Defined as a non-healing exposed necrotic bone of the jaw.
Risk factors include radiation therapy to the head and neck, periodontal disease, dental surgery involving bone, edentulous areas trauma from poorly fitting dentures, presence of an underlying malignancy, chemotherapy, corticosteroids regional or systemic infections, denosumab and bisphosphonate treatment.
The condition may involve the mandible or maxilla.
Coagulopathies, impaired blood flow from edema or osteomyelitis have been implicated as possible risk factors.
Pathogenesis unclear but possibly due to inhibition of resorption, thrombotic microangiopathy and angiogenesis inhibition leading to avascular necrosis and poor wound healing after dental work.
From radiation may be a result from loss of osseous cellular elements as well as vascular damage that results in relative ischemia of the bone.
Incidence and severity of radiation induced osteonecrosis are related to the dose, field and fraction given.
Incidence from radiation in the range from 0.4-8.2%, with large variation among centers.
Associated with pain, infection, disability and diminished quality of life.
Most cases associated with radiation therapy develop following dental extractions.
Osteonecrosis of the jaw following radiotherapy can occur spontaneously, without a precipitating event, or secondary to denture induced trauma or periodontal disease.
The median time to the development of radiation to osteonecrosis of the jaw is 13 months.
Pretreatment oral care reduces the risk and severity of oral complications, allows for prompt identification and treatment of infections, improves the likelihood that the patient will successfully complete planned cancer treatment, prevents, eliminates, or reduces pain, prevents nutritional compromise, prevents or reduces incidence of bone necrosis, improves oral health, improves quality of life, and decreases cost of care.
Oral evaluation should take place 1 month before cancer treatment starts to allow adequate time recovery from any required invasive dental procedures.
It is standard of care for patients to undergo dental evaluation prior to radiation therapy of the head and neck region to have infected teeth, teeth at high risk for infection, or teeth with a poor prognosis extracted at that time.
Pretreatment evaluation includes a thorough examination of hard and soft tissues, and radiographs to detect possible sources of infection, carious and compromised teeth, and tissue pathology.
Teeth that are nonrestorable or may pose a future problem are removed to prevent later extraction-induced osteonecrosis.
After radiation the remaining dentition must be well-maintained in order to avoid future extractions and risk of developing osteonecrosis of the jaw.
The dose of radiation to the mandible and maxilla should be minimized when possible to decrease risk of jaw osteonecrosis.
Medication-related osteonecrosis of the jaw (MRONJ) is defined as exposed bone or bone that can be probed through an intraoral or extra oral fistula or fistulae in the maxillofacial region and that does not heal within eight weeks, occurring in a patient who is received a bone modifying agent or an angiogenic inhibitor agent with no history of head and neck radiation.
Associated with bisphosphonates and denosumab and patients may present as numbness and heaviness of the jaw, pain, swelling, exposure of bone and loosening of teeth.
Majority of cases reported with pamidronate and zoledronic acid but has been observed with oral alendronate (Fosamax), risendronate (Actonel).
To date not reported with ibandronate (Boniva).
Not reported with etidronate (Didronel).
The type produced by oral bisphosphonates is different from intravenous induced jaw osteonecrosis in that the a longer period of exposure to oral agents is necessary and the amount of exposed bone is smaller and symptoms less severe.
Induced by oral agents may improve with cessation of oral agent and spontaneous healing may occur, and is more responsive to debridement after 6 months to a year.
95% of cases associated with zoledronic acid or pamidronate given intravenously.
Patients generally present with exposed necrotic bone that does not heal for 6-8 weeks.
Zervas and others reported a 9.5 fold greater risk for zoledronic acid compared with pamidronate.
Typically develops in patients who have received intravenous bisphosphonates for 1.5-3 years.
When given intravenously for patients with malignancy the incidence ranges from 1.3% to 4-7% in various studies with multiple myeloma and breast cancer the most associated cancers.
Among millions of patients on oral agents only a handful have developed this entity among persons treated for osteoporosis.
Estimated that 1 in 100,000 patient-years for the incidence in patients receiving oral nitrogen containing bisphosphonates for osteoporosis.
Fewer than 5 cases reported among patients taking bisphosphonates for Paget’s disease of the bone.
Histologically the osteonecrosis of the jaw lesion is the same as that of osteoradionecrosis.
Hypothesized that the physiological stresses on the jaw demanding repair of micro-defects are inhibited by hypovascular and hypodynamic effects induced by bisphosphonates causing decreased ability for repair, resulting in osteonecrosis.
The doses of bisphosphonates used for metastatic cancers are typically 4-12 times higher than those used for osteoporosis.
Presents as exposed bone in the maxilla and or mandible with appearing necrotic, nonvital and surrounded by inflamed mucosa secondary to infection.
May involve the palate.
Typically heals poorly or does not heal over 6-8 weeks.
Not all patients have pain.
Approximately two thirds of the lesions occur in the mandible and the rest involve the maxilla.
A rare case can involve the external auditory canal.
Diagnosis is a clinical one.
Predisposing factors include dental disease, dental procedures, such as tooth extraction, oral trauma, periodontal disease, and poor oral hygiene.
Patients frequently have received chemotherapy and corticosteroids.
Presently, there is no consensus for the prevention or management of osteonecrosis of the jaw.
Conservative management includes minimal surgical debridement, rinses with cyclohexidine or hydrogen peroxide, intermittent antibiotics and analgesic agents.
Treatment ranges form conservative surgical approaches, such as local debridement, and sequestrectomy, to resection with or without osteomyocutaneous flaps.
Adjunctive approaches to surgery include antibiotics, pentoxifyline and hyperbaric oxygen.
Suggested benefits of hyperbaric oxygen therapy in osteonecrosis of the jaw by facilitating wound healing by increasing local tissue oxygen tension, resulting in enhanced collagen production, angiogenesis, bone regeneration and oral tissue epithelialization, overcoming hypoxia, hypocellularity and hypovascularity due to effects of radiation therapy.
In a review of 7 studies there was no consistent evidence supporting hyperbaric oxygen therapy for either the prevention or management of osteonecrosis of the jaw(Sultan A, Dana Farber Cancer Institute).
In a 2004 multicenter trial of hyperbaric oxygen, the study was terminated due to worse outcomes in the hyperbaric arm -19% resolution with hyperbaric oxygen and 32% resolution with placebo (Annane).
Recommended to have dental evaluation before beginning intravenous bisphosphonates therapy to optimize dental hygiene and perform necessary procedures in advance.
The risk of osteoporosis of the jaw after IV bisphosphonates in patients with cancer is estimated as 1-5% over five years.
The rate of jaw osteoporosis after IV bisphosphonates given for osteoporosis is lower than for cancer.
Targeted therapies such as tyrosine kinase inhibitors in addition to bisphosphonates may increase the risk of osteonecrosis of the jaw by decreasing VEGF activity.