Hypertension favors the inflammatory process in rats with experimentally induced periodontitis.
OBJECTIVE
Cardiovascular diseases are significantly correlated with chronic periodontitis. The aim of this study was to evaluate bone-loss level, neutrophil migration, CXCL2/CINC-2α, CXCL5/LIX, CCL20/MIP-3α and tumor necrosis factor-α (TNF-α) production, inducible nitric oxide synthase (iNOS) expression and C-reactive protein (CRP) release in spontaneously hypertensive rats (SHRs) and normotensive (WTK) rats after experimental induction of periodontal disease.


METHODS
Periodontitis was induced by placement of silk yarn ligatures around the first molar counterparts. The levels of CRP, CCL20/MIP-3α and CXCL5/LIX were evaluated in the peripheral blood, and bone-loss level, neutrophil recruitment, the production of myeloperoxidase, CXCL2, CXCL5, CCL20 and TNF-α, and the expression of iNOS were evaluated in the gingival tissue. Histological sections were taken to evaluate and measure bone resorption and neutrophil recruitment in the furcation region.


RESULTS
Rats with periodontitis had alveolar bone resorption. SHRs with periodontitis showed marked bone loss and increased neutrophil infiltration in comparison with WTK rats. SHRs with periodontitis showed increased levels of TNF-α and CXCL2, and a slight tendency for increased levels of CXCL5, in the gingival tissue but no increase in the level of CCL20. In SHRs, even without periodontitis, the levels of TNF-α, CXCL2, CXCL5 and CCL20 showed a slight tendency to increase. In the WTK rats, TNF-α, CXCL2 and CXCL5 levels were increased with periodontitis, but the level of CCL20 was not. iNOS was expressed in the gingival tissue of WTK rats and SHRs with periodontitis; however, SHRs appeared to express a higher level of iNOS than did WKT rats. The CRP level was elevated in both types of rats with periodontitis; however, the CRP level was higher in SHRs with periodontitis than in WTK rats with periodontitis.


CONCLUSIONS
In SHRs, the hypertensive condition per se seems to favor the inflammatory processes that become potentiated with periodontitis, when compared with WKT rats.
Undergraduate Dentistry Student, School of Dentistry of Araçatuba, Universidade Estadual Paulista, UNESP, Araçatuba, São Paulo, Brazil.
C F
CF
Bonato
C C F
CC
do-Amaral
L
L
Belini
L M P
LM
Salzedas
S H P
SH
Oliveira
D016301:Alveolar Bone Loss / Q000097:blood / Q000503:physiopathology; D000818:Animals; D002097:C-Reactive Protein / Q000032:analysis; D018925:Chemokines / Q000096:biosynthesis / Q000097:blood; D055113:Chronic Periodontitis / Q000097:blood / Q000209:etiology / Q000503:physiopathology*; D005881:Gingiva / Q000378:metabolism; D006973:Hypertension / Q000097:blood / Q000150:complications*; D018836:Inflammation Mediators / Q000378:metabolism*; D020556:Neutrophil Infiltration; D052247:Nitric Oxide Synthase Type II / Q000096:biosynthesis; D009195:Peroxidase / Q000096:biosynthesis; D051381:Rats; D011918:Rats, Inbred SHR; D017208:Rats, Wistar; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
D018925:Chemokines; D018836:Inflammation Mediators; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein; D009195:Peroxidase; D052247:Nitric Oxide Synthase Type II