I find it surprising, in a period when bisphosphonate-associated osteonecrosis (BON) is such a "hot" subject, that JADA’s reviewers did not properly vet the October article by Dr. Michael Siegel and colleagues, "Exposed Bone in the Palate" (
Siegel MA, Migliorati CA, Velez I, Forrest M. JADA 2007;138[10]:1341–3[Free Full Text]
), before publishing it.
It is a well-known fact that the mucosa covering palatal and lingual tori is very thin and fragile when subjected to trauma. The mucosa and its thin layer of periosteum is the main source of the blood supply to these large, dense, cortical, compact bone tori. When this blood supply is lost as a result of trauma (hard foods) during mastication, it causes an ulceration. The exposed bone, over time, will slough in a superficial fashion. When it does, granulation tissue has formed to re-establish the blood supply by secondary intention beneath this slough of bone. Unless the new tissue is protected from the trauma of eating and deglutition by a prosthetic appliance, the process just continues over and over.
In my 44 years of private oral and maxillofacial surgery clinical practice, I have seen this at least three to four times each year. I have successfully treated all of these cases without antibiotics in young and old patients, with total healing in four to six weeks, by prosthetic protection of the ulcer. Some of my patients had chronic ulcers for two to four months before being referred to me.
In older patients, compliance with instructions is difficult; hence, the ulceration becomes chronic. Keep in mind that the vast bulk of my cases, identical to these cases to which I refer, took place in the era prior to bisphosphonate therapy. Just because the patient was on a bisphosphonate does not automatically mean that this is BON.
