development of VAP. VAP is associated with high morbidity, longer hospital stay, higher health care costs and increased mortality rate [8, 10, and 14]. Simple oral care interventions such as toothbrushing and mouth rinsing with chlorhexidine may reduce the incidence of VAP and consequently morbidity as well as mortality in ICU patients [15, 16].
Objectives
Data on oral hygiene practice of ICU staff in Croatian hospitals is lacking and up to date no research articles on this topic have been published. Aim of this study was to assess the awareness and knowledge concerning VAP as well as current oral hygiene practice of ICU medical staff in order to identify potential possibilities for improvement.
Subjects and Methods

The study was conducted from November 2010 to February 2011 among 249 members of ICU nursing staff from 14 Croatian hospitals. The research was approved by the Ethical Committee of the School of Dental Medicine, University of Zagreb. ICUs staff, who participated in this study, were informed about the research and signed informed consent. A written survey comprising questions divided into two groups: staff knowledge and oral hygiene practice was used. Ten true/false statements were used to assess knowledge and attitudes of respondents regarding VAP:
1. 2. 3. 4. 5. 6. 7. 8. 9. VAP is infection caused by specific pathogens. VAP is infection caused by non-specific pathogens. VAP may be caused by multi-resistant strains. The most common cause of VAP is air or droplet transmitted pathogens. The most common cause of VAP is oral cavity pathogens. VAP has high mortality rate. VAP is easy to cure and patients usually recover well. VAP is one of the most common nosocomial infections. Appropriate oral hygiene in intubated patients may reduce the incidence of VAP. Pneumonia may also occur in patients who are not intubated.
10.
The following questions were used to assess staffs education and interest for future education and training:
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1. 2. Are you familiar with the VAP? When were you first acquainted with the VAP? (during education, while working in hospital, during professional training, in some other occasion) Do you want additional training and education? (yes, no, do not care) 8. 9. 10. 11. rinsing with some other agent cleaning with sponge and gauze artificial saliva gauze soaked with paraffin oil something else
12.
3.
The following limiting factors were listed (multiple answers are possible):
1. 2. 3. 4. 5. lack of time lack of education lack of staff lack of resources something else
In terms of practice, respondents were asked about commonly performed oral hygiene procedures and limiting factors in the implementation of adequate oral hygiene. The following list was given and participant was asked to mark procedures which he/she routinely performs (multiple answers are possible):
1. 2. 3. 4. 5. 6. 7. cleaning teeth with toothbrush cleaning teeth with toothbrush and toothpaste tongue brushing rinsing with chlorhexidine rinsing with hydrogen peroxide rinsing with povidone iodine rinsing with saline
___________________________________________ ___________________________________________
Results
In terms of knowledge, ten true/false statements were given. Percentage of correctly marked statements is shown in Figure 1. Statement VAP is infection caused by specific pathogens showed the least percentage of correct answers (29.3%, n=73). Statement with most correct answers was Appropriate oral hygiene in intubated patients can reduce the incidence of VAP (90.8%, n=226). Overall percentage of correct answers was 65.8%.
100 90 80 70 60 50 40 30 20 10 0
87,9
84,3 70,2 70,6 69,8
90,7 71,8
% correct answers
40,1 29,3
42,5
10
Question No.
Figure 1: Percentage of correctly marked true/false statements.
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1. 2. 3. 4. 5. 6. 7. 8. 9. 10.
VAP is infection caused by specific pathogens. VAP is infection caused by non-specific pathogens. VAP may be caused by multi-resistant strains. The most common cause of VAP is air or droplet transmitted pathogens. The most common cause of VAP is oral cavity pathogens. VAP has high mortality rate. VAP is easy to cure and patients usually recover well. VAP is one of the most common nosocomial infections. Appropriate oral hygiene in intubated patients may reduce the incidence of VAP. Pneumonia may also occur in patients who are not intubated.
Most of respondents (94.7 %, n=236) declared they were familiar with the VAP (Figure 2).
250 Number of respondents 200 150 100 50 7 0 YES Are you familiar with the VAP? NO 236
Missing data= 3
Figure 2: Answers to question Are you familiar with the VAP?
The most of nurses (86.3%, n=215) have received education concerning VAP during their work in the hospital, and significantly smaller number (28.9%, n=73) during formal school education.
250 Number of respondents 200 150 100 50 0 during education while working in hospital during professional training in some other occasion
When were you acquainted with the VAP?

Figure 3: Answers to question When were you acquainted with the VAP? (Multiple answers are possible)
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When asked about possible additional education, 16% (n=38) of respondents declared they do not want any additional training and education, and 22% (n=54) of them do not care. Most of subjects (62%, n=151) noted they are interested in future education (Figure 4).
Do you want additional training and education?
DO NOT CARE 22%
NO 16%
YES 62%
Missing data= 6
Figure 4: Answers to question: Do you want additional training and education?
Oral care practice varied within each hospital. Gauze soaked with paraffin oil was the primary material used (75.1%, n=187), and the most common mouthwash was chlorhexidine (57%, n=142). Tongue brushing was reported by only 42.1% (n=105) nurses (Figure 5).
200 180 160 140 120 100 80 60 40 20 0
187 142 128 114 94 105 77 48 35 13 0 7 8 9 10 11 12 110
Number of respondents
Which oral hygiene procedures are commonly used?

Figure 5: Commonly performed oral hygiene procedures. (Multiple answers are possible)
1. 2. 3. 4. 5. 6. 7. 8.
cleaning teeth with toothbrush cleaning teeth with toothbrush and toothpaste tongue brushing rinsing with chlorhexidine rinsing with hydrogen peroxide rinsing with povidone iodine rinsing with saline rinsing with some other agent
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9. 10. 11. 12.
cleaning with sponge and gauze artificial saliva gauze soaked with paraffin oil something else
The most common factors limiting adequate oral hygiene are listed in Figure 6. Lack of time has been noted as the most common limiting factor (57.4%, n=143).
160 Number of respondents 140 120 100 80 60 40 20 0
143 120 111
23 6 lack of time lack of education lack of staf f lack of resources something else
Lim iting factors in the im ple m e ntation of ade quate oral hygie ne
Figure 6: Limiting factors in the implementation of adequate oral hygiene. (Multiple answers are possible)
Discussion
Most of respondents (94.7%, n=236) declared they are familiar with the VAP, but only 36.6% (n=91) provided correct answer to the question about etiology of VAP. This indicates great discrepancy between self- perceived and real level of knowledge. Generally low level of knowledge is the possible cause of staff's unawareness and false impression they are well informed about the VAP. This is indicated by relatively low overall score average score for all 10 questions is only 65.7%. Also, significant variability between scores for individual questions was noted. Percentage of correct answers ranges from 29.3% up to 90.7% (Figure 1). This indicates great variability in knowledge of different aspects of VAP. For instance, the worst results were scored for two questions dealing with etiology of VAP (29.3 and 40.1% accordingly) and the best result (90.7%) was scored for the statement Appropriate oral hygiene in
intubated patients may reduce the incidence of VAP. High percentage of correct answers (84.3%) was also noted for statement The most common cause of VAP are oral cavity pathogens, which implies that nurses are relatively well informed about the role of oral bacteria in VAP etiology. Considering that the majority of nurses stated they got familiar with VAP only at work (Figure 2, 3), presumably by word of mouth from older colleagues, and not during formal school education, it is somewhat contradictory that many of them havent shown interest for additional training and education (38%, n=95) (Figure 4). This finding also suggests that current curriculum of Croatian nursing schools lacks some crucial lessons and therefore should be revised. We suggest that oral hygiene in critically ill patients should be integrated in nursing schools curriculum as a nursing activity of very high priority. A high percentage of nurses (90.1% n=226) are aware that appropriate oral hygiene in ICUs
75
could reduce the incidence of the VAP, but they reported some limiting factors (Figure 6). Lack of time has been noted as the most common limiting factor (57.4%, n=143). A possible cause of this problem is relatively small number of nurses employed in Croatian ICUs, which seems to be insufficient to fulfill all required nursing tasks. In such situation, nurses are more likely to dedicate their time to some other tasks they consider more crucial for patient well- being [1, 2, and 3] rather than performing oral hygiene measures. Increasing number of nurses would probably enable them to distribute their nursing activities more evenly and to avoid neglecting of oral care. Literature dealing with oral care of critically ill often emphasizes the correlation of poor oral hygiene in ICUs with the lack of awareness [19, 20]. According to these studies, low awareness of the problem is the main cause of neglecting oral hygiene in critically ill patients. Since recommended measures [18] are relatively simple and inexpensive, simple rising of awareness (without any other interventions) should motivate nurses to perform oral care more efficiently. Considering poor economic situation in Croatia, as well as insufficient nursing education, we assume that mentioned lack of awareness plays important role in oral hygiene inadequacy. It is important to note the long- term efficiency of improved oral care for critically ill patients. Evidence shows that correctly maintained oral hygiene could greatly reduce the incidence of VAP [15, 16]. Lower incidence of VAP is correlated with less complication during hospitalization, shorter hospital stay, lower mortality and better postoperative recovery [8, 10, and 14]. This is beneficial not only for patients, but also for hospitals and healthcare system as a whole, since it greatly reduces hospital expenses. It is therefore rational to encourage education and enforcement of oral care in critically ill patients. The first step in accomplishing this goal should be raising awareness of the problem through formal school education, as well as during continuing lifelong education. The next step should be introducing a written evidence-based protocol (AACN) and providing staff with adequate materials and resources. 63.1% (n=157) of respondents perform oral hygiene measures as recommended by American Association of Critical- Care Nurses (AACN), i.e. brushing and rinsing with chlorhexidine [18]. There is some evidence available indicating that measures recommended by AACN are effective in prevention of VAP [22]. Even if AACN protocol isnt generally accepted as an effective measure for prevention of VAP, we consider its practical implementation useful for dealing with the problem. Several studies demonstrated that enforcement of protocol recommended by AACN successfully reduced VAP morbidity and mortality in clinical environment [15, 16, and 18]. Since it is the only protocol which is as-to-date supported by evidence, it should be taught in nursing schools and introduced to nursing staff. Also, tongue brushing, combined with tooth brushing and rinsing with chlorhexidine has desirable effects [22, 23, 24], but this survey has shown that it is performed by only 42.2% (n=105) of nurses. The most common oral hygiene procedure is swabbing with gauze soaked in paraffin oil, what we found very unique to Croatian ICUs. Little information has been found in the available literature regarding this method. In one Croatian medical high school textbook [21] paraffin is listed as an agent for oral hygiene in ICUs, but as dental professionals we are dubious about the potential benefit of this agent, except lubrication, moistening and mechanical protection of mucosa. It certainly lacks required antibacterial properties and combined with gentle swabbing isnt very effective in plaque removal. This practice should be replaced with brushing in order to mechanically remove the plaque. Using chlorhexidine after brushing inhibits
76
formation of new plaque and recolonization of bacteria to mechanically cleansed tooth surfaces [25, 26]. A great variety of performed procedures (Figure 5) is probably the result of lack of written oral hygiene protocol in Croatian hospitals. Having no precise guidelines, nurses perform oral hygiene procedures at their own discretion and in accordance with available materials. Many different materials for oral hygiene are used (Figure 5), presumably depending on their availability in individual hospitals. care patients receiving mechanical ventilation. Am J Crit Care. 2007;16:552-62. 7. Berry AM, Davidson PM. Beyond comfort: oral hygiene as a critical nursing activity in the intensive care unit. Intensive Crit Care Nurs. 2006;22:318-28. 8. Craven DE, Duncan RA. Preventing ventilator-associated pneumonia. Am J Crit Care Med. 2006; 173:1297-99. 9. http://www.ihi.org/knowledge/Pages/Changes/I mplementtheVentilatorBundle.aspx 10. Craven DE, Driks MR. Nosocomial pneumonia in the intubated patient. Semin Respir Infect. 1987; 2:20-33. 11. Torres A, el-Ebiary M, Gonzalez J, et al. Gastric and pharyngeal flora in nosocomial pneumonia acquired during mechanical ventilation. Am Rev Respir Dis. 1993; 148:352-7. 12. Valles J, Artigas A, Rello J, et al. Continuous aspiration of subglottic secretions in preventing ventilator-associated pneumonia. Ann Intern Med. 1995; 122:17986. 13. Levine SA, Niederman MS. The impact of tracheal intubation on host defenses and risks for nosocomial pneumonia. Clin Chest Med. 1991;12:523-43. 14. Hutchins K, Karras G, Erwin J, Sullivan KL. A comprehensive oral care program reduces rates of ventilatorassociated pneumonia in intensive care unit patients. Am J Intensive Care. 2008;36(5):81-2. 15. Yao LY, Chang CK, Maa SH, Wang C, Chen CC Brushing teeth with purified water to reduce ventilator-associated pneumonia. J Nurs Res. 2011 Dec;19(4):289-97. 16. Garcia R, Jendresky L, Colbert L, Bailey A, Zaman M, Majumder M. Reducing ventilator-associated pneumonia through advanced oral-dental care: a 48-month study 17. Schwartz SN, Dowling JN, Benkovic C et al. Sources of gram-negative bacilli colonizing the tracheae of intubated patients. J Infect Dis 1978;138:227-31.
Conclusion
The results of this survey indicate that present level of knowledge among nurses and oral practice currently performed in Croatian ICUs may be ineffective in prevention of VAP. Implementation of standardized written protocols, as well as additional nurse training should be done.
References
1. Munro CL, Grap MJ. Oral health and care in the intensive care unit: State of the science. Am J Crit Care.2004; 13:25-34. 2. Binkley C, Furr La, Carrico R, McCurren C. Survey of oral care practices in US intensive care units. Am J Infect Cont. 2004; 32(3):161-9. 3. Jones H, Newton J, Bower EJ. A survey of the oral care practices of intensive care nurses. Intensive Crit Care Nurs. 2004; 20:6976. 4. Cutler CJ, Davis N. Improving oral care in patients receiving mechanical ventilation. Am J Crit Care. 2005; 14:389-94. 5. OReilly M. Oral care of the critically ill: a review of the literature and guidelines for practice. Austral Crit Care. 2003;16(3):101-10. 6. Berry AM, Davidson PM, Masters J, Rolls K. Systematic literature review of oral hygiene practices for intensive
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25. Scannapieco FA, Yu J, Raghavendran K, Vacanti A, Owens SI, Wood K, Mulotte JM: A randomized trial of chlorhexidine gluconate on oral bacterial pathogens in mechanically ventilated patients. Crit Care 2009, 13:R117. 26. Munro CL, Grap MJ, Jones DJ, McClish DK, Sessler CN: Chlorhexidine, toothbrushing and preventing ventilator-associated pneumonia in critically ill adults. Am J Crit Care 2009, 18:428-437. ______________End of article________________
18. AACN Web site: http://www.aacn.org/WD/Practice/Docs/Practic eAlerts/oral%20care%2004-2010%20final.pdf. Accessed March 31, 2012 19. Adams R 1996 Quali.ed nurses lack knowledge related to oral health, resulting in inadequate oral care of patients on medical wards. Journal of Advanced Nursing 24(3): 552560 20. Price B 1990 Body Image-nursing Concepts and Care. Prentice Hall, London 21. Prli N. Zdravstvena njega za ucenike I. II. razreda srednjih medicinskih kola, u zanimanju medicinska sestra. 12. izd. kolska knjiga. Zagreb. 2009. 22. Feider LL, Mitchell P, Bridges E. Oral care
practices for orally intubated critically ill adults. Am J Crit Care. 2010 Mar;19(2):17583.
23. Wilkins EM. Clinical Practice of the Dental Hygienist. Philadelphia: Lippincott Williams & Wilkins, 1999. 24. Christensen GJ. Why clean your tongue? Journal of the American Dental Association 1998; 129 (11):1605-1607.
78 REVIEWSTUDY
ARETROSPECTIVESTUDYONOCCUPATIONRELATED MAXILLOFACIALFRACTURESINCHONGQING,CHINAFROM 2008(YEAR)TO2011(YEAR)

Piyush Sharma1a, Zhao Ningbo1b, Yang Kai2 Graduate Student, Department of Oral and Maxillofacial Surgery, Chongqing Medical University, Yuzhong district, Chongqing, China
1aPost
Corresponding Author Prof. Wang Tao DDS PhD (Oral and Maxillofacial Surgery), Affiliated hospital of Stomatology, Chongqing Centre of Oral and Biomedical Research, Chongqing medical university Chongqing, China E-Mail: taosan@126.com Access this Article Online
Graduate Student, Department of Oral and Maxillofacial Surgery, Chongqing Medical University, Yuzhong district, Chongqing, China
1bPost
2Professor,
DDS PhD (Oral and Maxillofacial Surgery), Affiliated hospital of Stomatology, Chongqing Centre of Oral and Biomedical Research ,Chongqing medical university Chongqing, China
Note: Authors 1a and 1b are Co-First Authors
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Abstract
Background Maxillofacial trauma constitutes of hard and soft tissue injuries, in this study we have discusses the fractures in maxillofacial region related to occupations .Fractures constitute a substantial proportion of cases of maxillofacial trauma. This retrospective study was designed to analyze the sex, age, cause, site distribution and treatment of maxillofacial fractures and their relationship with patients occupations in Chongqing, China. Methods A retrospective study on maxillofacial fractures was carried out in the Department of Oral and Maxillofacial Surgery, the First Affiliated Hospital of Chongqing Medical University (Chongqing, China) between January 1, 2008 and December 31, 2011. The study included 173 patients with 248 maxillofacial fractures. Sex, age, cause, occupation site distribution of patients and treatment modalities in hospital were recorded. Results The males consisted 67.6% of maxillofacial fractures and females (32.4%) Middle-aged had more fractures than young and old-aged, and the yearly distribution showed no significant variation. Road traffic accident was the most common causative factor (33.6%), followed by fall of an object 20.2%, and falls (18.5%). Taxi/truck drivers (24.3%) were most prone to have maxillofacial fractures, followed by construction workers (19.6%) and mine workers (16.2%). Regarding the site distribution of mandibular fractures, the majority (32.4%) occurred in the parasymphysis, 19.8% in the angle, and 12.6% in the condylar region. 71.3% of patients had rigid fixation with plates and 15.3% had inter maxillary fixation (IMF). Conclusion Occupation distribution and causes of maxillofacial fractures reflected trauma patterns within the community and can provide guidelines for the design of programs geared toward prevention and treatment. In our study the drivers and construction workers were more prone to maxillofacial fractures, proper safety measures while driving and working will significantly reduce the incidence of such injuries. Key Words: maxillofacial fractures, occupation-related, mandible fractures, rigid internal fixation (RIF), prevention
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Introduction
Many studies have reported the anatomic localization, causes, age and gender distributions, treatments, treatment results, and incidences of maxillofacial fractures.[1-3] As reported in previous studies the major cause of maxillofacial fractures was traffic accidents.[4] Other causes are assaults, falls, sports-related injuries, and civilian warfare.[5] Some studies shown assault was the most common cause of maxillofacial fractures in many developed countries, whereas traffic accidents was the most frequent causes in many developing areas.[6,7] The causes, types, and site distributions of these fractures seem to change with geographic locations. [1] Treatment of maxillofacial fractures includes fixation with miniplates, wire fixation, intermaxillary fixation, elevation and reduction. Moreover, graft and proplast applications for reconstruction of bone defects and elevation by Gillies method in the case of zygoma fracture are the most common treatments used worldwide and also in our department. Nevertheless, the treatment protocols of the patients with maxillofacial fracture may vary according to the types and locations of the fracture as well as the surgeons experience and preference. Because of cultural, social and environmental factors, both the incidence and etiology of maxillofacial fractures change from country to country.[8] China is the fastest growing economy in the world and is a developing country, this study was carried out in a major municipal province, Chongqing, which geographically locates in southwest China and is a fast-developing city. However, there have been few detailed reports about the occupation-related maxillofacial fractures in Chongqing. This article presents the sex, age, cause, site distribution, treatment and their relationship with patients occupations for 173 patients treated for maxillofacial fractures from January 2008 to December 2011 in the Department of Oral and Maxillofacial Surgery, the First Affiliated Hospital of Chongqing Medical University (Chongqing, China).
Materials and methods

We retrospectively investigated 173 patients with maxillofacial fractures who were treated in our department between January 2008 and December 2011. Various parameters including sex, age, cause, occupation and site distribution, treatment modalities and duration in hospital were recorded. The site distribution of fractures was classified into frontal, nasal and nasoethmoidal, zygomatic, orbital, dento-alveolar, maxillary and mandible.
Results
This retrospective study included 173 patients (117male and 56 female) with maxillofacial fractures treated in the Department of Oral and Maxillofacial Surgery, the First Affiliated Hospital of Chongqing Medical University (Chongqing, China) from January 2008 to December 2011. In addition to the sex, age, yearly distribution, cause and occupation of maxillofacial fractures in Tables 1-4, site distribution of maxillofacial fractures are shown in Table 5 and the treatment protocols for each patient and the number of the patients treated with each protocol are presented in Table 6.
Table 1. Sex and age distribution of maxillofacial fractures
Age groups Upto20 20-40 40-60 Above 60 Total
Total number 38 47 46 42 173
Male 23 34 31 29 117
Female 15 13 15 13 56
80
Table 2. Yearly distribution of occupation related fracture cases
50 40 30 20 10 0 2008 2009 2010 2011
Table 3. Causes of fractures
Causes of fracture
Number of patients
Percentage
Traffic accidents Fall of an object Falls Blows Assaults Work related injuries/sports injuries Total
58 35 32 24 17 7 173
33.6 20.2 18.5 13.8 9.9 4.0 100
Table 4. Occupations of patients with maxillofacial fractures
Occupation Number of patients Percentage
Driver 42 24.3
Construction workers 34 19.6
Mine workers 28 16.2
Factory workers 22 12.7
Forest workers 18 10.4
farmers 15 8.7
Others 14 8.1
Total 173 100
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Table 5. Site distribution of maxillofacial fractures
Sites of fracture Frontal Nasal and nasoethmoid Zygomatic Orbit Dentoalveolar Maxilla Mandible Total 248
Driver 3 12 8 6 11 9 18 67
Construction workers 6 7 6 4 6 5 10 44
Mine workers 7 8 5 2 5 1 8 36
Factory workers 4 4 5 1 8 6 8 36
Forest workers 4 3 1 1 3 2 7 21
Farmers 2 3 4 2 11 22
Others 3 2 6 2 9 22
Anatomic location of mandibular fractures
Site Symphysis Parasymphysis Condylar Coronoid Angle Body Ramus
Number 7 23 9 3 14 4 11
Percentage 9.9 32.4 12.6 4.3 19.8 5.6 15.4
Table 6. Treatment protocols of patients with maxillofacial fractures
Treatment Intermaxillary fixation(imf) Rigid fixation with plates Fixation with wire Elevation reduction Iliac bone graft Total
Number of patients 38 177 12 17 4 248
Percentage 15.3 71.3 4.8 6.9 1.7 100
Discussion
In general, our results were concordant with earlier studies. [9] The male is likely to have more maxillofacial fractures (67.6%) than female, which is possibly because more males engaged in more physical and dangerous works than females. The sex ratio was about 2:1, which was lower than previous reports from Nigeria, [10] Austria, [11] and Japan, [12] and higher that report from Libyan children. [13]
The number of patients was found mostly in the 20-40-year-old group. This was similar to results reported in previous studies. And the yearly distribution almost had no change. The most common cause of maxillofacial fractures in our study is traffic accidents (33.6%). A higher incidence of traffic accidents had been reported from Saudi Arabia, [10] Austria, [11] and Japan, [12]. More recent studies have shown assault as the most common cause of maxillofacial fractures in many developed countries, whereas traffic accidents remain the most frequent cause in
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many developing areas. [14] ,the results of our study are in accordance with other developing countries having higher incidence of traffic accidents .We found fall of an object was the second most frequent cause (20.2%) of maxillofacial fractures. This incidence was higher than in the United Arab Emirates (4.1%) [15] But similar with the results from Brazil (22.5%) [16]. Occupations like forestry construction and mining are more prone to suffer injuries due to fall of an object due to lack of appropriate safety measures and equipments. The results reflect the socioeconomic conditions had great relationship with the causes of maxillofacial fractures. Our study Fractures in drivers. It is acknowledged that the most common mandibular fracture location was the condyle (36%) followed by the corpus by previous studies [4,16] .Earlier studies showed the corpus region as the most common location.[1,2] However, our findings are similar to other studies in this regard, demonstrating the parasymphysis(32.4%) as the most common region followed by angle(19.8%) and condyle. Different site distributions of fractures appeared to relate to the nature of the work and the cause of the injury. Road traffic accidents appear to be the cause in most sites of facial fractures. There are many treatment regimens of maxillofacial fractures, and the selection may vary according to the types and size distributions of the fractures, patients characteristics, and the surgeons experiences and preference. Each fracture and patient has particular character; therefore, standardization is hard to meet. However, the common applications are rigid fixation using mini-plates or wire inter-maxillary fixation using arch bars, extraoral bandage, elevation and reduction procedures for zygoma fractures, [17] or a combination of these methods. We preferred rigid fixation with plates in most cases (71.3%). Other protocols we used were intermaxillary fixation, fixation with wires, and elevation reduction or a combination of these protocols. In conclusion, maxillofacial fractures are observed with different causes and site distributions of each patient. Age and sex variations may also contributed to incidences. showed traffic accidents was the first highest cause and fall of an object the second highest, like in other developing countries like Brazil. [16] Our study found that taxi/truck drivers (24.3%) were the most to have maxillofacial fractures, followed by construction workers. Workers in these occupations carried a (24.3+19.6)/ (10.4+8.7) =2.3-fold while compared to workers in forestry and farm. The road conditions in the Mountain city Chongqing is not so good, heavy traffic in the city and lack of safety measures while driving may be the possible reasons leading to higher incidence of maxillofacial fractures. Also we found that maxillofacial fractures are occupation-related with the most happened in bus/taxi drivers. The best way of treating occupation-related maxillofacial fractures is through prevention. That should include recognition of possible occupational hazards, safety training of workers and implementation of safety measures in the road and work place. The treatments are not the same in each case and the surgeon should evaluate the patients and fractures individually.
References
1. Gven O. A comparative study on maxillofacial fractures in central and eastern Anatolia. A retrospective study. J Craniomaxillofac Surg 1988;16:126-9. 2. Ellis E 3rd, Moos KF, el-Attar A. Ten years of mandibular fractures: an analysis of 2,137 cases. Oral Surg Oral Med Oral Pathol 1985;59:120-9. 3. Taher AA. Maxillofacial injuries due to road traffic accidents in Kuwait. Br J Oral Maxillofac Surg 1986;24:44-6. 4.Haug RH, Prather J, Indresano AT. An epidemiologic survey of facial fractures and concomitant injuries. J Oral Maxillofac Surg 1990;48:926-32. 5.Telfer MR, Jones GM, Shepherd JP. Trends in the aetiology of maxillofacial fractures in the United Kingdom (1977-1987). Br J Oral Maxillofac Surg 1991;29:250-5. 6.Brown RD, Cowpe JG. Patterns of maxillofacial trauma in two different cultures.
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A comparison between Riyadh and Tayside. J R Coll Surg Edinb 1985;30:299-302. 7.Adi M, Ogden GR, Chisholm DM. An analysis of mandibular fractures in Dundee, Scotland (1977 to 1985). Br J Oral Maxillofac Surg 1990;28:194-9. 8.Cheema SA, Amin F. Incidence and causes of maxillofacial skeletal injuries at the Mayo Hospital in Lahore, Pakistan. Br J Oral Maxillofac Surg 2006;44:232-4. 9.Ashar A, Samerr Khateery, Adam Kovacs. Etiology and patterns of facial fractures in Al Ain, United Arab Emirates. Saudi Dent J 1999;11:109-13 10.Lawoyin DO, Lawoyin JO, Lawoyin TO. Fractures of the facial skeleton in Tabuk North West Armed Forces Hospital: a five year review. Afr J Med Med Sci 1996;25:385-7. 11.Hackl W, Hausberger K, Sailer R, Ulmer H, Gassner R. Prevalence of cervical spine injuries in patients with facial trauma. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2001;92:370-6. 12. Iida S, Kogo M, Sugiura T, Mima T, Matsuya T. Retrospective analysis of 1502 patients with facial fractures. Int J Oral Maxillofac Surg 2001;30:286-90. 13. Jaber MA, Porter SR. Maxillofacial injuries in 209 Libyan children under 13 years of age. Int J Paediatr Dent 1997;7:39-40. 14.Adi M, Ogden GR, Chisholm DM. An analysis of mandibular fractures in Dundee, Scotland (1977 to 1985). Br J Oral Maxillofac Surg 1990;28:194-9. 15.Muraoka M, Nakai Y, Nakagawa K, Yoshioka N, Nakaki Y, Yabe T, et al. Fifteenyear statistics and observation of facial bone fracture. Osaka City Med J 1995;41:49-61. 16.Brasileiro BF, Passeri LA. Epidemiological analysis of maxillofacial fractures in Brazil: a 5-year prospective study. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2006;102:2834. 17.Khalil AF, Shaladi OA. Fractures of the facial bones in the eastern region of Libya. Br J Oral Surg 1981;19:300-4.
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4 HarshRajvanshi ExecutiveEditor I.T.SCentreforDentalStudiesandResearch India

AyeshaZaka ExecutiveEditor HamdardMedical&DentalCollege Pakistan

ORAL MUCOSITIS MANAGEMENT PROTOCOL BY ORAL PHYSICIAN

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Oral Hygiene Assessment

1 Smooth,pink,moist and intact

2 Slightly wrinkled and dry; one or more isolated reddened areas

Gingiva and oral mucosa

Smooth,pink,moist and intact

Smooth,pink,moist and intact

Thin, watery, plenty

Minimal debris; mostly between teeth Increase in amount

Oral dysfunction Score

Mild dysfunction 6-10

Corresponding Author Dr. Annie Mehnaz Mirza E-Mail: annie.mirza24@gmail.com

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Types of Informed Consent

Consent to Disclose/Release of Information

Consent for Children or minors

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Discussion & Conclusion

ENDODONTIC THERAPY IN A 3ROOTED MANDIBULAR SECONDMOLAR:ACASEREPORT

Intern, School of Dental Sciences, Sharda University, Greater Noida, India

School of Dental Sciences, Sharda University, Greater Noida, India

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with three roots, which is a rare clinical entity.

Fig. 3 _____________End of article______________

SEMEVALUATIONOFEFFECTOF37%PHOSPHORICACIDGEL, 24%EDTAGELAND10%MALEICACIDGELONTHEENAMEL ANDDENTINFOR15AND60SECONDS:ANINVITROSTUDY

Jodhpur Dental Hospital, Jodhpur

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Materials and Methods

subgroups of 5 teeth each. Ia Ib IIa IIb IIIa IIIb

Photograph 1: Armamentarium used for the study

Photograph 2: Materials used in the study

Photograph 3: Scanning Electron Microscope

The parameters to be observed were:*

The etching patterns on enamel surface.

Type 4 Pitted enamel surface. Type 5

Preferential dissolution prism cores resulting honeycomb appearance

Type 2 Etch pattern showing preferential

A more random etch pattern, areas of which corresponded to type 1 and

Insignificant Significant Insignificant

Significant Significant Significant

7.67 8.58 10.43 9.26 8.4 8.86

Photograph 4: Etching Time-15 Seconds

9.64 9.31 11.96 14.34 12.15 11.48

Photograph 5: Etching Time- 60 Seconds

Photograph 6: Etching Time- 15 Seconds Photograph 8: Etching time - 15 seconds

Photograph 7: Etching Time- 60Seconds

Photograph 9: Etching time - 60 seconds

1.73 2.54 1.52 2.01 1.88 1.94 Table : 3

0.00 0.00 0.00 0.00 0.00 0.00

Photograph 11: Etching time - 60 seconds

ETCHING OF DENTIN WITH 24% EDTA GEL (Open Dentinal Tubules)

2.76 2.59 2.29 3.02 2.72 2.67 Table : 4

3.7 5.14 3.85 2.9 4.02 3.92

Photograph 12: Etching time - 15 seconds

ETCHING OF ENAMEL WITH 24% EDTA GEL (Type 4 Etching Pattern)

Photograph 10: Etching time - 15 seconds

Photograph 13: Etching time - 60 seconds

Fig. 3 _End of article__