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Oral Bisphosphonates and Optimal Oral Health

Bisphosphonates are widely used for the treatment of osteoporosis, hypercalcemia of malignancy, osteolytic lesions of multiple myeloma, and bone metastasis of solid tumors. The association between osteonecrosis of the jaw (ONJ) and the use of bisphosphonates in compromised patients has been established in the literature.1-10 By suppressing osteoclasts, bisphosphonate drug mechanisms increase overall bone mass.8 In osteoporosis, it inhibits osteoclast-mediated bone resorption, which reduces the gradual reduction of bone mass with aging.2,3,8,9 This effect, however, may carry a potential for severe suppression of bone turnover, which may impair wound healing and reparative properties. Although the exact mechanism of bisphosphonate-related osteonecrosis (BRONJ) has not been determined, in most cases, the pathogenesis is consistent with a suppression of bone physiologic remodeling and wound healing. The profound inhibition of osteoclast function also can inhibit normal bone turnover to an extent that local microdamage from normal mechanical loading or an injury cannot be repaired.10 

 

Clinical Manifestations

The clear understanding of the various manifestations of BRONJ is critical to prevention, early recognition, and treatment. The clinical presentation of BRONJ is variable, ranging from asymptomatic soft tissue swelling to painful exposed necrotic bone and infection. The majority of patients present with an area of exposed bone—with or without pain—in the mandible alone (ie, 68.1%), in the maxilla (ie, 27.7%), or, less commonly, in both (ie, 4.2%).8 Mobile teeth, cutaneous fistula, mucosal fistula, or bone exposed through the skin are less frequent.1 Some patients may have more subtle complaints (eg, feelings of heaviness in the jaw, numbness).

 

Imaging and Laboratory Examination

Radiographic evaluation is not particularly effective during the early stages of the disease. Periapical and panoramic radiographs may, however, be of assistance in ruling out other causes of dental pain, as well as metastatic lesions. The most common findings are hyperostotic lamina dura and widened periodontal ligament.1

 

The C-terminal cross-linked telopeptide (CTx) test has been used in metabolic studies as an indicator of the rate of bone renewal. Serum CTx values < 100 pg/ml have been associated with a high risk of developing BRONJ, values of 100 to 150 pg/dl have been associated with a moderate risk, and values > 150 pg/dl generally indicate a minimal risk (11). The CTx test, however, measures primarily metabolism of trabecular bone and not cortical bone, and is representative of skeletal bone in general. Therefore, this test may not be reflective of the cortical plate of bone which supports the dentition.

Staging

Establishing the diagnosis and careful evaluation of the extent and severity of bone involvement are paramount in the management of patients and prognosis of BRONJ. While the American Association of Oral and Maxillofacial Surgeons (AAOMS) established a working definition for BRONJ, Wade and Suzuki subsequently established a modification of the AAOMS-proposed staging system to include treatment strategies using the CTx serum test.1

 

Stage 0

Therapy can be deferred when patients are generally asymptomatic and are receiving IV bisposphonates (stage 0iv) or have been taking oral bisposphonates for more than three years (stage 0or), until serum CTx levels are obtained. Ctx levels > 150 pg/ml indicate that odontoalveolar surgery is relatively safe. For patients with serum level < 150 pg/dL, the prescribing physician should be contacted regarding withdrawal of bisphosphonate therapy for a period of three months if possible. If repeated CTx levels are > 150 pg/dl, dental treatment may be rendered. Otherwise, the period is extended in three month intervals until levels are > 150pg/dl. If emergency treatment must be performed, CTx levels should be obtained as soon as possible, and the physician should be contacted.

 

Stage I

When patients present with asymptomatic exposed bone, a detailed oral examination and noninvasive treatment plan should be undertaken. The patient should be educated regarding the exposed bone, instructed in proper oral hygiene of the area, and placed on a maintenance regimen of chlorhexidine oral rinses. Frequent follow-up visits should be implemented, including close monitoring for any signs of soft or hard tissue infection or additional exposed bone. A baseline CTx level should be obtained, and the treating physician should be contacted to investigate the possibility of temporarily discontinuing bisphosphonate medication.

 

Stage II

When patients present with exposed bone, pain, and soft tissue or bone infections, they should have cultures taken to determine appropriate antibiotic treatment. Empiric therapy is recommended if results are inconclusive. The standard regimen is penicillin V potassium 500 mg every six hours and an oral rinse using chlorhexidine 0.12% twice daily. In refractory cases, metronidazole 500 mg every six hours is added for seven to 10 days. For patients who are allergic to penicillin, levofloxacin 500 mg daily has proven to be an excellent alternative. A baseline CTx level should be obtained, and more extensive treatment may proceed when the level exceeds 150 pg/dl. Empiric data, however, does not indicate that increasing CTx level will result in reduction of BRONJ risk.

 

Stage III

Patients present with all of the preceding signs and symptoms and at least one of the following: pathologic fracture, extraoral fistula, or osteolysis extending to the inferior border. In these patients, more conservative treatment methods may have already failed. Therefore, to alleviate pain and eliminate infection, it may be necessary to debride or resect large areas of bone. This approach has met with some success. To date, however, no standardized treatment protocols exist.

Therapy

As efficacy of treatment is limited, prevention of BRONJ is very important and begins with identifying patients at increased risk.12,13 These include patients with a history of dentoalveolar trauma and those with prolonged exposure to bisphosphonate therapy.10 In the majority of BIONJ reported cases to date, recent dentoalveolar trauma was the most prevalent and consistent risk factor. Patients with inflammatory dental diseases (eg, periodontal disease, dental abscesses) are at seven-fold increased risk for developing BRONJ. This underscores the importance of maintaining good oral health and avoiding extractions, especially in high-risk patients such as women and men with prolonged (ie, more than three years) exposure and those with concomitant steroid therapy.

 

Conclusion

Oral bisphosphonate therapy is the first-line treatment option for patients who require osteoporosis treatment and is highly effective in preventing fractures. Although a definitive causal relationship between the use of oral bisphosphonate and ONJ has yet to be established, the potential risk of bone necrosis and associated morbidity cannot be ignored. Prevention is superior to treatment, and the establishment of meticulous oral hygiene is important to prevent pathology necessitating surgical management.

 

*Resident in the Department of Periodontology and Oral Implantology, Temple University, Kornberg School of Dentistry, Philadelphia, Pennsylvania.

†Professor of Microbiology and Immunology, School of Medicine; Professor of Periodontology and Oral Implantology, Department of Periodontology and Oral Implantology, Temple University, School of Dentistry; Associate Dean for Graduate Education and International Affairs and Program Director of Graduate Periodontics, Temple University, Philadelphia, Pennsylvania.

 

References

 

  1. Wade ML, Suzuki JB. Issues related to diagnosis and treatment of bisphosphonate-related osteonecrosis of the jaws. Grand Rounds Oral-Sys Med 2007;2(2):46-53.
  2. Nase JB, Suzuki JB. Osteonecrosis of the jaw and oral bisphosphonate treatment. J Am Dent Assoc 2006;137(8):1115-1119.
  3. Suzuki JB, Klemes MA. Osteoporosis and osteonecrosis of the jaw. Access 2008(suppl):1-16.
  4. Advisory Task Force on Bisphosphonate-Related Ostenonecrosis 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):369-376.
  5. King AE, Umland EM. Osteonecrosis of the jaw in patients receiving intravenous or oral bisphosphonates. Pharmacotherapy 2008;28(5):667-677.
  6. Abu-Id MH, Warnke PH, Gottschalk J, et al. “Bis-phossy jaws” - High and low risk factors for bisphosphonate-induced osteonecrosis of the jaw. J Craniomaxillofac Surg 2008;36(2):95-103.
  7. Marx, RE. Pamedronate (aredia) and zoledronate (zometa) induced avascular necrosis of the jaws: A growing epidemic. J Oral Maxillofac Surg 2003;61(9):1115-1117.
  8. Sawatari Y, Marx RE. Bisphosphonates and bisphosphonate induced osteonecrosis. Oral Maxillofac Surg Clin North Am 2007;19(4):487-498.
  9. American Dental Association Council on Scientific Affairs. Dental management of patients receiving oral bisphosphonate therapy: Expert panel recommendations. J Am Dent Assoc 2006; 137(8):1144-1150.
  10. Ruggiero SL. Bisphosphonate-related osteonecrosis of the jaws. Compend Contin Educ Dent 2008; 29(2):96-105.
  11. Marx RE. Oral and intravenous bisphosphonate-induced osteonecrosis of the jaws. 1st ed. Hanover Park, IL: Quintessence, 2006.
  12. Jeffcoat M, Watts NB. Osteonecrosis of the jaw: Balancing the benefits and risks of oral bisphosphonate treatment for osteoporosis. Gen Dent 2008;56(1):96-102.
  13. Hewitt C, Farah CS. Bisphosphonate-related osteonecrosis of the jaws: A comprehensive review. J Oral Pathol Med 2007;36(6): 319-328.

 

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