Osteomyelitis is a rare complication of tooth-
related infections (incidence of 25 in 100,000).  
In most cases, it is the result of spread of
infection from a
dento-alveolar (tooth) or
periodontal (pyorrhoea / gum disease) abscess
or from the
para-nasal sinuses, by way of
continuity through
tissue spaces and planes.  It
occasionally occurs as a complication of jaw
fractures or as a result of manipulations during
surgical procedures.

Most patients are adult males with infection of the
mandible (lower jaw).

Osteomyelitis of the maxilla (upper jaw) is a rare disease
neonates (newly born) or infants after either birth
injuries or uncontrolled middle ear infection.

It is classified as
acute or chronic osteomyelitis.

Acute Osteomyelitis

In the acute form (which rarely, may also be of
hæmatogenous origin
[i.e. seeded from the blood
stream]), the infection begins in the
medullary cavity (bone
marrow) of the bone.  The resulting increase of
pressure leads to a decreased blood supply (and hence
diminution of white blood cells and other immune
components) and spread of the infection, by way of the
Haversian canals of the bone, to the cortical bone
and periosteum (below the periosteum, a thick
fibrous two-layered membrane covering the surface of
bones).  This aggravates the
ischæmia (decreased blood
supply), resulting in
necrosis (the death of cells or tissues
from severe injury or disease, especially in a localised
area of the body.  Causes of
necrosis include inadequate
blood supply [as in
infarcted tissue], bacterial infection,
traumatic injury and
hyperthermia) of the bone.

Acute Osteomyelitis of the Jaws — Potential Sources of

  • Peri-apical infection
  • A periodontal pocket involved in a fracture
  • Acute gingivitis or pericoronitis (even more rarely)
  • Penetrating, contaminated injuries (open fractures or
    gunshot wounds)
The mandible (lower jaw), due to decreased vascularity (blood supply & flow), is
involved 6 times more often than the maxilla (upper jaw).

mandible has a relatively limited blood supply and dense bone with thick bony
cortical) plates.  Infection causes acute inflammation in the medullary (bone
marrow) soft tissues and inflammatory
exudate (a fluid with a high content of
protein and cellular debris which has escaped from blood vessels and has been
deposited in tissues or on tissue surfaces, usually as a result of inflammation. It
may be septic or non-septic) spreads infection through the marrow spaces.  It also
compresses blood vessels confined in the rigid boundaries of the vascular canals.

Thrombosis (the formation or presence of a thrombus [a clot of coagulated blood
attached at the site of its formation] in a blood vessel) and obstruction then lead to
further bone

Dead bone is recognisable microscopically by
lacunae (a cavity, space, or
depression, especially in a bone, containing cartilage or bone cells) empty of
osteocytes (a cell characteristic of mature bone tissue.  It is derived from
osteoblasts and embedded in the calcified matrix of bone. Osteocytes are found in
small, round cavities called
lacunae and have thin, cytoplasmic branches) but filled
neutrophils (white blood cells) and colonies of bacteria which proliferate in the
dead tissue.

Pus, formed by liquefaction of necrotic soft tissue and inflammatory cells, is forced
along the
medulla and eventually reaches the sub-periosteal region by resorption
(an organic process in which the substance of some differentiated structure that
has been produced by the body undergoes
lysis and assimilation) of bone.  
Distension of the
periosteum by pus stimulates sub-periosteal bone formation but
perforation of the
periosteum by pus and formation of sinuses on the skin or oral
mucosa are rarely seen now.

At the boundaries between infected and healthy tissue,
osteoclasts (a specialised
bone cell that absorbs bone)
resorb the periphery of the dead bone, which
eventually becomes separated as a
sequestrum (a fragment of dead bone
separated from healthy bone as a result of injury or disease).  Once infection starts
to localise, new bone forms around it, particularly

Where bone has died and been removed, healing is by granulation with formation of
coarse fibrous bone in the proliferating connective tissue.  After resolution, fibrous
bone is gradually replaced by compact bone and remodelled to restore normal
bone tissue and structure (and function).

Piercing, deep and constant pain predominates in the clinical presentation in adults,
while low or moderate fever,
cellulitis, lymphadenitis, or even trismus may also be

In the
mandible, changes in sensation affecting the lower lip (paræsthesia or
dysæsthesia of the lower lip) may accompany the disease.  When the disease
spreads to the
peri-osteum (definition) and the surrounding soft tissues, a firm
œdema (definition) of the region is observed, while the tooth becomes loose
and there is discharge of
pus from the periodontium.  Radiographic examination
osteolytic (definition) or radiolucent (definition) regions

Therapy entails combined surgical (incision, drainage, extraction of the tooth and
removal of
sequestrum) and chemo-therapeutic treatment (with antibiotics).

Summary of Treatment of Osteomyelitis

Essential Measures

  • Bacterial sampling and culture
  • Vigorous (empirical) antibiotic treatment
  • Drainage
  • Give specific antibiotics based on culture and sensitivities
  • Give analgesics
  • Debridement
  • Remove source of infection, if possible

Adjunctive Treatment

  • Sequestrectomy
  • Decortication if necessary
  • Hyperbaric oxygen*
  • Resection and reconstruction for extensive bone destruction

*Mainly of value for
osteo-radionecrosis and possibly, anærobic infections.

Anæsthesia of the lower lip usually recovers with elimination of the infection.  Rare
complications include pathological fracture caused by extensive bone destruction,
osteomyelitis after inadequate treatment, cellulitis due to spread of
exceptionally virulent bacteria or
septicæmia in an immuno-deficient patient.

Chronic Osteomyelitis

Chronic osteomyelitis is characterised by a clinical course lasting over a month.  It
may occur after the acute phase or it may be a complication of tooth-related
infection without a preceding acute phase.  The clinical presentation is milder, with
painful exacerbations and discharge of pus or sinus tracts.


Patient UK

Useful Articles:

Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology & Endodontology
2005. Diagnosis and Classification of Mandibular Osteomyelitis

Gülhane Týp Dergisi 2007.  Mandibular osteomyelitis developing due to a failed
root canal treatment in a patient with multiple myeloma

Journal of Dental Research, Dental Clinics, Dental Prospects 2009.  Localized
Osteomyelitis of the Mandible Secondary to Dental Treatment - Report of a Case

Dental Update 2010.  Osteomyelitis of the Mandible Secondary to Pericoronitis of
an Impacted Third Molar.

British Dental Journal 2010.  Osteomyelitis presenting in two patients - a
challenging disease to manage.
Important Predisposing Conditions for Osteomyelitis

Local Damage to / Disease of the Jaws
  • Fractures, including gunshot wounds
  • Radiation damage
  • Paget's disease
  • Osteopetrosis

Impaired Immune Defences

  • Acute leukaemia
  • Poorly-controlled diabetes mellitus
  • Sickle cell anaemia
  • Chronic alcoholism or malnutrition
  • AIDS

  • Infection from micro-organisms with great virulence.  In such cases, even a
    peri-apical abscess may be implicated in osteomyelitis.

Acute Osteomyelitis of the Jaws — Key Features

  • Mandible mainly affected, usually in adult males
  • Infection of dental origin - anærobes are important
  • Pain and swelling of jaw
  • Teeth in the area are tender; gingivæ (gums) are red and swollen
  • Sometimes paræsthesia of the lip
  • Minimal systemic upset
  • After about 10 days, X-rays show 'moth-eaten' pattern of bone destruction
  • Good response to prompt antibiotic treatment and debridement
Last Updated 26th December 2014