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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

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

Etiology.  In these conditions.  Pathogenesis of Sclerosing osteomyelitis. Microbiology Common organisms:  α-hemolytic Streptococci  Peptostreptococcus  Fusobacterium .This island of necrotic bone is called sequestrum. which separates the diseased necrotic bone from surrounding healthy bone .  Genral health status of the host . malnourished individuals are suceptible. the inflammation decreases. Two host related factors contribute to the occurrence of osteomyelitis apart from the virulence of the organism. Irradiated bone. the pus tracks it’s way through epithelium to open to the external environment as a sinus tract. immuno supressed.  If the host defense or antimicrobial regimen manage to control the rapid progression of the disease. The point of entry for the invading organism is from local injury or odontogenic infections. the site is revascularised and granulation tissue is formed.  Pathogenesis & Disease progression If there is continued accumulation of is called an involucrum.  If the surrounding granulation tissue promotes the laying down of a layer of new bone surrounding the sequestrum. fibro-osseous lesions and destructive osseous lesion of bone render them suceptible.  Health of the bone at the site of invasion.  Haematogenous spread is rare. 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. Immunocompromised. Predilection  The common site of occurrence is the mandible since the maxilla is highly vascular and contains lesser medullary bone.  The involucrum is sometimes perforated by pus draining channels called Cloacae.

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

2. Imaging. regions of sclerotic bone that do not show trabeculations are found. 1. Using these methods an accurate 3D picture of the extent of the lesion can be obtained.  In garre’s type.  In focal sclerosing osteomyelitis.. 2. 3. Absence of pain or tenderness over the expanded bone. similar the cotton-wool appearance of paget’s disease. Occurs in children and young adults.RADIOGRAPHY Regions of radiolucency become apparent only after 14 days. Investigations. obscuring the intrinsic bone architecture. Densification of bone due to deposition of subperiosteal bone. Islands of sequestra are found among areas of bone destruction.They are sensitive within the 3rd day of onset.  Incidental radiological finding during the investigation for the offending tooth. Unilateral swelling involving the lateral and inferior aspects of the mandible 3.  Mild pain may be present. IMAGING . Focal sclerosing osteomyelitis. They maybe surrounded by a sheath of involucrum. 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. CT and MRI are done in special cases where the bone scan is not conclusive. Principles of treatment. Hematology: Leukocytosis & elevated ESR.  Definitive findings occur after 3 weeks and are described by Worth.Garre’s periostitis.     In diffuse sclrerosing osteoeomyelitis. 1. by when 30% -60% of the bone loss has occurred. a mass of sclerotic bone is found adjacent to the offending tooth. Scattered areas of bone loss giving a moth eaten appearance. Pus culture: To identify the organism. These are taken up by reactive bone. .

. 4.Removal of loose teeth and sequestra. decortication. 3. 8. 5.Imaging to study the extent of lesion. 2.Reconstruction. 7. 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.Correction of compromised host defences.Emprical antibiotic administration. 6.Sequestrectomy.        1.Sensitivity guided antibiotics. Inpatient therapy Aq penicillin 2 mill u IV 4hrly + Metronidazole 500mg IV 6hrly for 48-72 hrs. resection.Testing culture sensitvity. Antibiotic Therapy.5-3gm IV/IM 6hrly for 48-72 hrs. PenicillinV 500mg PO 4hrly + Metronidazole 500mg 6hrly for 4-6 weeks Or Ampicillin/sulbactam 1.

the sequestra are removed and granulation tissue curetted.  The pack is removed every 3-4 days replaced till epithelization occurs   Decortication . During the acute phase.  Emprical antibiotic therapy is started.  The cortex is reduced with burs or rongeurs till there is a healthy bleed  The marrow cavity is thorougly debrided.Two perforated polyethelene Tubes are introduced through skin incisions to lie on the infected bone.Healing is by secondary intention.  The flap is trimmed and a pack is given to fill the dffect. The wounds are closed in a watertight manner.  A buccal mucoperiosteal flap is elevated. Saucerisation is the unroofing of the cortex for thorough debridement of the medullary cavity. Neomycin polymixin can also be introduced and left for 3hrs. Antibiotics such as Clindamycin. Irrigant is introduced into one and a low volume suction attached to the other.  Supportive therapy includes hydration . Removal of mobile and infected teeth and excision of the granulation tissue followed by the insertion of a drain. High protien and a high vitamin diet  Sequestrectomy & Saucerisation. It takes at least two weeks for sequestra to form after which they persist. with removal of loose teeth Sequestrectomy Saucerisation Decortication Stabilisation by internal fixation Resection Reconstruction        Debridement. extensive debridement of bone until active bleeding is encountered.They are stabilised to the bone by catgut sutures. folowed by intermittant suction  Surgical options. Debridemant and drainage.

A stage 1 nonresponder directly goes to stage 3 treatment.Decortication refers to the removal of the lateral and the inferior border of the mandible for upto 2cm beyond the affected area.  If the removal is extensive and a risk of fracture is feared.  If the lesion remains static recontouring is done Focal sclerosing osteomyelitis  Endodontic therapy or removal of the causative tooth Diffuse sclerosing osteomyelitis . Pathological fracture & Resorption of inf Border of mand. Each dive is 100% O2 For 90mins At 2.4 atm Non-suppurative osteomyelitis Garre’s periosteitis  Resolution occurs with removal or endodontic treatment of the causative tooth.  Hyperbaric Oxygen Therapy Direct bacteriostatic action Neoangiogenesis. fibroblast proliferation Enhances phagocytic function.  The defect is primarily closed with pressure bandaging (10-14days) and a two way suction drain or antibiotic beads may be placed . the mandible is stabilised with plates. 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.

Clinical features  Facial cellulitis  Hyperpyrexia & malice  Dehydration  Involvement of the orbit  Pus exudation from the nose  Intraorally. a swollen maxilla with sinuses. Infantile osteomyelitis Etiology  Perinatal trauma.Disodium clodronate(300-900mg)IV  Decortication  Resection  Calcitonin therapy. Treatment  Drainage  Culture sensitvity  Antibiotics Ampicillin/sulbactam IV or Clindamycin Until acute symptoms come Similar antibiotic PO 2-4 week.  Contaminatrd artificial nipples.  Bisphophonates .  Special considerations. till all symptoms are down totally resolved .Long term antibiotic therapy with roxithromycin(300mg/d PO) for upto 66months. Complications  Optic damage  Dural sinus involvement  Neural damage  Loss of tooth buds.

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 .

on biopsy Treatment  Debridement  Antibiotic therapy  Ultrasound therapy  Bone resection  Hyperbaric oxygen therapy .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.