Cholesterol, C-Reactive Protein, and Periodontitis: HMG-CoA-Reductase Inhibitors (Statins) as Effect Modifiers

Abstract

Common risk factors of periodontitis and cardiovascular diseases fuel the debate on interrelationships between them. The aim is to prove whether statins may influence periodontal parameters by affecting either of these factors. Out of the 4,290 subjects of SHIP (Study of Health in Pomerania), we included subjects aged >30 years (219 with statins, 2937 without) and excluded edentulous. We determined periodontal measures, cholesterol fractions, and inflammation markers. Statin use and periodontal risk factors were assessed. Gingival plaque and periodontal attachment loss were associated with systemic LDL cholesterol (P < 0.001) and C-reactive protein CRP (P = 0.019) revealing interaction with statin use. When adjusted for age, sex, smoking, diabetes, education, and dental service, statins were identified as effect modifiers abolishing the relationship between attachment loss and LDL and between gingival plaque and LDL (interactions P < 0.001). No statin-related interaction was detected with increase in CRP. The interaction supports the view of inter-relationships between periodontal and systemic inflammatory mediators.

Figure 1

(a) Mean LDL-c concentration related to increasing extent of gingival plaque (in tertils) without and with statin use. ANOVA: statins P < 0.001, plaque tertils P = 0.475, interaction P < 0.001. (b) Mean LDL-c dependent on severity of attachment loss (mean CAL tertils) without and with statin use. ANOVA: statins P = 0.003, CAL tertils P = 0.366, interaction statins ∗CAL P = 0.002. Lowest periodontal tertil—white columns, 2nd tertil—dark columns, 3rd tertil—hatched columns.

Figure 2

Severe periodontitis (mean CAL > 4 mm, dark columns; white columns CAL ≤ 4 mm) is associated with an increase in CRP, which is attenuated by statins. ANOVA: statins P = 0.992, CAL P = 0.019, interaction P = 0.024.