Hypertension May Affect Tooth-Supporting Alveolar Bone Quality: A Study in Rats Marta Ferreira Bastos,* Felipe Vilhena Brilhante,* Tiago Eduardo Dias Gonc xalves,* Amanda Gonc xalves Pires,* Marcelo Henrique Napimoga † Marcelo Rocha Marques, ‡ and Poliana Mendes Duarte* Background: This study evaluates the ligature-induced bone loss (BL) and quality of tooth-supporting alveolar bone in spontaneously hypertensive rats (SHRs) by histometric, histochemical, and immunohistochemical analyses and as- sesses the effects of lercanidipine on these parameters. Methods: Wistar rats and SHRs were assigned to one of the following groups: normotensive rats (n = 15), untreated SHRs (n = 15), and treated SHRs (n = 15). The latter group was treated daily with lercanidipine for 45 days. Two weeks after the beginning of drug administration, the first right mandibular molar received a cotton ligature, whereas the contralateral tooth was left unligated. The following parameters were ana- lyzed in the furcation area of decalcified histologic sections: BL, bone density (BD), number of positive cells for tartrate- resistant acid phosphatase (TRAP+), and expression of recep- tor activator of nuclear factor-kappa B ligand (RANKL) and osteoprotegerin (OPG). Results: In ligated teeth, no significant differences among groups were found regarding BL, TRAP+ cells, and the ratio of RANKL/OPG+ cells (P >0.05), although the expression of RANKL was decreased in the treated SHR group (P <0.05). In- creased BL and decreased BD were observed around unli- gated teeth of the untreated and treated SHR groups (P <0.05). In the furcation area of the unligated teeth, the un- treated SHR group presented a higher number of TRAP+ cells and higher ratio of RANKL/OPG+ cells compared to the other groups. Conclusions: SHRs present harmful alterations in the qual- ity of tooth-supporting bone, independently of inflammation. In addition, the administration of lercanidipine for 45 days decreased the expression of bone-resorption markers. J Peri- odontol 2010;81:1075-1083. KEY WORDS Alveolar bone loss; hypertension; RANK ligand; rats; tartrate-resistant acid phosphatase. H uman essential hypertension is a highly prevalent chronic vas- cular disorder that has a multi- factorial etiology and complications such as cardiovascular and kidney diseases, which are major public-health prob- lems. 1 Various experimental and clinical studies showed that hypertension pres- ents prejudicial effects on bone density (BD) and quality. 2-7 The physiologic, cellular, and molecular mechanisms by which essential hypertension may affect bone tissues have not been fully eluci- dated. It was suggested that a hyperten- sive status causes increased mobilization of calcium from bone, increased excre- tion of calcium from kidneys, secondary activation of the parathyroid hormone, and alterations in the activity and differ- entiation of bone cell mediated by angio- tensin (Ang) II. 8-11 The relationship between hyperten- sion and periodontal tissues/periodonti- tis was previously evaluated in earlier studies. 12-17 With the emergence of periodontal medicine, most studies 18-22 focused on periodontal infection as a source of pathogenic species and inflammatory mediators that can create a systemic inflammatory burden and increase the risk for hypertension and the development of other cardiovascular disorders. However, some studies 12,13,16,23 focused on the impact of the hypertensive status on periodontal tissues, and even * Department of Periodontics, Dental Research Division, Guarulhos University, Guarulhos, Sa ˜o Paulo, Brazil. † Laboratory of Molecular Biology, University of Uberaba, Uberaba, MG, Brazil. ‡ Department of Morphology, Division of Histology, School of Dentistry at Piracicaba, University of Campinas, Piracicaba, Sa ˜o Paulo, Brazil. doi: 10.1902/jop.2010.090705 J Periodontol • July 2010 1075