Exposed bone in the palate
Michael A. Siegel, DDS, MS,
Cesar A. Migliorati, DDS, MS, PhD,
Ines Velez, DDS, MS and
Mark Forrest, DMD
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THE CHALLENGE
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An 86-year-old woman visited her periodontist (M.F.) for diagnosis and treatment of a persistent palatal ulceration (Figure 1
). At the time the patient first noted the palatal lesion, the periodontist believed that the ulceration represented a traumatized maxillary torus. He constructed a clear palatal stent to cover the lesion and prevent further trauma (Figure 2). The periodontist also prescribed triamcinolone ointment for topical application.
During the ensuing four-month period, the lesion did not resolve, which prompted the periodontist to refer the patient to an oral medicine health care provider (M.A.S.) for a consultation. The patient was concerned about the possibility of having oral cancer. She reported that during the four-month period, she had a sharp area of bone that had resolved spontaneously.
The patient had a complex medical history, but her medical conditions were well-controlled at the time of the consultation. She was ambulatory, lived alone and was able to carry out her daily activities without limitation. She was being treated for cardiovascular disease, hypertension, mild anxiety, hypothyroidism, osteopenia and hypokalemia. The patient’s medications included atenolol (50 milligrams), zolpidem (10 mg), amlodipine (5 mg), clopidogrel (75 mg), aspirin (1 mg), levothyroxine (0.05 mg), fludrocortisone (0.1 mg), hydrochloro-thiazide (25 mg), fenofibrate (130 mg) and alendronate (70 mg weekly), and she also took a multi-vitamin. Previous significant surgeries included a coronary artery bypass graft. The patient denied having any allergies.
The results of the extraoral examination were completely normal. The oral medicine health care provider did not note any ocular or cutaneous lesions. The intraoral examination revealed a large lobulated torus extending from the premaxilla to the soft palatal aponeurosis in an anterior-posterior direction and from the vertical aspects of the alveolar ridges laterally. The middle of the torus was ulcerated (8 x 6 millimeters) to the right of the mid-line, and necrotic bone was clinically evident centrally.
Can you make the diagnosis?
- minor salivary gland tumor
- angiocentric T-cell lymphoma (midline lethal granuloma)
- squamous cell carcinoma
- fixed drug reaction
- bisphosphonate-associated osteonecrosis
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THE DIAGNOSIS
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E. bisphosphonate-associated osteonecrosis
Reports of bisphosphonate-associated osteonecrosis (BON) (also referred to as osteonecrosis of the jaws and osteochemonecrosis) of the jaw associated with the use of intravenous bisphosphonates were first published in 2003.1 Intravenous bisphosphonates are used in patients with skeletal lesions resulting from multiple myeloma; breast, lung and other cancers; and Paget’s disease of bone. The majority of reported cases of BON have been reported after dental procedures such as tooth extractions. However, BON also appears to occur spontaneously in some patients taking these drugs.2
By 2005, the literature also contained reports of cases of BON in patients taking orally administered nitrogen-containing bisphosphonates, which are used for the treatment of osteoporosis.3 For alendronate (the most commonly prescribed oral bisphosphonate), a BON incidence of approximately 0.7 cases per 100,000 person-years of exposure has been estimated.4 To date, a true cause-and-effect relationship has not been established.5 Migliorati and colleagues6 published a model for the pathogenesis of BON. Although there are no definitive diagnostic criteria or known risk factors, BON has been defined as the unexpected appearance of necrotic bone anywhere in the oral cavity of a patient receiving bisphosphonate treatment who has not received radiation therapy to the head and neck region. The necrotic bone persists for at least six to eight weeks in spite of standard therapy.6 Guidelines have been published to assist the clinician in the prevention and treatment of BON.5,7,8
In this case, the oral medicine health care provider carefully considered the fact that the lesion had not healed during a four-month period in a patient with an essentially uncompromised immune system. This patient had been receiving alendronate therapy weekly for seven years. The dentists involved in her treatment (M.F., M.A.S.) did not remove any sequestrum. However, the oral medicine health care provider considered the patient’s history of having had a self-resolving sharp area of bone to be consistent with the presence of a small nidus of necrotic bone.
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DIFFERENTIAL DIAGNOSIS
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The midline of the hard palate is an uncommon site for a fixed drug reaction. On palpation, a salivary gland tumor does not have the bony hard consistency of a torus, but it appears firm or soft. The soft-tissue margins of the palate were not rolled or indurated, signs that might have suggested neoplastic disease such as a squamous cell carcinoma or a malignant minor salivary gland tumor. Angiocentric T-cell lymphoma (midline lethal granuloma) results in the destruction of the midline structures of the palate and nasal cavity; the lesion in this case exposed only palatal bone.
The oral medicine health care provider rendered a presumptive diagnosis of BON. The physician of record discontinued the patient’s alendronate therapy, as she did not have osteoporosis and was being treated prophylactically only for osteopenia. The physician of record felt that the alendronate therapy was not essential to her medical management. During the six-week healing period, the patient did not receive any bisphosphonate therapy. The bisphosphonate therapy was not discontinued for the purpose of treating the palatal lesion. The clinicians agreed that if the patient’s bone density decreased progressively into clinical osteoporosis, the physician of record would reinstitute the alendronate therapy. The oral medicine health care provider instructed the patient to take clindamycin (150 mg) four times daily for two weeks and apply topical chlorhexidine gluconate (0.12 percent) twice daily directly onto the ulceration using a cotton swab.
After two weeks, the lesion had begun to heal, but the patient was complaining of gastrointestinal distress related to the systemic antibiotic. For the following four weeks, until the lesion healed completely, the patient applied topical metronidazole 1.0 percent gel to the lesion twice daily. The oral medicine health care provider also instructed her to use the clear plastic stent until the lesion had resolved (Figures 3 and 4).
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CONCLUSION
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BON has been defined as the unexpected appearance of necrotic bone anywhere in the oral cavity of a patient receiving bisphosphonate treatment who has not received radiation therapy to the head and neck region. To date, a true cause-and-effect relationship has not been established.5 Guidelines have been published to assist the clinician in the prevention and treatment of BON.5,7,8 The necrotic bone persists for at least six to eight weeks despite standard therapy.6 The published guidelines stress that patients with BON should be treated conservatively. The patient described here had localized BON that resolved with systemic and topical antibiotic therapy, along with use of a plastic stent to protect the lesion.
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FOOTNOTES
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Dr. Siegel is a professor and the chairman, Department of Diagnostic Sciences, College of Dental Medicine, Nova Southeastern University, 3200 S. University Drive, Fort Lauderdale, Fla. 33328-2018, e-mail "masiegel{at}nova.edu". Address reprint requests to Dr. Siegel.
Dr. Migliorati is a professor, Department of Diagnostic Sciences, College of Dental Medicine, Nova Southeastern University, Fort Lauderdale, Fla.
Dr. Velez is an associate professor and the director, Oral and Maxillofacial Pathology Service, College of Dental Medicine, Nova Southeastern University, Fort Lauderdale, Fla.
Dr. Forrest is an adjunct associate professor, Department of Periodontology, College of Dental Medicine, Nova Southeastern University, Fort Lauderdale, Fla.
Diagnostic Challenge is published in collaboration with the American Academy of Oral and Maxillofacial Pathology and the American Academy of Oral Medicine.
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REFERENCES
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- Migliorati CA. Bisphosphonates and oral cavity avascular bone necrosis. J Clin Oncol 2003;21(22):4253–4.[Free Full Text]
- Ruggiero SL, Mehrotra B, Rosenberg TJ, Engroff SL. Osteonecrosis of the jaws associated with the use of bisphosphonates: a review of 63 cases. J Oral Maxillofac Surg 2004;62(5):527–34.[Medline]
- Marx RE, Sawatari Y, Fortin M, Broumand V. Bisphosphonate-induced exposed bone (osteonecrosis/osteopetrosis) of the jaws: risk factors, recognition, prevention, and treatment. J Oral Maxillofac Surg 2005;63(11):1567–75.[Medline]
- Advisory Task Force on Bisphosphonate-Related Osteonecrosis of the Jaws, American Association of Oral and Maxillofacial Surgeons. American Association of Oral and Maxillofacial Surgeons position paper on bisphosphonate-related osteonecrosis of the jaws. J Oral Maxillofac Surg 2007;65(3):369–76. Available at: "www.aaoms.org/docs/position_papers/osteonecrosis.pdf". Accessed Aug. 29, 2007.[Medline]
- American Dental Association Council on Scientific Affairs. Dental management of patients receiving oral bisphosphonate therapy: expert panel recommendations. JADA 2006;137(8):1144–50.[Abstract/Free Full Text]
- Migliorati CA, Siegel MA, Elting LS. Bisphosphonate-associated osteonecrosis: a long-term complication of bisphosphonate treatment. Lancet Oncol 2006;7(6):508–14.[Medline]
- Migliorati CA, Casiglia J, Epstein J, Jacobsen PL, Siegel MA, Woo SB. Managing the care of patients with bisphosphonate-associated osteonecrosis: an American Academy of Oral Medicine position paper. JADA 2005;136(12):1658–68.[Abstract/Free Full Text]
- Woo SB, Hellstein JW, Kalmar JR. Narrative (corrected) review: bisphosphonates and osteonecrosis of the jaws (published correction appears in Ann Intern Med 2006;145[3]:235). Ann Intern Med 2006;144(10):753–61.[Abstract/Free Full Text]
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TRAUMATIC INJURY OR BON?
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January 1, 2008;
139(1):
16 - 17.
[Full Text]
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THE CHALLENGE
THE DIAGNOSIS
