title: Hypertension may affect tooth-supporting alveolar bone quality: a study in rats.
abstract: 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 assesses 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 analyzed 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 receptor 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). Increased BL and decreased BD were observed around unligated teeth of the untreated and treated SHR groups (P <0.05). In the furcation area of the unligated teeth, the untreated 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 quality of tooth-supporting bone, independently of inflammation. In addition, the administration of lercanidipine for 45 days decreased the expression of bone-resorption markers.
authors.affiliation: Department of Periodontics, Dental Research Division, Guarulhos University, Guarulhos, São Paulo, Brazil. mfbastos@prof.ung.br
authors.forename: Marta Ferreira
authors.initials: MF
authors.lastname: Bastos
authors.forename: Felipe Vilhena
authors.initials: FV
authors.lastname: Brilhante
authors.forename: Tiago Eduardo Dias
authors.initials: TE
authors.lastname: Gonçalves
authors.forename: Amanda Gonçalves
authors.initials: AG
authors.lastname: Pires
authors.forename: Marcelo Henrique
authors.initials: MH
authors.lastname: Napimoga
authors.forename: Marcelo Rocha
authors.initials: MR
authors.lastname: Marques
authors.forename: Poliana Mendes
authors.initials: PM
authors.lastname: Duarte
mesh_terms: D000135:Acid Phosphatase / Q000032:analysis; D016301:Alveolar Bone Loss / Q000473:pathology / Q000503:physiopathology; D000539:Alveolar Process / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology*; D000818:Animals; D000959:Antihypertensive Agents / Q000627:therapeutic use; D015415:Biomarkers / Q000032:analysis; D015519:Bone Density / Q000187:drug effects / Q000502:physiology; D004095:Dihydropyridines / Q000627:therapeutic use; D006973:Hypertension / Q000188:drug therapy / Q000503:physiopathology*; D007150:Immunohistochemistry; D007527:Isoenzymes / Q000032:analysis; D008297:Male; D008963:Molar / Q000473:pathology; D053244:Osteoprotegerin / Q000032:analysis; D053245:RANK Ligand / Q000032:analysis; D051381:Rats; D011918:Rats, Inbred SHR; D017208:Rats, Wistar; D000071681:Tartrate-Resistant Acid Phosphatase; D014092:Tooth Root / Q000473:pathology
chemical_list: D000959:Antihypertensive Agents; D015415:Biomarkers; D004095:Dihydropyridines; D007527:Isoenzymes; D053244:Osteoprotegerin; D053245:RANK Ligand; D000135:Acid Phosphatase; D000071681:Tartrate-Resistant Acid Phosphatase; C060343:lercanidipine