Sir, in reply to the request from Z. Harrison for evidence-based protocols dealing with the problem of bisphosphonate-associated osteonecrosis (BDJ 2006; 200: 242–243), I am afraid that there are no randomised trial results at present. However, an excellent comprehensive review paper was published in the December edition of the Journal of the American Dental Association and this should be essential reading for all dentists.1 Their observations included the following.

Bisphosphonates are used to treat resorptive bone diseases and to control bone loss in malignancies such as multiple myeloma and metastatic solid tumours. They act by inhibiting osteoclastic activity and therefore severely compromise normal bone deposition and remodelling. The complication of bisphosphonate-associated necrosis (BON) associated with their long-term use has recently been recognised although the exact mechanism which leads to this condition is still unknown.

BON has been reported with the use of the intravenous agents pamidronate (Aredia) and zoledronic acid (Zometa). The most common history is lack of healing following dental extractions, although other dental procedures have been implicated. The oral lesions are similar to those of radiation-induced osteonecrosis and are often progressive, leading to extensive areas of bone exposure. Since there is no successful therapy at present, prevention is of vital importance.

All patients about to begin bisphosphonate treatment and those who have recently started should undergo a full dental evaluation in order to achieve an excellent state of dental health and eliminate all potential sites of infection. Periodontal therapy and restorative procedures should be provided and any extractions completed as soon as possible. Following active treatment, there should be regular visits for oral examination and reinforcement of oral hygiene measures.

For patients who have developed BON, routine dental care may be provided but scaling and prophylaxis should be as atraumatic as possible. Ideally extractions should be avoided, except in the case of very mobile teeth, and endodontic treatment considered. Any extractions should be performed with the minimum of trauma and patients should be followed up weekly for the first four weeks and then monthly until the sockets are completely closed and healed. Where antibiotics are indicated, amoxicillin alone, or in combination with clindamycin, may reduce the incidence of local infection. The area of BON should only be treated with the object of eliminating trauma from sharp edges of bone. A chlorhexidene mouthrinse is recommended four times a day and any odontogenic infections treated aggressively with systemic antibiotics. It is important that any prosthetic appliances should fit well and these may be relined with a soft liner to prevent soft-tissue trauma and pressure.

There is no scientific evidence to support discontinuation of the bisphosphonate therapy to promote healing of necrotic tissue and this should not be done without full consultation with the patient's specialist. Since the half-life of intravenous bisphosphonates is reported to be years, cessation of therapy for a few months will have little effect on the bone environment.

For a complete account of the problem I would advise full reading of this excellent article which may be obtained from the Journal of the American Dental Association website at jada.ada.org.