osis of the Jaws: n
A Challenge, a Responsibility, and an Opportunity
In the period since bisphosphonate-induced osteonecrosis of the jaws (BIONJ) was first identified in 2003,1more than 300 publications have appeared, and more than 3,600 cases have been reported to the US Food andDrug Administration (FDA). Since most cases are seen and treated in dental offices throughout the world andnever reported to the FDA, this number represents only a small fraction of the actual number of patients affected.
Like the radiated patient who develops radiation caries, xerostomia, periodontal bone loss, or even osteoradio-necrosis, patients with BIONJ depend on their dental providers to recognize, understand, treat, and preventBIONJ. This formidable challenge also carries a responsibility for the dental profession to take the lead in edu-cating their medical colleagues about this drug-induced complication of the jaws, in the same tradition as radiation-induced complications of the jaws.
The Challenge: Perhaps the greatest challenge for dental practitioners is to avoid either under- or overstating theBIONJ problem. Dental providers should understand that some publications minimize the risk of BIONJ and under-state its impact on oral health, using its low incidence as justification for being unprepared.2,3 Conversely, it is impor-tant not to overreact or be fearful either of caring for patients who are taking bisphosphonates or of treating thosewho have BIONJ. In addition to following established protocols,4–8 dentists should know that this group of patientsrequires more frequent monitoring and oral maintenance schedules than others, a greater effort made toward pre-ventive dentistry, and a well-planned and executed treatment program.
The Responsibility: The first responsibility for dental providers is to include a history of bisphosphonate use in theirhealth history forms. Questions should be asked regarding not only the use of a bisphosphonate, but also the form(intravenous vs oral) and type (intravenous: pamidronate [Aredia] or zoledronate [Zometa]; oral: alendronate[Fosamax], residronate [Actonel], or ibandronate [Boniva]), along with the dosage, frequency, and most importantly,the duration of therapy. The responsibility continues with the need to be informed and to educate others as to themechanism of BIONJ and its incidence related to each form and type of bisphosphonate, clinical and radiographicappearance, and treatment and prevention protocols. This information is readily available through the publishedposition papers of several organizations and individual authors.4–9
The Opportunity: Dental professionals can minimize the impact of bisphosphonates on the quality of life of thoseaffected by educating the medical profession and seeking their understanding and cooperation in the care theyprovide. Specific to intravenous bisphosphonates, prevention involves completing needed oral surgical and peri-odontal surgical procedures prior to or at least within the first 3 months of intravenous bisphosphonate use.
Restorative prevention and periodontal maintenance procedures also enable these patients to avoid the need forinvasive surgical procedures once they have started receiving intravenous bisphosphonates. This requires dentiststo consult the treating oncologist as to the patient’s dental needs and recommendations for a reasonable time framein which to accomplish them consistent with medical treatment goals. The mainstay of treatment for patients whohave developed intravenous bisphosphonate–induced osteonecrosis is palliation with 0.12% chlorhexidine aloneor in combination with various antibiotic courses to control secondary infections and hence pain. Resection is nec-essary in only rare instances of refractory BIONJ or pathologic fracture. In either case, coordination with the patient’soncologist provides the best control and keeps him/her apprised of the treatment course.
Similar to intravenous bisphosphonates, prevention of BIONJ in those patients receiving oral bisphospho-
nates is best achieved by completing all necessary invasive oral surgical and periodontal procedures and evenelective procedures, such as ridge augmentation and dental implant placements, prior to the start of their riskperiod. The critical difference in oral BIONJ risk is that it does not begin until after about 3 years of oral bisphos-phonate use and can be assessed with the morning fasting serum C-terminal telopeptide (CTX) test. This infor-mation needs to be conveyed to the physicians treating osteopenia and osteoporosis. Ideally, physicians willlearn to refer patients for dental evaluations before or during their early treatment course with an oral bisphos-phonate. By following these guidelines, dental and medical professionals can work together to prevent a largepercentage of potential BIONJ cases from developing.
om that of intravenous BIONJ. Because oral bisphosphonates accu-
mulate in bone at a much slower rate, osteoclast function can be restored by discontinuation of the oral bisphos-phonate, often described as taking a “drug holiday.” The patient’s CTX values are monitored throughout thisperiod. Such drug holidays can be initiated only by the prescribing physician at the request of the dentalprovider. During this period, exposed bone may spontaneously heal or be resolved by minor office-baseddebridements, something that is not usually possible with intravenous BIONJ.7,9 The safety of such drug holi-days or of even longer periods of suspended use has been documented in the medical literature.10,11
This recently identified disease has in some ways reversed the old tradition of dentists seeking a “medical
clearance” to proceed with their dental care. With BIONJ, medical providers also need to consult dentists andwork equally to provide optimum therapeutic care while preventing the complications that sometimes resultfrom it.
Robert E. Marx, DDSProfessor of Surgery and ChiefDivision of Oral and Maxillofacial SurgeryUniversity of Miami Miller School of MedicineMiami, Florida
1. Marx RE. Pamidronate (Aredia) and Zoledronate (Zometa)–induced
7. Marx RE, Sawatari Y, Fortin M, Broumand V. Bisphosphonate-
avascular necrosis of the jaws. A growing epidemic [letter]. J Oral
induced exposed bone (osteonecrosis/osteopetrosis) of the jaws:
Maxillofac Surg 2003;61:1151–1157.
Risk factors, recognition, prevention, and treatment. J Oral
2. Schwartz H. Bisphosphonate-associated osteonecrosis of the jaws.
Maxillofac Surg 2005;63:1567–1575.
J Oral Maxillofac Surg 2005;63:1248–1249.
8. Migliorati CA, Casiglix J, Epstein J, Jacobson PL, Siegel MA, Woo
3. Jeffcoat MK. Safety of oral bisphosphonates: Controlled studies on
SB. Managing the care of patients with bisphosphonate-associat-
alveolar bone. Int J Oral Maxillofac Implants 2006;27:349–353.
ed osteonecrosis. An American Academy of Oral Medicine PositionPaper. J Am Dent Assoc 2005;136:1658–1668.
4. American Association of Oral and Maxillofacial Surgeons Position
Paper on Bisphosphonate-Related Osteonecrosis of the Jaws. J Oral
9. Marx RE, Cillo JE, Ulloa JJ. Oral bisphosphonate–induced
osteonecrosis: Risk factors, prediction of risk using serum CTX test-ing, prevention, and treatment. J Oral Maxillofac Surg
5. American Dental Association Council on Scientific Affairs. Dental
management of patients receiving oral bisphosphonate therapy:Expert panel recommendations. J Am Dent Assoc 2006;
10. Black DM, Schwartz AV, Ensrud KE, Cauley JA, Levis S, Quandt SA,
et al. Effects of continuing or stopping alendronate after 5 years oftreatment. The Fracture Intervention Trial Long-term extension
6. Ruggiero S, Gialow J, Marx RE, et al. Practical guidelines for the pre-
(FLEX). A randomized trial. JAMA 2006;296:2927–2938.
vention, diagnosis, and treatment of osteonecrosis of the jaw inpatients with cancer. J Oncol Pract 2006;2:7–14.
11. Colón-Emeric CS. Ten vs five years of bisphosphonate treatment for
postmenopausal osteoporosis: Enough of a good thing. JAMA2006;296:2968–2969.
The International Journal of Periodontics & Restorative Dentistry
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