DISEASES OF THE ORAL MUCOSA

The oral mucosa is divided into 3 types:

1. Keratinized mucosa (functional mucosa) e.g.: gingival and hard palate. 2. Nonkeratinized mucosa (lining mucosa) e.g.: floor of the mouth, check. 3. Specialized mucosa e.g.: dorsal surface of the tongue & it is carrying taste buds.

A lesion: is any wound or pathologic alteration of tissue. Oral mucosal diseases are characterized by one or more lesions that can be categorized into these basic types; *Macule: A focal area of color changes which is not elevated or depressed in relation to its surroundings. e.g.: amalgam tattoo, rash of secondary syphilis.

 *Papule: A solid, raised lesion which is less than 5 mm in diameter. e.g.: popular lichen planus.

 *Nodule: A solid, raised lesion which is greater than 5mm in diameter. e.g.: fibroma.

 *Sessile: Describing a tumor or growth whose base is the widest part of the lesion. *Pedunculated: Describing a tumor or growth whose base is the narrower than the widest part of the lesion.

 *Papillary: Describing a tumor or growth show numerous surface projections. *Verrucous: Describing a tumor or growth show a rough, warty surfaces.

 *Vesicle: A superficial blister, 5mm or less in diameter usually filled with clear fluid. e.g.: burns, herpetic lesions. *Bulla: A large blister, greater than 5mm in diameter, it may form when several vesicles coalesce. e.g.: pemphigus & penphigoid.

 Vesicles can be of two types: Sub epithelial vesicles (accumulation of fluid is beneath the stratum basalis so that all the layers of epithelium are raised). Intra epithelial vesicles are those in which the fluid collects within the epithelial layer, usually the stratum spinosum, and the basal layer remains attached to the C.T.

 Pustule: A blister filled with purulent exudates (pus).

 Ulcer: A lesion characterized by loss of the necrosis appears as white or yellow membrane & is surrounded by a red halo; the border may be punched out, undermined, rolled & raised. e.g.: aphthous, cancer.

 Erosion: Refers to a partial loss of the surface epithelium e.g.: traumatic erosion caused by tooth brushing.

 *Fissure: A narrow, slit like ulceration or groove. *Plaque: Is a small or large demarcated patch that can be smooth or fissured e.g.: leukoplakia.

 *Petechia: A round, pinpoint area of hemorrhage. *Ecchymosis: A non elevated area of hemorrhage larger than petechia. *Telangiectasia: A vascular lesion caused by dilatation of a small, superficial blood vessel.

 *Cyst: A pathological epithelium lined cavity after filled with fluid or semi fluid contents & surrounded by a fibrous C.T. capsule.

 *Tumor: Is a swelling of a part, considered as neoplastic solid growth projecting outward or infiltrates downward. e.g.: a hemangioma(benign tumor) Carcinoma or cancer is malignant tumor.

 *Atrophy: Refer to reddened area of the mucosa where the epithelium is thin & the blood supply of the C.T. is seen, it differ from erosion in that there are less cells in the epithelium due to atrophy of the epithelium, not because of trauma. e.g.: geographic tongue where the filiform papillae are lost as well as in vitamin deficiency states, anemia.

 *Scar: Is a white depressed mark line or area that represents healing after injury. It is rare in the oral cavity but is seen following gingivectomy, apicectomy.

 *Crust: Is a scab or dry outer layer usually seen with brown pigmentation of skin or outer surface of lips.

 CHANGES IN THE COLOR OF ORAL MUCOSA The normal color of the oral mucosa is pink or pinkish red which comes from the reflecting color of the highly vascular sub mucosa. Changes in the color of oral mucosa can be seen as brown or black mucosa due to the presence of pigmentation in the mucosa, some times the case may be very dangerous like in melanoma.

 Any change in color or consistency of the normal oral mucosa may indicate a pathologic condition which may be very simple like erosion or serious like sq.cell ca. The cause of such change may be physical like trauma or chemical like long term aspirin use or some time microbial cause (fungal, bacterial or viral) also some time we see oral manifestation of systemic disease thats why it is said that the oral cavity is the mirror of the body.

 MICROSCOPIC CHANGES OF THE ORAL MUCOSA The microscopical changes seen in the oral mucous membrane consequent to pathologic condition can be divided into those of the epithelium and those of the C.T. These changes may be more striking in the epithelium or in the C.T. or even both.

 **Epithelial changes: Hyperkeratosis: Refers to an increase or widening in the stratum cornium. This result in excess keratin(hyper ortho keratosis) or parakeratin(hyper para keratosis) at the surface & yields a white appearance clinically.

 This hyperkeratinization can occur in keratinized area or occurs abnormally or nonkeratinized area. If the white surface is in the form of a patch it is called leukoplakia.

 Hyperplasia: Refer to increase in the thickening of epithelium from the surface down to the basal cell layer. Hyperplasia of the epithelium occurs with the widening or increase in the number of cells in the stratum spinosum we called this (A canthosis). This thickening also would result in a white lesion.

 Epithelial dysplasia (dyskeratosis) or epithelial atepia It is a serious condition refers to the abnormal growth pattern or disorientation of the normal layer of epithelium. It generally indicates premalignant changes. The changes can be so sever that they resemble cancer in which case the term carcinoma in situ is used because all the cellular characteristics of cancer are present but are confined to the epithelium with no invasion into the C.T. This also can be a white or red lesion. Once the lesion invades the C.T. it is also called sq.cell carcinoma or intra epithelial carcinoma.

 SPONGIOSIS Refer to the accumulation of fluid within the cells of fluid within the cells of the stratum spinosum. This reflects a degeneration of these cells & the microscopic picture resembles a sponge. Clinically the lesions appear white and are most commonly seen on the buccal mucosa as leukoedema.

 **CONNECTIVE TISSUE CHANGES Inflammatory infiltrates are common. Most often chronic inflammatory cells are present e.g.: gingivitis. Hyperplasia of C.T. refers to an increase in the amount of collagen fibers. Glandular and ductal destination can be seen in the many accessory mucous glands due to pressure and obstruction.

**Generally, oral mucosal lesions are divided into: White lesions. Red lesions. Vesiculo-ulcerative lesions. Infectious disease: bacterial fungal viral

 Tuberculosis Is a chronic infectious disease caused by (mycobacterium tuberculosis) the tubercle bacillus. The most frequent type is pulmonary tuberculosis; this type may remain localized but may spread as well through the blood stream to among other organs as in kidney or liver (milliary tuberculosis) or through the lymph vessels. Tuberculous infection of the submandibular & cervical lymph nodes also referred to as (scrofula) may locally give rise to abscess formation or may remain stationary as a granulomatous lesion. Tuberculosis may also primarily affect the skin; this type is called (lupus vulgaris) such primary tuberculous lesion rarely affect the oral mucosa.

More than 1 billion people are infected with TB. 8 million new cases per y . 3 million death per y. 1940 ( declined due to effective anti microbials ) 1980 stop decline as result of a combination of several factors 1-HIV epidemic 2- increased immigration from countries with endemic TB 3- transmission of TB in crowded enviroment. 4- decline of health care infrastructure .

 The mechanism of spreading of microorganism to the oral mucosa has not been identified. **It appears most likely that: The microorganism is carried to the oral tissue by the sputum. The microorganism may be carried by hematogenous route. Primary oral tuberculosis without pulmonary involvement is rare, when present the oral involvement of primary tuberculosis usually involve the gingival, mucobuccal fold, and area of inflammation adjacent to teeth.

 Secondary oral lesion mostly present on the tongue, palate & lip. The typical lesion is an ulcer on the middorsum of the tongue, the ulcer is typically angular with over hanging edges which appear indurate and hard.

 Histological features of tuberculosis: The cell-mediated hyper sensitivity reaction is responsible for the classical histological formation of granuloma. One granuloma called tubercle. Area of infection demonstrates the formation of granulomas which are circumscribed collection of epitheliod histiocytes, lymphocytes & multinucleated giant cells (langhans cell) with central caseous necrosis. Tubrculous osteomylitis occasionally occur Spcial stain Ziehl Neelsen or other acid fast stain.

 Management of tuberculosis: Tuberculin test ( Mantoux ) skin test + indicate exposure to the org and doesnt distinguish infection from active diseases. Diagnosis is confirmed by biopsy, chest radiography & a specimen of sputum. Mycobacterial infection is confirmed by culture.(4-6 w)(PCR POLYMERASE CHAIN REACTION to identify M TUBERCULOSIS DNA may accelerate this diagnosis with out the need to wait on culture result. Oral lesion clears up rapidly, if there is effective multi drug chemotherapy for the pulmonary infection. No local treatment is needed. Isoniazid (INH)+ RIFAMPIN for 9 M. Refadin cap, ethyanbutal & INH. Tab.

 SYPHILIS (LUES) It is a veneral disease caused by a spirochete the treponema palladium. The spirochetes are transmitted from one person to another by intimate sexual contact or by close body contact involving the sex organs, mouth or rectum. The organism are fragile & can not live long in light and air, they require warm & moist area for survival. 1940 y 1995 y (12 million) (50-100 ) 1- cocaine abuse. 2-illegal use drugs for sex. M to F ratio 3.5:1-----1-1

 To enter the body the spirochetes must penetrate mucosa or skin, usually through a wound or area that is not intact. **syphilis may be classified as either: Acquired type. Congenital type.

 Acquired type: The infection takes place through sexual intercourse with an infected partner. A physician or dentist may be infected by a patient with a lesion of the oral mucosa during the second stage of the disease which is extremely contagious stage. The disease has a natural course of three stages with tow periods of remission if preventive measures are not taken.

Primary stage: Is characterized by the appearance of chancre, this primary chancre develop at the site of initial inoculation about 3-4 weeks following intimate contact. 90% of the lesions occur on the genitalia & 10% occur in or about the mouth, on the lip, tongue or palate. Chancre consist initially of a firm nodule in which the surface break down after a few days, leaving a rounded hard ulcer with raised indurate edges, this may resemble a carcinoma if present on the lip.

 A chancre is typically painless but regional lymph nodes are enlarged. The ulcer heals spontaneously in weeks, serological test are negative at first & the diagnosis depend on finding treponema palladium by dark-ground illumination of a smear from the chancre.

Secondary stage: The secondary stage develops 1-4 months after infection. It typically caused mild fever with malaise, headache, sore throat soon followed by a rash & stomatitis. The skin rash is composed of numerous red macule and papules. These eruptions can occur in the mouth usually on the palate. In the oral cavity multiple, a symptomatic white-grey plaques may appear on the tongue, gingive, palate & the check mucosa. The discharge from the ulcers contains many spirochetes & saliva is highly infective. The serological findings are always positive in this stage. Treatment in this stage with long acting antibiotic, mostly penicillin.

 In compromised immune system Secondary syphilis can exhibit an explosive and wide spread form known as Lues maligna ( fever , headache and myalgia followed by the formation of necrotic ulceration( face and scalp), 30 % of affected patients will show oral lesions, malaise ,pain and arthralgia.

Tertiary syphilis: Between the secondary & tertiary stages there is latent period which is about 1-30 years. The third stage of syphilis manifests itself primarily with changes in the nervous system and cardiovascular system. There is tissue destruction without regeneration & patient suffers from insanity, lose motor control & balance. The aorta of the heart in some patient is damaged & caused heart disease. Beside these major findings, there can be oral lesion at this stage:

A tropic glossitis: The tongue appears smooth, shiny due to loss or atrophy of the papilla. The gamma is other lesions of tertiary syphilis that can involve the oral cavity mostly affect the palate, tongue or tonsils. Vary from one to several inches in diameter.

 It begin as a swelling some times with yellowish center which undergo necrosis leaving a painless deep ulcer. The ulcer is rounded with soft punched-out edges. The floor is depressed & pale. In the palate the destruction may cause a perforating through the soft tissue and bone of the hard palate leaving a permanent opening from the mouth to the floor of the nose.

 **.

Leukoplakia of the tongue may also develop during the late stage. *the lesions are not contagious at this stage.

 Congenital syphilis: Is not veneral but is passed on to the fetus by an infected pregnant woman. If the woman is treated within the first three months of pregnancy the fetus will not be affected. The classical symptoms of congenital syphilis consist of the triad of Hutchinson:

Hypoplasia of the incisors and molars (mulberry molars), central notching of the incisal edge & a tapering screw-driver appearance. Deafness due to involvement of the 8th nerve (a coustical nerve). Interstitial keratitis. Various other abnormalities have been described such as under development of the maxilla, a high arched palate & a saddle nose.

 DIAGNOSIS: Dark field examination of a smear : spiral Morg. False-positive result.(T.microdentium,T.macrodentium, T.mucosum ) Specific IF antibody or serologic test. NON specific,not highly sensitive (VDRL ,RPR ) 1 and 2 + ,latency -. Specific and highly sensitive 1-FTA 2-TPHA + from 1 to life

 ACTINOMYCOSIS Is caused by gram-positive, anaerobic actinomysis israelli. Actinomycosis proceeds as a granulomatous infection producing abscesses, the pus often contains yellow sulpher granules. **There are 3 anatomic variant: The cervicofecial type. The abdominal type. The pulmonary type.

 The actinomycetes commonly inhabit the oral cavity with out giving rise to symptoms. However if a portal of entry has been created in the oral mucosa by trauma or by extraction of tooth, for instance the microorganism can penetrate the underlying tissue. Although actinomycosis may involve the jaws causing osteomylitis, most of the lesions are localized in the soft tissue and in the tongue.

 Histologically: On microscopic examination of removed tissue, granulation tissue can be seen with central abscess formation within which may be seen the characteristic colonies of M.O., the individual clones appear lobulated or round with peripheral radiating filaments. There are also multinucleated giant cells & macrophages particularly around the periphery of the lesion.

 Diagnosis & treatment: History & clinical appearance suggest cervicofacial actinomycosis. Demonstration of the M.O. on the tissue. Culture of the M.O. Demonstration of sulpher granules. Flurescen-conjucated antiserum can be used on the granules to identify the actinomyces species. Treatment by penicillin and tetracycline in a high dose over along period of time is in general most successful.

 Diagnosis & treatment: History & clinical appearance suggest cervicofacial actinomycosis. Demonstration of the M.O. on the tissue. Culture of the M.O. Demonstration of sulpher granules. Flurescen-conjucated antiserum can be used on the granules to identify the actinomyces species. Treatment by penicillin and tetracycline in a high dose over along period of time is in general most successful.

NOMA ( Concrum oris : Gangrenous Stomatitis : Necrotizing Stomatitis ) Noma is a creek word meaning to devour. It is a rapidly progressive opportunistic infection caused by components of the normal oral flora that become pathogenic during periods of compromised immune status.

The predisposing factors: 1-Poverty. 2-Malnutrition or dehydration . 3-Poor oral hygiene. 4-Recent illness. 5-Malignancy . 6-An immune defficiency disorders include AIDS. 7- Poor sanitation . 8- Proximity to livestock .

 The infection begins as necrotizing ulcerative gingivitis. Clinically : typically arise in childern age 1 to 10 y and start in the gingiva as NUG ( inflamed interdental papillae , punched-out necrosis that cover with gray pseudomembrane , bad odor , pain , spontaneous hemorrhage lymphadenopathy , fever, and malaise ) which may extend facially or lingually to involve the adjacent soft tissue and form area of NUM .

 Treatment : Appropriat antibiotic ( penicillin and metronidazole) Local wound care . Correcting the inadequate nutrition , hydration and electrolyte imbalances.

FUNGAL LESION (Candidosis Candidiasis) Is a disease caused by infection with yeast- like fungal organism candida albicans. In about half of the population candidaalbican can be shown in the normal oral flora without causing any clinical evidence of infection.

 Factors predisposing to candidal infection are: Immunodeficiency or immunosuppression. Anemia. Suppression of the normal flora of the mouth by antibacterial drugs. Xerostomia.

Candidal infection can cause a variety of lesions: Acute candidosis. Thrush Acute antibiotic stomatitis. Chronic candidosis. Denture- induced stomatitis. Chronic hyperplastic candidosis. Chronic mucocutanous candidosis. Erythematous candidosis. Angular stomatitis.

 THRUSH (Pseudomembranous candidosis) Thrush clinically is seen as white creamy lesion or patch seen on the tongue, palate, check. These white patches resemble curdled milk which can be removed by scraping them with wooden spatula or with dry gauze.

 The underlying mucosa may appear normal or erythematous, the white lesion contain candidal hyphi and yeast together with desquamated epithelial cells & debris. Thrush may be initiated by exposure of the patient to broad spectrum antibiotic or by impairment of the patients immune system. The immune dysfunction seen in leukemic patients or those with human immunodeficiency virus (HIV), infant may also be affected because of their under developed immune system.

 **Management of thrush: Control of any local cause, such as topical antibiotic treatment, may alone cause thrush to resolve. If not a course of nystatin or amphotericin lozenges. Failure of response to topical antifungal suggests immune deficiency. HIV infection should always be suspected when thrush is seen in an adult male in which there is no other detectable cause.

 Acute antibiotic stomatitis: This can follow topical use of antibiotics especially tetracycline, which can cause suppression of normal flora. Clinically the whole mucosa is red & sore; spot of thrush can be present. Resolution may follow with removal of the antibiotic.

 Denture induces stomatitis (chronic) This lesion is seen in patients wearing a well filling upper denture which cuts off the underlying mucosa from the protective action of the saliva. This condition is characterized by varying degree of erythema, sometimes accompanied by petechial hemorrhage, localized to the denture bearing area of a maxillary removable dental prosthesis.

 Whether this represents actual infection by C.albicans or is simply a tissue response by the host to the various M.O. living beneath the denture remain controversial, or this reaction could be due to improper design of the denture, allergy of the denture base or inadequate curing of the denture acrylic.

 Chronic hyperplastic candidosis or candidal leukoplakia: This lesion characterized by the appearance of white plaque or patch that can not be removed by scraping, such lesions are usually located on the anterior buccal mucosa and can not clinically be distinguished from a leukoplakia only by taking a biopsy.

 It is not clear whether this lesion is caused by candida or candida is superimposed on preexisting leukoplakia. In H&E stained section, hyphae are difficult to see but by using PAS (periodic acid Schiff) stain clearly shows the hyphae growing through the full thickness of the keratin to the prickle cell layer.

 Chronic mucocutanous candidosis (syndromes) There are a rare group of immunologic disorders which characterized by sever oral candidosis. There are four main types: Familial (limited) type. Diffuse type (candida granuloma). Endocrine candidosis syndrome. Late onset (thymoma syndrome).

 Familial (limited) mucocutaneous candidosis: Inherited as an autosomal recessive trait. The onset typically in infancy as persistent thrush, then the lesion will gradually transformed into leukoplakia like lesion. There may be mild cutaneous involvement with sidropenia (iron deficiency anemia).

 Diffuse type mucocutaneous candidosis: This is the most sever type also termed monilial granuloma because of the extensive warty overgrowth on the skin. Pulmonary & superficial suppurative infections associated in diffuse C.M.C.C. with gross candidal epithelial proliferation.

 Endocrine candidosis syndrome: In this form C.M.C.C. is associated with multiple glandular deficiencies & organ specific autoantibody production. Addisons disease (supra renal gland) & hypoparathyroidism are most frequently associated with endocrine candidosis but oral candidosis frequently mild.

 Late onset M.C.C.: In this type thymoma cause defective cell mediated immunity. Myasthenia gravis (thymus) & pure red cell aplasia may be associated.

 Erythemtous candidosis This lesion clinically appear as patchy red mucosal macules, and some time appear as smooth or granulated red or fissures , this lesion mostly occur in hard palate ,dorsum of the tongue and soft palate and mostly associated with HIV-positive patients

 There are varying form of erythematous candidosis :

Acute atrophic candidosis or antibiotic sore mouth .

Due to long term antibiotic therapy the patients suffer from burning sensation which may be accompanied by a diffuse loss of the filiform papilla of the dorsal tongue.

 Median rhomboid glossitis or central papillary atrophy In the past this was thought to be a developmental defect of the tongue , but now consideras onetype of candidal infection. This lesion is a symptomatic as a well demarcated red zone in the mid line of post dorsal tongue.

 Angular stomatitis or Perleche

This occur in the angles of the mouth which appear as red, fissured and scale. This seen typically in an older person with reduced vertical dimension and many folds at the corner of the mouth so the saliva tend to poolor flow in these folds keeping the moist and thus inducing a yeast infection. This may be caused by candida albicans alone or combined with other M.O such as Staphylo coccus aureus .

VIRAL INFECTION Herpes simplex infection: A\ Primary herpes simplex infection B\ Secondary herpes simplex infection Recurrent herpes labialis Herpetic whitlow

Herpes simplex infection: It is an acute infectious disease caused by HSV type one. The infection in human can be seen in two types: Primary infection in a person without circulating antibodies.

This develops in children & young adult, rarely seen in children less than 6 month because the infant has inherited the antibodies from the mother. The attack is characterized by the development of fever, irritability, headache, pain on swallowing & regionally lymphadenopathy.

In the oral cavity primary infection characterized by multiple vesicular eruptions located on the attached gingiva & movable mucosa, chiefly the lips & buccal mucosa, palate, pharynx & tonsil may be involved also. These vesicles rupture forming painful ulcers covered by a gray membrane & surrounded by erythematous area. Gingival inflammation precedes the formation of the ulcers by several days. The ulcer vary considerably in size & heal spontaneously within 14-7 days have no scar.

The virus does not remain latent at the site of the original infection but reaches to nerve ganglia and remain latent their until reactivated, the usual ganglia involved are the trigeminal ganglia. By an unknown triggering mechanism the virus is reactivated and spread along the nerve pathway to produce vesicles in epithelial at peripheral location.

Factors associated with the out break of lesions are: Trauma, emotions, fever, infections, menstruation and allergy. In most individuals the disease is sub clinical meaning antibodies are produced but no sign and symptoms of the disease appear.

Histologically : intra epithelial vesicle formations seen with necrotic exudates and neutrophile infiltrate accompanied by epithelial cells showing nuclear ballooning degeneration (because replication of herpes virus within the cells cause degeneration and death of epithelial cells).

Treatment: supportive care, consist of prescribing a soft diet, anti -fibril drug to reduce the fever and pain; with anti-biotic to prevent secondary infection, soothing mouth wash could be used also.

 Type two HSV infections affected the genital area and transmitted by sexual contact.

 SECONDARY HSV INFECTIONS RECURRENT HERPES LABIALIS HERPETIC WHITTLOW

Recurrent herpes labialis: It is usually seen in adult patients and represents reactivation of virus, by trauma, fatigue, menstruation, upper respiratory tract infection, stress allergy and exposure to sun light. The virus will spread to the epithelial cells and produce the recurrent infection and this occur most commonly on the lips (herpes labialis) ,usually there is a prodromal symptom of tingling or slight pain ,followed by the eruption of a vesicle which soon rupture

The vesicle occur mostly on firmly attached mucosa , such as hard palate and attached gingiva and not movable mucosa (this is important in distinguishing the herpetic ulcer from aphthous ulcer). The ulcer heal in about 7 days, no treatment is required unless symptoms demand it .

Herpetic whitlow (Herpetic cross- infection)(Terminal pulp infection) Contact with infected patients by dentists and oral health auxiliary personal who have never been exposed to the disease may result in herpetic whitlow, a viral dermatitis of the finger.

Varicella_ zoster infection: primary varicella_zoster (chicken pox) secondary varicella_zoster (shingles)

Primary varicella_zoster infection (chicken pox): Is an acute infectious viral disease caused by the varicella_zoster virus. The incubation periods lasts 2-3 weeks, the lesions are located primarily on the trunk, face. The infections commonly appears as vesicles with an erythematous boundary and are extremely pruritic, fever, malaise &mild generalized lymphadenopathy are present. Oral manifestations are common with early onset of vesicles that rapidly rupture & leave erosions with a surface pseudo membrane. The palatal mucosa is the predominant oral location, the lesion resolve within 5-8 days.

Secondary varicella_zoster infection (shingles): This viral disease caused by reactivation of the chicken pox virus, the disease erupts along peripheral nerves leading from the dorsal root ganglion, where the virus was dominant. H_zoster usually affect adults of middle age or over but occasionally attacks even children. Starting as painful vesicular eruption on skin but may affect the oral cavity when the trigeminal is infected.

The vesicular eruption in herpes zoster occur unilaterally is striking because it is unilateral in distribution. Malaise, fever & enlarged lymph nodes are usually associated. Patients some times unable to distinguish the pain of trigeminal zoster from sever toothache.

**Histopathology: The varicella_zoster virus produces similar epithelial lesions to those of herpes simplex. **Treatment: By antiviral drugs Acyclovir (IV).

Herpangina Is a viral disease caused by coxsackie A virus, it affects the posterior part of the mouth. There is a predromal period of fever &ill feeling, following these groups of vesicles appears mainly on the soft palate & tonsilar areas, the vesicle will then rupture. Patients complain of a sever sore throat. The disease runs its course in 7-10 days, symptomatic treatment is required.

Hand-foot &mouth disease: This is caused by coxsackie A virus, affect children & young adults, is more often seen in spring & summer, the distribution of lesion is pathognomonic in that, after a short incubation periods which is probably between 3-10 days vesicles with erythematous halo appear in the oral cavity, on hand & feet. The disease typically resolves within a week. No specific treatment is needed but myocarditis or encephalitis is rare complication.

Rubella (Measles) Caused by a paramyxo virus, the most characteristic oral manifestation of the measles are lesions known as Kopliks spots, which develop early in the course of the infection. Multiple areas of the mucosal erythema are visible on the buccal & labial mucosa & within these areas there are numerous small bluish-white macules. Kopliks spots are not the only manifestation that may be associated with measles, candidosis acute necrotizing ulcerative gingivitis & necrotizing stomatitis may occur if significant mal nutrition is also present, sever measles in early childhood can affect odontogenesis and result in pitted hypoplasia of the developing permanents teeth.

AIDS The acquired immune deficiency syndrome (AIDS) was recognized as a disease entity in the early 1980 in the United States. The disease is caused by a virus known as human immunodeficiency virus (HIV) mainly HIV-type I, HIV-type II is as yet only widely prevalent in West Africa. Transmission of HIV occurs mainly by sexual contact or by blood; also infected pregnant women can transmit the infection to the fetus.

The incubation period of AIDS is highly variable, in male homosexual it average approximately 5 years but in sometimes as long as 10 years. The virus multiplies in T- helper lymphocytes cells, the virus kill T-helper & reverse the ratio of helper to suppressor lymphocytes. The main affect of the immunodeficiency and chief cause of death is infection by a great variety of microbes. The earliest clinical manifestation of HIV infection can be a transient illness resembling glandular fever associated with antibody production.

Later in progressive cases: there will be generalized lymph adenopathy syndrome with wide spread persistent enlargement of lymph nodes is a typical early sign. The full syndrome of AIDS is characterized by multiple infections by bacteria, fungi, parasite & virus. Though infections are main cause of death, there is also a greatly raised incidence of tumors particularly Kaposis sarcoma & lymphoma which is frequently affect the oral or perioral tissue.

AIDS is transmissible to health care personal particularly surgeons, dental surgeons& nurses, via needles or other sharp instrument, however the risk of acquiring HIV infection by such means is considerably smaller than that of hepatitis B.