Abstract

Managing modifiable risk factors, such as cholesterol and blood pressure, is the conventional strategy to combat heart disease, the number 1 cause of death in the United States. Medications for lowering cholesterol and blood pressure have also been shown to play a role in bone metabolism. As such, these medications are of potential interest to the osseointegration and health of dental implants. Given the widespread use of these medications, it is imperative to understand their role in enhancing or deteriorating the health of dental implants. The most common class of cholesterol-lowering medications (known as statins) lower serum cholesterol by inhibiting the rate-limiting enzyme in the hepatic cholesterol biosynthesis pathway. Animal studies have shown statins to increase osteogenesis around dental implants, which has been explained by increased expression of bone morphogenic protein-2 and osteoblast differentiation. The applicability of these results to dental implant health in humans, however, remains unclear.1 Many pharmacologic mechanisms exist for lowering blood pressure, and as such, antihypertensives can affect bone physiology in different ways. For example, thiazide diuretics increase renal calcium absorption, beta adrenergic blockers inhibit osteoclasts, and drugs targeting the renin-angiotensin-aldosterone system block the bone resorptive activity of angiotensin II. These mechanisms have been used to explain an association between decreased implant failure and antihypertensive medications.2 This study aims to elucidate how cholesterol-lowering and antihypertensive medications affect long-term peri-implant health. A retrospective cohort study was performed to evaluate implants placed between 2006 and 2013. Medical and dental encounter notes were used to determine which medications a patient had been prescribed. Peri-implantitis was defined as radiographic evidence of bone loss of osseointegrated implants in conjunction with inflammatory signs, such as bleeding on probing, peri-implant probing depth of 5 or more millimeters, with or without suppuration. A minimum follow-up period of 5 years after placement was necessary to be included in the analysis. Of the 1362 implants placed in 398 patients, 881 implants in 284 unique patients met the inclusion criteria. Descriptive statistics were computed using the SAS system (SAS Institute Version 9.4, 2002-2012, Cary, NC). The predictive variables were prescriptions for cholesterol-lowering and antihypertensive medications. The primary outcome variable was peri-implantitis, with P < .05 used to define statistical significance. Of the implants that met the inclusion criteria, 456 (52%) were placed in patients’ prescribed statins. Risk of developing peri-implantitis was 77% higher in patients’ prescribed statins (OR: 1.772; 95% CL 1.285-2.445) compared to non-users (P = .0005). Peri-implantitis risk was not associated with overall antihypertensive medications or specific classes of antihypertensives, including angiotensin converting enzyme inhibitors, angiotensin II receptor blockers, beta adrenergic blockers, calcium channel blockers, diuretics, or clonidine. Peri-implantitis risk was also not associated with other cholesterol-lowering medications, fibrates, or ezetimibe. The results from this retrospective cohort study reveal an increased risk of peri-implantitis in patients taking statins. This finding is clinically significant because there is substantial overlap between patients in need of dental implants and patients taking statins for cardiovascular protection, as evidenced by the numbers in our study. Further studies are needed to expound this association and establish recommendations for increasing long-term implant success in patients taking statins.

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