OSTEOMYELITIS A brief review.

HISTOLOGY of BONE THE MATURE BONE Histologically each adult bone is composed of two different architectures. Compact bone or cortical bone Spongy or marrow bone The cortex forms the outer circumference of the bone, enclosing the spongy bone within. Both the architectures are composed of lamellae sandwiched one over the other. Lamellae Each lamellus is a thin plate of bone composed of minerals and collagen fibres in agelatinous ground substance. The smallest piece of bone is made up of a number of layers of lamellae. The space between each lamellus is a lacuna and it contains entrapped osteoblasts, now quiesent and called osteocytes.

Compact Bone. Here the lamellae are arranged in concentric circles, encircling a HAVERSIAN CANNAL, containing blood vessels and nerves. This entire unit is called an osteon.

Spongy Bone. Here the bone arranged in a meshwork called TABECULAE in gross section. Each trabeculus is again composed of a lamellar archetecture.

Mature and Woven Bone. Woven bone or immature bone found at fracture sites where new bone is forming consists of a NON LAMELLAR random arrangement of collagen fibres. This lack of architecture sets it apart from mature bone.

OSTEOMYELITIS. Osteomyelitis is an inflammatory condition that begins as an infection of the medullary portion of the bone, but quickly breaches the endosteum, and spreads along the lacunae, through the haversian system, and rapidly involves the periosteum.

Classification of Osteomyelitis

Waldovel Classification: This was the proposed classification for long bone osteomyelitis in the year 1970. Haematogenous Contiguous Vascular insufficiency. Classification of Osteomyelitis Cieny-Mader classification: based upon the anatomy of the bone infection and the physiology of the host. The stages may be altered by therapy outcome or change in host status. Stage 1, or medullary osteomyelitis, denotes infection confined to the intramedullary surfaces of thebone. Stage 2, or superficial osteomyelitis an exposed infected necrotic surface of bone lies at the base of a soft tissue wound. Stage 3 full-thickness cortical sequestration that can be removed surgically without compromising bony stability. Stage 4 or diffuse osteomyelitis is a through-and-through process requiring resection An A host is a patient with normal physiologic, metabolic, and immunologic capabilities. A B host has systemic compromise, local compromise, or both. The C host is a patient in whom the morbidity of treatment is worse than that of the disease itself.

Classification of Osteomyelitis Suppurative Oteomyelitis Acute Chronic Primary Secondary Infantile osteomyelitis Non-suppurative type Diffuse sclerosing Focal sclerosing Proliferative periosteitis Osteeoradionecrosis.

Etiology. Two host related factors contribute to the occurrence of osteomyelitis apart from the virulence of the organism. Genral health status of the host . Immunocompromised, immuno supressed, malnourished individuals are suceptible. Health of the bone at the site of invasion. Irradiated bone, fibro-osseous lesions and destructive osseous lesion of bone render them suceptible. The point of entry for the invading organism is from local injury or odontogenic infections. Haematogenous spread is rare.

Pathogenesis & Disease progression If there is continued accumulation of pus, the pus tracks its way through epithelium to open to the external environment as a sinus tract. If the host defense or antimicrobial regimen manage to control the rapid progression of the disease, the inflammation decreases, the site is revascularised and granulation tissue is formed, which separates the diseased necrotic bone from surrounding healthy bone .This island of necrotic bone is called sequestrum. If the surrounding granulation tissue promotes the laying down of a layer of new bone surrounding the sequestrum,it is called an involucrum. The involucrum is sometimes perforated by pus draining channels called Cloacae.

Pathogenesis of Sclerosing osteomyelitis. In these conditions, there is no ischemia and the inflammation induced by a low grade organism results in irritation of the infected site with a result that dense sclerotic bone is laid down instead of bone destruction. Predilection
The common site of occurrence is the mandible since the maxilla is highly vascular and contains lesser medullary bone.

Microbiology Common organisms: -hemolytic Streptococci Peptostreptococcus Fusobacterium

Other microbes: Stapylococcus aureus Mycobacterium tuberculosis Actinomycete israelii Klebsiella Troponema pallidum Pseudomonas aeruginosa Clinical Features: Acute suppurative osteomyelitis. 1. Deep intense pain 2. High intermittent fever 3. A clearly identifiable cause 4. Paresthesia of the nerve Swelling is usually minimal. There are no sinus tracts, but there is pus Exudation from the infected extraction socket. The sub acute phase (10-14 days later). 1. Deep pain, fever and malaise, anorexia. 2. Pus exudation from the sulcus & fetid odor. 3. Fistulas may be present. 4. Firm cellulites, that is tender. 5. Bone expansion may be present. Chronic suppurative osteomyelitis. 1. Indurated soft tissues with wooden character of the affected area 2. Sinus tracts, both extra oral and intraoral, fixed to the bone. 3. Dull pain & Tenderness of the affected area. 4. Exposed bone with sloughing and pus. Chronic diffuse Sclerosing osteomyelitis. 1. Occurs only in the mandible. 2. Occurs in older individuals(3rd decade) 3. Bone is mildly expanded and tender 4. Reccurent episodes of pain, sometimes excruciating and swelling. Nerve, paresthesia may also be present.

Garres periostitis. 1. Occurs in children and young adults. 2. Unilateral swelling involving the lateral and inferior aspects of the mandible 3. Absence of pain or tenderness over the expanded bone. Focal sclerosing osteomyelitis. Incidental radiological finding during the investigation for the offending tooth. Mild pain may be present. Investigations. Hematology: Leukocytosis & elevated ESR. Pus culture: To identify the organism. Imaging. IMAGING ..RADIOGRAPHY Regions of radiolucency become apparent only after 14 days, by when 30% -60% of the bone loss has occurred. Definitive findings occur after 3 weeks and are described by Worth. 1. Scattered areas of bone loss giving a moth eaten appearance. 2. Islands of sequestra are found among areas of bone destruction. They maybe surrounded by a sheath of involucrum. 3. Densification of bone due to deposition of subperiosteal bone, obscuring the intrinsic bone architecture.

In diffuse sclrerosing osteoeomyelitis, regions of sclerotic bone that do not show trabeculations are found, similar the cotton-wool appearance of pagets disease. In focal sclerosing osteomyelitis, a mass of sclerotic bone is found adjacent to the offending tooth. In garres type, the occlusal radiograph reveals a thickened outer cortical bone which can sometimes be distinguished as a discreet layer.

IMAGING ADVANCED ADIS Bone scans using Tc99 are done. These are taken up by reactive bone.They are sensitive within the 3rd day of onset. CT and MRI are done in special cases where the bone scan is not conclusive. Using these methods an accurate 3D picture of the extent of the lesion can be obtained.

Principles of treatment.

1.Correction of compromised host defences. 2.Testing culture sensitvity. 3.Imaging to study the extent of lesion. 4.Emprical antibiotic administration. 5.Removal of loose teeth and sequestra. 6.Sensitivity guided antibiotics. 7.Sequestrectomy, decortication, resection. 8.Reconstruction.

Antibiotic Therapy. Inpatient therapy Aq penicillin 2 mill u IV 4hrly + Metronidazole 500mg IV 6hrly for 48-72 hrs. PenicillinV 500mg PO 4hrly + Metronidazole 500mg 6hrly for 4-6 weeks Or Ampicillin/sulbactam 1.5-3gm IV/IM 6hrly for 48-72 hrs. Amoxycillin/clavulanic acid 875/125mg PO Bid for 4-6 weeks Outpatient therapy PenicillinV 2g PO + Metronidazole 500mg PO 8hrly for 2 to 4 weeks Or

Clindamycin 600-900mg IV 6hrly Clindamycin 300-450mg PO 6hrly Or Cefoxitin 1-2g IV/IM 4hrly or 8hrly until no symptoms Cephalexin 500mg 6hrly for 2-4 weeks Closed wound irrigation.

Two perforated polyethelene Tubes are introduced through skin incisions to lie on the infected bone.They are stabilised to the bone by catgut sutures. The wounds are closed in a watertight manner. Irrigant is introduced into one and a low volume suction attached to the other. Antibiotics such as Clindamycin, Neomycin polymixin can also be introduced and left for 3hrs, folowed by intermittant suction

Surgical options. Debridemant and drainage; with removal of loose teeth Sequestrectomy Saucerisation Decortication Stabilisation by internal fixation Resection Reconstruction

Debridement. During the acute phase, extensive debridement of bone until active bleeding is encountered. Removal of mobile and infected teeth and excision of the granulation tissue followed by the insertion of a drain. Emprical antibiotic therapy is started. Supportive therapy includes hydration , High protien and a high vitamin diet

Sequestrectomy & Saucerisation. It takes at least two weeks for sequestra to form after which they persist. Saucerisation is the unroofing of the cortex for thorough debridement of the medullary cavity. A buccal mucoperiosteal flap is elevated. The cortex is reduced with burs or rongeurs till there is a healthy bleed The marrow cavity is thorougly debrided, the sequestra are removed and granulation tissue curetted. The flap is trimmed and a pack is given to fill the dffect.Healing is by secondary intention. The pack is removed every 3-4 days replaced till epithelization occurs

Decortication

Decortication refers to the removal of the lateral and the inferior border of the mandible for upto 2cm beyond the affected area. The defect is primarily closed with pressure bandaging (10-14days) and a two way suction drain or antibiotic beads may be placed . If the removal is extensive and a risk of fracture is feared, the mandible is stabilised with plates.

Hyperbaric Oxygen Therapy Direct bacteriostatic action Neoangiogenesis, fibroblast proliferation Enhances phagocytic function. 30 dives Examine bone + + 10 dives + 10 dives Reconstruction after 3 10 dives

Stage1

Stage 2 Surgery

Stage 3 Excision of bone & Fixation months

In Case of Cutaneous fistula, Pathological fracture & Resorption of inf Border of mand, A stage 1 nonresponder directly goes to stage 3 treatment. Each dive is 100% O2 For 90mins At 2.4 atm

Non-suppurative osteomyelitis Garres periosteitis Resolution occurs with removal or endodontic treatment of the causative tooth. If the lesion remains static recontouring is done Focal sclerosing osteomyelitis Endodontic therapy or removal of the causative tooth

Diffuse sclerosing osteomyelitis

Long term antibiotic therapy with roxithromycin(300mg/d PO) for upto 66months. Bisphophonates - Disodium clodronate(300-900mg)IV Decortication Resection Calcitonin therapy.

Special considerations. Infantile osteomyelitis Etiology Perinatal trauma. Contaminatrd artificial nipples. Clinical features Facial cellulitis Hyperpyrexia & malice Dehydration Involvement of the orbit Pus exudation from the nose Intraorally, a swollen maxilla with sinuses. Complications Optic damage Dural sinus involvement Neural damage Loss of tooth buds. Treatment Drainage Culture sensitvity Antibiotics Ampicillin/sulbactam IV or Clindamycin Until acute symptoms come Similar antibiotic PO 2-4 week, till all symptoms are

down totally resolved

Actinomycotic osteomyelitis Etiology Endogenous Clinical features Firm soft tissue masses Multiple sinuses discharging granular material No response to conventional antibiotic Diagnosis Biopsy or culture Gram staining Innunoflorescence

Treatment PenicillinG 10-20mill U/day IV for 4 to 6 weeks PenicillinV 6hrly PO For 6 12 months Or Ampicillin 2.5 3g/day IV For 4 6 weeks Amoxycillin 500mg 8hrly PO For 6 12 months Tuberculous Osteomyelitis Etiology Haematogenous spread. Clinical features Cheesy exudate from sinus tract Symptoms of systemic tuberculosis Diagnosis Culture/biopsy Monteux test Radiography to check for systemic manifestations

Treatment Anti tubrculous therapy Sequestrectomy Decortication Osteoradionecrosis Etiology Extractions Mucosal ulcers Dental infections in irradiated bone Clinical findings History of radiation therapy Pain and exposed bone Diagnosis History Organisms only on bone surface, on biopsy

Treatment Debridement Antibiotic therapy Ultrasound therapy Bone resection Hyperbaric oxygen therapy