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| IMC Wiki | Osteomyelitis


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Osteomyelitis is inflammation of the medullary cavity of a bone caused by an infection.
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is inflammation of the bone tissue originating from the vessels of the Haversian canals, in the strict sense (in contrast to osteomyelitis that originates from the medullary cavity).


is inflammation of the periosteum.


is localised inflammation within a dental alveolus.

Aetiology of osteomyelitis

Osteomyelitis is primarily caused by extension of odontogeneous infections into bone.
Spread of focal infection is almost the single cause of osteomyelitis in the maxillo-facial region.
Other infections by foreign body, iatrogenic measures, trauma and haematogeneous spread are of inferior significance.

Most pyogenic infections can be sealed off within the bone marrow and healed completely by the organism after elimination of the primary focus.

The involved bone marrow becomes necrotic or undergoes chronical changes, which cannot heal spontaneously after elimination of the primary focus.
The mandible is affected 3-15 times more frequently than the maxilla (Adekeye et Cornah 1985).
Less frequently the osteomyelitis of the maxilla occurs predominantly in infancy.
The most common route of infection is via an avital or dislocated tooth.
Beside the spectrum of oral germs, Staphylococcus aureus ist the commonest causative agent.

Forms of osteomyelitis

Osteomyelitis may be an acute or a chronic disease.
The significance of acute osteomyelitis has decreased since the development of modern antibiotic therapy.
The prevalence of acute osteomyelitis in realation to chronic osteomyelitis is 1:25.

Acute osteomyelitis

Clinical features and diagnosis

Local symptoms of inflammation: #pic#
  • spongy, red gingiva
  • perimandibular infiltration (in mandibular localisation)
  • oedematous swelling of adjacent soft tissues
  • severe pain
  • discharge of pus from periodontium (take smear for microbial detection)
  • tooth loosening
  • pain on percussion on bone
  • massive swelling with formation of fistula and abscess upon penetration of cortical bone
  • Vincent symptom:
    decrease or loss of sensation in the mental nerve region of the mandible (by alteration of the N. alveolaris inferior)
  • pyrexia
  • general fatigue, severe clinical picture
  • In the first week the radiograph shows no or only mininmal signs of de-mineralisation.

Chronic osteomyelitis

Chronic osteomyelitis is characterised by bone formation and resorption processes as well as bone marrow necrosis with variable subliminal clinical course leading frequently to diagnostic and therapeutical problems.
Clinically, primary chronic and secondary chronic osteomyelitis can be distinguished. A classification in pseudo-Paget disease (osteomyelitis sicca), non-purulent, chronic, diffuse and sclerosing-, as well as chronic juvenile ostomyelitis has been attmpted based on different reaction muster of the affected bone.

Clinical features of chronic osteomyelitis

  • diffuse pain
  • non-healing soft tissue and bone wounds
  • recurrent swelling
  • sequestrum formation
  • pathologic fractures
  • formation of fistula into oral cavity and sometimes into dermis
Clinical appearance and course are primarily dependent on local rate of perfusion.

The vascular supply to bones is a significant pathogenetic factor. It is composed of multiple arterial loops which function as end-arteries without terminal anastomoses (Wannfors et Gazelius 1991).
Vascular insufficiencies, caused by infection-related thromboembolic processes, lead to impairement of microcirculation and trophic deficit with secondary cell- and tissue necrosis, comparable to infarction.
Some bone areas excluded from normal supply become necrotic. Bone sequestra develop, surrounded by granulation tissue (x-ray).
Sequestration hampers immune response, since immunocompetent cells do not achieve the centre of inflammation.

Reenforcing pathogenetic factors are: persistent, atherosclerosis-related deficit in microcirculation, arterial occlusion diesease or hyperergic conditions.
New perfusion of the affected bone area should be built up by neovascularisation to enable bone regeneration.

Predisposing factors

Systemic predisposing factores are: aseptic chronic osteomyelitis foci, state of the immune system and microcirculation.

Predisposing systemic factors

  • low patient's compliance (lacking oral hygiene)
  • diabetes mellitus
  • chronic hypoxia
  • immune suppression/deficit
  • malignant tumours
  • hypertension
  • tobacco and alcohol consumption

Predisposing local factors

  • chronic lymphoedema
  • impaired venous drainage
  • vascular diseases
  • extensive scars
  • radiation-induced fibrosis
  • paraesthesia

Diagnostic imaging

Conventional radiographs

Bone morphology regarding shape, structure and outlines can be assessed by conventional radiography (e.g. OPG).
Because osteolytic processes can be first visualised after loss of more than 50 % of anorganic substance, conservative radiology is more meaningful in chronic osteomyelitis.

Radiological findings:
  • osteolysis
  • sclerosis
  • irregular, unsharp borders
  • sequestra (shadowing encircled by a brighter surrounding)



Intensity and extension of osteomyelitis can be assessed by scintigraphy. In areas of osteomyelitis there is increased activity of the used radioactive agent secondary to increased bone tissue metabolism (activity of osteoblasts and osteoclasts).

Scintigraphy can be used for:
  • early diagnosis
  • identification of osteomyelitic areas after two days of disease (Reinert et al 1999)
  • assessment of extension
  • monitoring of course of disense
  • monitoring of integration following reconstruction

Laboratory findings

  • leukocytosis (acute osteomyelitis, rarely in case of chronic osteomyelitis
  • increase of sedimentation rate and C-reactive protein (CRP)

Histological findings

Histology of punch biopsies helps in the differentiation against malignant bone tumours and systemic bone diseases.

  • infiltration of medullary cavity by granulocytes
  • lacunar resorption of bone substance by osteoclasts
  • tissue liquefaction with necrotic bone trabecules

Microbiological findings (intraoperative biopsy)

  • most commonly, mixed infections from the oral flora
  • gram-positive bacteria, with preponderance of aerobics
  • increased prevalence of anaerobic and rare bacterial infections

Further examinations

  • computertomography
  • magnetic resonance tomography
  • positron emission tomography
  • sonography

Differential diagnosis

The following diseases are considered in the differential diagnosis of chronic osteomyelitis:
  • fibrous dysplasia
  • cemento-ossifying fibroma
  • malignant non-Hodgkin-lymphoma
  • osteosarcoma
  • chondrosarcoma
  • Ewing-sarcoma
  • carcinomatous metastases other organs
Exclusion of malignant tumours is essential!

Conservative therapeutical options

  1. antibiotic therapy
    early introduction of antibiotic therapy, if possible (prior to transport and referral), especially in case of acute osteomyelitis
    Clindamycin (Sobelin®) 3 x 300 mg/d
    • penetrate bone
    • concentration in macrophages and granulocytes
  2. medicamentous-rheological therapy: Pentoxifyllin (Trental®)
    • increases microcirculation by
      • increasing erythrocyte plasticity
      • decreasing blood viscosity
      • inhibiting platelet aggregation
    • dosage 3 x 400 mg/d
    Naproxen (Proxen®)
    • non-steroidal anti-inflammatory drug/analgetic, derivative of proionic acid
  3. physical therapy
    • microwave, occasionally, iodine iontophoresis
    • hyperbaric oxygen therapy, if necessary

Management of acute osteomyelitis

  • immediate antibiotic therapy
    Single antibiotic therapy is promising only in initial stage of disease as long as bone perfusion is present.
    Antibiotic should be continued for at least 3 weeks, also after control of the acute symtoms within a few days.
  • tooth splinting (no tooth extraction!)
  • trepanation of causing tooth, if necessary
  • early incision of soft tissue abscess (without lifting the periosteum!)

Management of chronic osteomyelitis

The surgical treatment is primary.
All conservative measures can be used additionally.

Surgical treatment options

The goal of surgical therapy is to remove all necrotic and connective tissue parts in order to enable sufficient neovascularisation.
  • removal of infected extraneous material and necrotic tissues
  • extraction of affected teeth
  • extensive curettage (up to vital bone)
  • decortication
  • removal of hyperplastic periosteum and scars
  • Segmental resection or continuity resection
  • followed by reconstruction using free autologous bone graft and modern methods of osteosynthesis
  • plastic reconstruction:
    • spongiosa graft (from the iliac crest) in case of alveolar crest resection
    • vascular soft tissue flap
    • microvascular pedided flap
  • osteosynthesis with plates


  • antibiotic resistency
  • spontaneus fractures
  • soft tissue abscesses
  • emphyema of maxillary sinus
  • pyarthros (purulent joint exsudation)
  • phlegmone of soft tissues in the head and neck region
  • intracranial expansion (abscess of the brain)
  • malignant transformation
  • massive bone loss
  • persisting osteomyelitis
  • impaired mastication
  • injury to or loss of adjacent anatomic structures (e. g. Vincent-syndrom)
  • affection and/or loss of teeth


The term angiogenesis relates to formation of capillaries from preexisting vessels.
The "vascular endothelial growth factor" (VEGF) has been identified as a key molecule from among endothelial growth factors.
It regulates proliferation of endothelial cells, angiogenesis, vasculogenesis and vascular permeability.
The influence of controlled release of vascular endothelial growth factor (VEGF) on angiogenesis and osteogenesis was investigated in a rabbit mandibular defect model. Significant increase and prolongation of angiogenesis as well as bone regeneration was observed under the influence of released VEGF (Kleinheinz et al.2002).


  • Adekeye EO, Cornah (1985) Osteomyelitis of the jaws: a review of 141 cases Br J Oral Maxillofac Surg. 23:24-35
  • Kleinheinz J, Wiesmann HP, Stratmann U, Joos U (2002) Evaluating angiogenesis and osteogenesis modified by vascular endothelial growth factor (VEGF) Mund Kiefer Gesichtschir. 6:175-82
  • Reinert S, Widlitzek H, Venderink DJ (1999) The value of magnetic resonance imaging in the diagnosis of mandibular osteomyelitis Br J Oral Maxillofac Surg. 37:459-63