Osteomyelitis of the jaws
Osteomyelitis of the jaws is osteomyelitis which occurs in the bones of the jaws. Historically, osteomyelitis of the jaws was a common complication of odontogenic infection. Before the antibiotic era, it was frequently a fatal condition.
Former and colloquial names include Osteonecrosis of the jaws, cavitations, dry or wet socket, and NICO. The current, more correct, term, osteomyelitis of the jaws, differentiates the condition from the relatively recent and better known iatrogenic phenomenon of bisphosphonate-caused osteonecrosis of the jaws. The latter is found primarily in post-menopausal women given bisphosphonate medications, usually against osteoporosis.
Classification
The classification is similar to the classification of OM generally, according to the length of time the inflammation has been present and whether there is suppuration. Acute osteomyelitis is loosely defined as OM which has been present for less than one month and chronic osteomyelitis is the term used for when the condition lasts for more than one month. Suppurative osteomyelitis of the jaws is uncommon in developed regions, and more common in developing countries. In Europe and the United States, most cases follow dental infections, oral surgery or mandibular fractures. There have been many reported cases occurring in Africa which are coexistent with acute necrotizing ulcerative gingivitis or cancrum oris.In the pre-antibiotic era, acute OM of the jaws was more extensive. Massive, diffuse infections commonly involved the whole side of the mandible, or the whole of one side and the opposite side as far as the mental foramen. Localized osteomyelitis tended to be described as either vertical, where a short segment of the body of the mandible from the alveolar crest to the lower border was involved, and alveolar, where a segment of alveolar bone down to the level of the inferior alveolar canal would sequestrate, including the sockets of several teeth. Treatment with antibiotics has significantly altered the natural history of OM of the jaws. Today, however, the condition is often a hidden infection, due in part to not being visible on most dental X-rays unless there is a substantial loss of bone density. In addition, some schools of dentistry do not recognize "silent" OM of the jaws—occurrence of the condition without visually obvious manifestations—in their curriculum. In addition, as circulation is intrinsically diminished in jawbones, antibiotics are frequently ineffective.
Signs and symptoms
The signs and symptoms depend upon the type of OM, and may include:- Pain, which is severe, throbbing and deep seated and often radiates along the nerve pathways.
- Initially fistula are not present.
- Headache or facial pain, as in the descriptive former term "neuralgia-inducing".
- Fibromyalgia.
- Chronic fatigue syndrome.
- Swelling. External swelling is initially due to inflammatory edema with accompanying erythema, heat and tenderness, and then later may be due to sub-periosteal pus accumulation. Eventually, subperiosteal bone formation may give a firm swelling.
- Trismus, which may be present in some cases and is caused by edema in the muscles.
- Dysphagia, which may be present in some cases and is caused by edema in the muscles.
- Cervical lymphadenitis.
- Aesthesia or paresthesia in the distribution of the mental nerve.
- Fever which may be present in the acute phase and is high and intermittent
- Malaise which may be present in the acute phase
- Anorexia.
- Leukocytosis which may be present in the acute phase
- Elevated erythrocyte sedimentation rate and C reactive protein are sometimes present.
- An obvious cause in the mouth such as a decayed tooth.
- Teeth that are tender to percussion, which may develop as the condition progresses.
- Loosening of teeth, which may develop as the condition progresses.
- Pus may later be visible, which exudes from around the necks of teeth, from an open socket, or from other sites within the mouth or on the skin over the involved bone.
- Fetid odor.
Cause
OM is usually a polymicrobial, opportunistic infection, caused primarily by a mixture of alpha hemolytic streptococci and anaerobic bacteria from the oral cavity such as Peptostreptococcus, Fusobacterium and Prevotella,. These are the same as the common causative organisms in odotonogenic infections. However, when OM in the jaws follows trauma, is the likely cause is still staphylococcal Leiden heterozygosity.Pathogenesis
OM may occur by direct inoculation of pathogens into the bone, by spread of an adjacent area of infection or by seeding of the infection from a non adjacent site via the blood supply. Unlike OM of the long bones, hematogenous OM in the bones of the jaws is rare. OM of the jaws is mainly caused by spread of adjacent odontogenic infection. The second most common cause is trauma, including traumatic fracture and usually following a compound fracture. In OM of the long bones, a single invading pathogenic micro-organism is usually found.The mandible is affected more commonly than the maxilla. This is thought to be related to the differences in blood supply between the mandible and the maxilla. The maxilla has a better blood supply, and has thin cortical plates and less medullary spaces. These factors mean that infections of the maxilla are not readily confined to the bone, and readily dissipate edema and pus into the surrounding soft tissues and the paranasal air sinuses. OM of the maxilla may rarely occur during an uncontrolled infection of the middle ear or in infants who have sustained birth injury due to forceps. The mandible in contrast has a relatively poor blood supply, which deteriorates with increasing age. The cortical plates are thick and there is a medullary cavity. The sites of the mandible most commonly affected by OM are the body, the symphysis, the angle, the ramus and finally the condyle. The mandible's blood supply is primarily via the inferior alveolar artery, and secondarily via the periosteum. Compromise of this supply is a critical factor in the development of OM in the mandible.
Most periapical and periodontal infections are isolated by the body which produces a protective pyogenic membrane or abscess wall to keep the area of infection localized. Micro-organisms which are sufficiently virulent may destroy this barrier. Factors which may contribute to this are decreased host resistance, surgery or repeated movement of fracture segments, as may occur with an untreated fracture. Mechanical trauma burnishes the bone, causing ischemia by crushing blood vessels and seeds micro-organisms into the tissues.
The events preceding OM are acute inflammatory changes such as hyperemia, increased capillary permeability and infiltration of granulocytes. Proteolytic enzymes are released, and thrombus formation in the blood vessels and tissue necrosis occur. Pus accumulates in the medullary spaces of the bone, which increases the pressure and leads to collapse of the blood vessels, venous stasis and ischemia. Pus may also spread to the sub-periosteal layer, dissecting it away from the surface of the bone and further reducing the blood supply. The inferior alveolar neurovascular bundle is compressed within the mandible, causing anesthesia or paresthesia in the distribution of the mental nerve. Pus may drain via sinuses on the skin and in the mouth, and these may in time become lined with epithelium, when they are termed fistulas.
Chronic OM is characterized by a degree of healing which takes place as a lesser degree of inflammation is present. Granulation tissue and new blood vessels form, and fragments of necrotic bone are separated from vital bone. Small sections of necrotic bone may be resorbed completely, and larger segments may become surrounded by granulation tissue and new bone. Sequestra may also be revascularized by new blood vessels, cause no symptoms or become chronically infected. Sometimes the involucrum is penetrated by channels through which pus drains to the skin or mouth.
OM of the jaws often occurs in the presence of one or more predisposing factors. These factors are related to compromised vascular perfusion locally, regionally or systemically, causes of immunocompromise and poor wound healing. Specific examples include familial hypercoagulation, diabetes, autoimmune diseases, Agranulocytosis, leukemia, severe anemia, syphilis, chemotherapy, corticosteroid therapy, sickle cell disease, acquired immunodeficiency syndrome, old age, malnutrition, smoking and alcohol consumption, radiotherapy, osteoporosis, Paget's disease of bone, fibrous dysplasia, bone malignancy and causes of bone necrosis such as Bismuth, Mercury or arsenic. Poor compliance or access to health care is also a risk factor.
Rarely, OM of the jaws may be a complication of trigeminal herpes zoster.