Osteomyelitis

Osteomyelitis

Osteomyelitis

Osteomyelitis is an extensive inflammation of a bone. It involves the cancellous portion, bone marrow, cortex, and periosteum

Conditions that alter HOST IMMUNITY

Leukemia, Severe anemia, Malnutrition, AIDS, IV- drug abuse, Chronic alcoholism, Febrile illnesses, Malignancy, Autoimmune disease, Diabetes mellitus, Arthritis, Agranulocytosis

Conditions that alter vascularity of bone

Osteoporosis, Paget’s disease, Fibrous dysplasia, Bone malignancy, Radiation, Virulence of the organisms

Certain organisms precipitate thrombi formation by virtue of their destructive lysosomal enzymes.

Organisms proliferate in enriched host medium while protected from host immunity.

Etiology

- Odontogenic infections
- Trauma
- Infections of oro facial region
- Infections derived from hematogenous route
- Compound fractures of the jaws.

PATHOGENESIS

DEV . OF INFECTION --> BACTERIAL INVASION -->  PUS FORMATION -->  SPREAD OF INFECTION --> INCREASED INTRAMEDULLARY PRESSURE , BLOOD FLOW , OSTEOCLASTIC ACTIVITY --> INFLAMMATORY RESPONSES --> INCREASED PERIOSTEAL PRESSURE --> PROCESS BECOMES CHRONIC GRANULATION TISSUE FORMATION --> LYSIS OF BONE --> SEQUESTRUM FORMATION

Classification

Classification based on clinical picture, radiology, and etiology

Suppurative osteomyelitis

I. Acute suppurative osteomyelitis

II. Chronic suppurative osteomyelitis

– Primary chronic suppurative osteomyelitis

– Secondary chronic suppurative osteomyelitis

III. Infantile osteomyelitis

Nonsuppurative osteomyelitis

I. Chronic sclerosing osteomyelitis

  – Focal sclerosing osteomyelitis

  – Diffuse sclerosing osteomyelitis

II. Garre's sclerosing osteomyelitis

III. Actinomycotic osteomyelitis

IV. Radiation osteomyelitis and necrosis

Related Questions Diseases of Bone and Joints

Infantile Osteomyelitis

  • Osteomyelitis Maxillaries Neonatarum, Maxillitis of infancy
  • Osteomyelitis in the jaws of new born infants occurs almost exclusively in maxilla.

Etiology

  • Trauma – through break in mucosa cause during delivery.
  • Infection of maxillary sinus
  • Paunz & Ramon et al  believe that disease caused through infection from the nose.
  • Hematogenous spread through streptococci & pneumococci

Clinical features

  • Fever, anorexia & intestinal disturbances.
  • swelling or redness below the inner canthus of the eye in lacrimal region.
  • Followed by marked edema of the eyelids on the affected side.
  • Next, alveolus & palate in region of first deciduous molar become swollen.
  • Pus discharge from affected sites

D/D for Infantile Osteomyelitis

  • Dacrocystitis neonatarum
  • Orbital cellulitis
  • Ophthalmia neonatarum
  • Infantile cortical hyperostosis

TREATMENT

  • Intravenous antibiotics, preferably penicillin.
  • Culture & sensitivity testing
  • Incision & drainage of fluctuant areas
  • Sequestrectomy
  • Supportive therapy

Infective osteomyelitis

  • Tuberculous osteomyelitis
  • Syphilitic osteomyelitis
  • Actinomycotic osteomyelitis

Tuberculous osteomyelitis

  • Non healing sinus tract formation
  • Age group affected is around 15 – 40 years.
  • Commonly seen in phalanges and dorsal and lumbar vertebrae.
  • Usually occurs secondary to tuberculosis of lungs.
  • Cases have been reported where mandibular lesions were not associated with pulmonary disease.
  • Another common entrance is through a carious tooth via open pulp.
  • Usually affects long bones and rare in jaws.
  • Results when blood borne bacilli lodge in cancellous bone. Usually in ramus , body of mandible. may mimic parotid swelling or submassetric abscess.

Syphilitic osteomyelitis

  • Difficult to distinguish syphilitic osteomyelitis of the jaws from pyogenic osteomyelitis on clinical & radiographic examination.
  • Main features are progressive course & failure to improve with usual treatment for pyogenic osteomyelitis.
  • Massive sequestration may occur resulting in pathologic fracture.
  • If unchecked, eventually causes perforation of the cortex.

Actinomycotic Osteomyelitis

  • The organisms thrive in the oral cavity, especially tissues adjacent to mandible.
  • May enter the bone through a fresh wound, carious tooth or a periodontal pocket at the gingival margin of erupting tooth.
  • Soft or firm tissue masses on skin, which have purplish, dark red, oily areas with occasional zones of fluctuation.
  • Spontaneous drainage of serous fluid containing granular material.
  • Regional lymph nodes occasionally enlarged.
  • Mimics parotitis / parotid tumors

Chronic Osteomyelitis

  • As soon as pus drains intra or extraorally, condition ceases to spread and chronic phase commences.
  • Infection is localized but persistent as bacteria are able to grow in dead bone inaccessible to body’s defenses.

Clinical features

  • Primary – insidious in onset , slight pain , gradual increase in jaw size.
  • Secondary - Pain is deep pain and intermittent, temperature fluctuations , pyrexia , cellulitis eventually leading to abscess
  • New bone formation leads to thickening causing facial asymmetry.
  • Thickened or “wooden” character of bone in cr sec osteomyelitis.
  • Eventually cures itself as the last sequestra is discharged.

Radiographic Features

  • Trabeculae in the involved area become thin or appear fuzzy & then lose their continuity.
  • After some time “moth eaten” appearance is seen
  • Sequestra appear denser on radiographs.
  • Where the subperiosteal new bone formation , the new bone is superimposed upon that of jaw, “fingerprint” or “orange peel” appearance is seen
  • Cloacae seen as dark shadows passing through opacity.

Histologic features

  • Areas of acute and subacute inflammation in the cancellous spaces of the necrotic bone.
  • Foci of acute inflammation
  • Active osteoclastic resorption of bone noted in peripheral portions

Chronic Subperiosteal Osteomyelitis

  • Cortical plate deprived of its blood supply undergoes necrosis, underlying medullary bone  is slightly affected.
  • Multiple small sequestra form, eventually discharged through sinuses with pus.
  • Following extrusion of sequestra, healing occurs.
  • Spontaneous drainage poor in submassetric area.
  • Much of  body of mandible is lost due to poor central blood supply of the region.

D/D

  • Paget’s disease – particularly wen periosteal bone is involved
  • Fibrous dysplasia
  • Osteosarcoma

Chronic sclerosing osteomyelitis

– focal

- diffuse

Focal Sclerosing Osteomyelitis

Clinical features

  • Most commonly in children and young adults, rarely in older individuals.
  • Tooth most commonly involved is the mandibular third molar presenting with a large carious lesion.
  • No signs or symptoms other than mild pain associated with infected pulp.

Radiographic features

  • Entire root outline always visible with intact lamina dura.
  • Periodontal ligament space widened.
  • Border smooth & distinct appearing to blend into surrounding bone

D/D for focal sclerosing osteomyelitis

  • Local bone sclerosis
  • Sclerosing cementoma
  • Gigantiform cementoma

Treatment & prognosis

  • Affected tooth may be treated endodontically or extracted.
  • Sclerotic bone  not attached to tooth and remains behind after tooth is removed.
  • This dense area may not get remodeled.
  • Recognizable on bone years later and is referred as bone scar.

Diffuse Sclerosing Osteomyelitis

  • May occur at any age, most common in older persons, esp in edentulous mandibles
  • vague pain, unpleasant taste.
  • Many times spontaneous formation of fistula seen opening onto mucosal surface to establish drainage
  • Slowly progressive, not particularly dangerous since it is non destructive & seldom produces complications

Radiographic features

  • Diffuse patchy, sclerosis of bone – “cotton wool” appearance
  • Radiopacity may be extensive and bilateral.
  • Due to diffuse nature, border between sclerosis & normal bone is often indistinct

D/D for DIFFUSE sclerosing osteomyelitis

FLORID OSSEOUS DYSPLASIA

SCLEROTIC CEMENTAL MASSES

TRUE CHR DIFFUSE SCLEROSING OSTEOMYELITIS

FIBROUS DYSPLASIA

Treatment & Prognosis

  • Resolution of adjacent foci of chronic infection often leads to improvement.
  • Usually too extensive to be removed surgically,
  • Acute episodes treated with antibiotics.

Acute suppurative osteomyelitis

  • Serious sequela of periapical infection.
  • Leads to spread of pus through the medullary cavities of bone.
  • Depending upon the main site of involvement of bone, can be of two types-
  1. Acute intramedullary
  2. Acute subperiosteal

Acute Intramedullary Osteomyelitis

CLINICAL FEATURES:

  • Patient experiences dull , continuous pain , indurated swelling forms over the affected region of jaw involving the cheek , febrile.
  • When mandible involved, loss of sensation occurs on lower lip on affected side due to involvement of inferior alveolar nerve.
  • Teeth become loose later along with tender on percussion
  • Pus discharge , trismus , foul smell , regional lymphadenopathy , weakness

RADIOGRAPHIC FEATURES

  • Earliest radiographic change is that trabeculae in involved area are thin, of poor density & slightly blurred.
  • Subsequently multiple radiolucencies appear which become apparent on radiograph.
  • In some cases there is saucer shaped area of destruction with irregular margins.
  • Loss of continuity of lamina dura, seen in more than one tooth.

HISTOLOGIC FEATURES:

  • Dense infiltration of marrow by polymorphonuclear leukocytes.
  • Bone trabeculae in involved site (sequestrum) are devoid of cells in the lacunae.
  • separation of considerable portions of devitalized bone.

 

Acute Subperiosteal Osteomyelitis

CLINICAL FEATURES

  • Pain , febrile condition , i/o and e/o swelling , parasthesia
  • Bone involvement limited to localized areas of cortex.
  • Pus ruptures rapidly through the overlying cortex, tracks along the surface of mandible under the periosteal sheath.
  • Elevation of periosteum from cortex is followed eventually by minute cortical sequestration.

Osteoradionecrosis

Clinical features

A reduction in vascularity, secondary to endarteritis obliterans, and damage to osteocytes as a consequence of ionising

Radiotherapy can result in radiation-associated osteomyelitis or Osteoradionecrosis. The mandible is much more  commonly affected than the maxilla, because it is less vascular. Pain may be severe and there may be pyrexia. The overlying oral mucosa often appears pale because of radiation damage. Osteoradionecrosis in the jaws arises most often following radiotherapy for squamous cell carcinoma.
 

Scar tissue will also be present at the tumour site, often in close relation to the necrotic bone.

 

Radiology
 

Osteoradionecrosis appears as rarefying osteitis within which islands of opacity (sequestra) are seen. Pathological

fracture may be visible in the mandible.

Pathology
The affected bone shows features similar to those of chronic osteomyelitis. Grossly, the bone may be cavitated

And discoloured, with formation of sequestra.
Acute inflammatory infiltrate may be present on a background of chronic inflammation, characterized by formation

Of granulation tissue around the non-vital trabeculae.

Blood vessels show areas of endothelial denudation and obliteration of their lumina by fibrosis.

Small telangiectatic vessels lacking precapillary sphincters may be present.

Fibroblasts in the irradiated tissues lose the capacity to divide and often become binucleated and enlarged.

Management

Prevention of Osteoradionecrosis is vital. Patients who  require radiotherapy for the management of head and

neck malignancy should ideally have teeth of doubtful prognosis extracted at least 6 weeks prior to treatment.

The dose of radiation,
The area of the mandible irradiated and
the surgical trauma involved in the dental extractions.
Surgical management of Osteoradionecrosis is similar to osteomyelitis.