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sues and recommendations regarding the most recent form of osteonecrosis described, osteonecrosis of the jaws (ONJ) related to bisphosphonate administration. The authors report that zoledronate administration poses the highest risk of developing ONJ, followed by pamidronate. Results from a longitudinal study1 have just been published and zoledronate, indeed, has been shown to be an independent risk factor for ONJ development when compared with ibandronate and pamidronate. Of note, ibadronate demonstrated the safest drug profile as far as ONJ complication is concerned, in the conditions (cancer) and dose schemas administered in the latter study (monthly, intravenous administration).1 The only issue not addressed by the JADA authors concerns the role of dentures as a risk factor for ONJ development. Some in the profession have believed that use of dentures could be a risk factor for ONJ development, and a year ago a case-control study confirmed use of dentures as a risk factor for ONJ development.2 A justpublished longitudinal study also reported on denture use as an independent risk factor for ONJ development.1 It has been proposed that ill-fitting dentures may cause breaches to the underlying mucosa, thereby initiating sequelae that drive local bone homeostasis toward ONJ.3 It has been suggested that denture wearers undergoing bisphosphonate treatment should receive additional care to avoid gingival trauma caused by their dentures.4 Consequently, dental practitioners may prevent a number of ONJ cases by regularly checking the fit of den-

tures and by re-treating those that are ill-fitting or modeling new ones for patients receiving bisphosphonates. Athanassios Kyrgidis, MD, DDS, MSc Konstantinos Vahtsevanos, MD, DDS, PhD Department of Oral and Maxillofacial Surgery Theagenio Cancer Hospital Thessalonik Greece 1. Vahtsevanos K, Kyrgidis A, Verrou E, et al. Bisphosphonate related osteonecrosis of the jaws: a longitudinal cohort study of risk factors in cancer patients. J Clin Oncol (in press). 2. Kyrgidis A, Vahtsevanos K, Koloutsos G, et al. Biphosphonate related osteonecrosis of the jaws: a case control study of risk factors in breast cancer patients. J Clin Oncol 2008; 26(28):4634-4638. 3. Kyrgidis A, Vahtsevanos K. Increased risk for biphosphonate related osteonecrosis of the jaws in patients wearing overdentures could be attributable to impaired mucosal cell wound healing. J Oral Maxillofac Surg 2009; 67(6):1355-1356. 4. Kyrgidis A, Triaridis S. Regular dental check-ups could be of benefit for patients receiving intravenous bisphosphonates: regarding “risks and benefits of bisphosphonates.” Br J Cancer 2009;100(4):670. Epub 2008 Aug 5.

Authors’ response: We thank Drs. Kyrgidis and Vahtsevanos for their letter. In our review article, we did state that trauma such as (although not limited to) tooth extractions is an important factor. However, since this was a review that discussed other factors related to osteonecrosis and not just bisphosphonate use, space constraints led us to omit articles that discussed other specific comorbid factors such as the use of dentures. In Drs. Kyrgidis and Vahtsevanos’ research, the use of dentures in 20 patients was a statistically significant factor (P = .018) in one of three analyses performed.1 We look forward to reading their latest research, which should be published soon.2 At this time, there appear to be two prevailing theories for the occurrence of bisphosphonateJADA, Vol. 140

related osteonecrosis. The “inside-out” theory is one in which the bone becomes necrotic in small foci, which then progress and enlarge,3 possibly as a result of local factors such as localized periodontal or periapical infection, or microdamage. Exposure of the necrotic bone occurs when there is trauma resulting from tooth extraction or from mucosal damage. As such, trauma does not “cause” the osteonecrosis but rather exposes and likely exacerbates a latent lesion when the mucosa breaks down. The other theory is the “outside-in” theory, in which the primary damage is to the mucosal keratinocytes that then leads to underlying bone damage and necrosis, possibly aggravated by bacterial ingress.4 Clearly, bisphosphonates affect both the bone and the keratinocytes, and there are supporters of both theories. However, the large size of many lesions that are “discovered” after a tooth extraction somewhat supports the first theory as a primary mechanism, although it is likely that mucosal damage plays an important but perhaps a secondary role. Soulafa Almazrooa, BDS Resident Department of Oral Medicine, Infection and Immunity Harvard School of Dental Medicine and Resident Division of Oral Medicine and Dentistry Brigham and Women’s Hospital Boston

Sook-Bin Woo, DMD Associate Professor Department of Oral Medicine, Infection and Immunity Harvard School of Dental Medicine and Attending Dentist Division of Oral Medicine and Dentistry

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Brigham and Women’s Hospital Boston 1. Kyrgidis A, Vahtsevanos K, Koloutsos G, et. al. Bisphosphonate-related osteonecrosis of the jaws: a case-control study of risk factors in breast cancer patients. J Clin Oncol 2008; 26(28):4634-4638. 2. Vahtsevanos K, Kyrgidis A, Verrou E, et al. Bisphosphonate related osteonecrosis of the jaws: a longitudinal cohort study of risk factors in cancer patients. J Clin Oncol (in press). 3. Burr DB, Allen MR. Mandibular necrosis in beagle dogs treated with bisphosphonates. Orthod Craniofac Res 2009;12(3):221-228. 4. Landesberg R, Cozin M, Cremers S, et al. Inhibition of oral mucosal cell wound healing by bisphosphonates. J Oral Maxillofac Surg 2008;66(5):839-847.

EARLY CHILDHOOD CARIES

I would like to congratulate Dr. Paul Casamassimo and colleagues on their June JADA article, “Beyond the dmft: The Human and Economic Cost of Early Childhood Caries” (Casamassimo PS, Thikkurissy S, Edelstein BL, Maiorini E. JADA 2009;140[6]:650-657). The incidence of early childhood caries (ECC) continues to rise to levels that we have not seen for decades,1,2 and the time has come to understand that when we discuss this disease, it’s about more than “just baby teeth.” If we are to eliminate this disease, we need to look beyond the mouth and develop an awareness program to convince the public that caring for the oral cavity affects the entire developing child. Dr. Carol Berkowitz, the past president of the American Academy of Pediatrics, stated that “the mouth is the gateway to the body, and if the mouth is not healthy, the rest of the body is not healthy either.”3 As a profession, we must produce hard research evidence to define the scope of the problem, and then make a compelling case for changing the public mindset about the prevention of a disease a former U.S. surgeon gen1218

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eral determined to be the most common of chronic infectious diseases in children.2 We must ask ourselves what concurrent and related events are transpiring during the critical age when ECC begins, including effects on the child’s neurodevelopment, social development and overall physical development. We must determine why these children are being exposed to foods that most precipitate ECC, and the relationship of ECC to spousal abuse and shaken baby syndrome. In these times of health care reforms, we must determine the private and public economic impact of this disease. If we can demonstrate what the true costs are and the value of prevention in reducing these expenses, then government and private industry will listen. All of this is achievable, but until we can provide the evidence to define and clarify these relationships, I fear that the incidence of ECC will continue to rise and our children will continue to suffer beyond the oral cavity. Leonard B. Smith, DDS, MSc Clinical Assistant Professor Department of Pediatrics Faculty of Medicine The University of Calgary Alberta, Canada 1. U.S. Department of Health and Human Services. Oral health. In: Healthy People 2010: Objectives for Improving Health. Vol II. 2nd ed. Washington: U.S. Department of Health and Human Services; 2000. “www. healthypeople.gov/Document/HTML/Volume2/ 21Oral.htm”. Accessed Sept. 11, 2009. 2. U.S. Department of Health and Human Services. Oral health in America: a report of the surgeon general—executive summary. Rockville, Md.: U.S. Department of Health and Human Services, National Institute of Dental and Craniofacial Research, National Institutes of Health; 2000. “www2.nidcr.nih. gov/sgr/execsumm.htm”. Accessed Aug. 24, 2009. 3. Smith LB. Prevention: what you should know—Dr. Berkowitz (video clip). “www. drgoodtooth.com/video_drberkowitz.php”. Accessed Aug. 24, 2009.

ORAL HEALTH, HEART HEALTH

Congratulations to Dr. Daniel J. Caplan and colleagues for their August JADA article, “The Relationship Between Self-Reported History of Endodontic Therapy and Coronary Heart Disease in the Atherosclerosis Risk in Communities Study” (Caplan DJ, Pankow JS, Cai J, Offenbacher S, Beck JD. JADA 2009;140[8]:1004-1012). The first theories of a connection between oral health and systemic health can be traced back to the 19th century. The classic and oft-quoted work is by W.D. Miller, who published his theories in 1891.1 Miller used knowledge garnered from working in the laboratory of Robert Koch. Also, a reference to the oral health–systemic health connection has been attributed to Dr. John Mankey Riggs (18111885), the father of periodontics, as far back as the 1870s.2 Dentists’ education and clinical experiences supply us with the proper armamentarium to investigate this relationship more fully and to expand on the existing knowledge base. In order to do this, dental professionals must partner with both basic science researchers and other health care professionals such as physicians and nurses. William J. Maloney, DDS Clinical Assistant Professor College of Dentistry New York University New York City

1. Miller WD. The human mouth as a focus of infection. Dent Cosmos 1891;33(9): 689-713. 2. Twain M. Happy memories of the dental chair. In: Hirst RH, ed. Who Is Mark Twain? New York City: Harper Collins; 2009:77-85.

October 2009

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OSTEONECROSIS OF THE JAW: Authors' response.

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