IADR Abstract Archives
Angiotensin-II AT1 Receptor Modulates Bone Markers Metabolism in Periodontal Disease
Objectives: Evaluate the effect of AT1 receptor blockade on the progression of experimentally-induced periodontal disease (PD) in rats.
Methods: After anesthesia, silk suture thread (4.0) was placed around the lower right first molar for 1, 3, 7 or 14 consecutive days. Gene expression for RAS-regulating genes and bone markers metabolism in the gingival tissue was evaluated. For bone loss analysis, mandibles were stained with 1% methylene blue, photographed and the area of bone loss around the lower first molar was evaluated through ImageJ software (version 1.48, USA). In addition to treatment with water and Losartan (AT1 receptor antagonist; 50mg/kg/day) on the same day of PD induction, groups of animals were previously treated with the same drug and at the same dosage for 30 days. Therefore, the present study comprised 4 groups with 5 rats per group: G1 - control without PD; G2 - animals with PD and treated with water; G3 – Losartan-treated animals (treatment started at the same day of PD induction) and G4 - animals previously treated with Losartan for 30 days followed by induction of PD and continuity of treatment.
Results: Water-treated animals (G2) had greater bone loss after 14 days of PD compared with control group (G1) and with Losartan-treated rats (G3 and G4). Moreover, PD promoted ACE, AT1a and AT1b receptors increased expression, but Losartan treatment did not modulate this response. On the other hand, PD alone did not influence the expression of ECA-2 and MAS receptor; however Losartan treatment promoted an increase in the expressions of these two genes, which may explain the blockade of bone loss observed in the animals treated with Losartan, since ECA-2 enzyme is capable of cleaving Angiotensin (Ang)-II into Ang 1-7, which in turn promotes anti-inflammatory actions when bound to MAS receptor. The results of bone formation/absorption markers also help to explain the blockade of bone loss in Losartan-treated rats, as it was possible to observe that treatment promoted increased expression of OPG, ALP, PHEX and RUNX2. RANK and RANKL levels increased with PD and were not modulated with Losartan.
Conclusions: Losartan attenuates bone loss possibly through modulation of gene expression of RAS components and bone markers metabolism in experimentally-induced periodontal disease in rats.
Methods: After anesthesia, silk suture thread (4.0) was placed around the lower right first molar for 1, 3, 7 or 14 consecutive days. Gene expression for RAS-regulating genes and bone markers metabolism in the gingival tissue was evaluated. For bone loss analysis, mandibles were stained with 1% methylene blue, photographed and the area of bone loss around the lower first molar was evaluated through ImageJ software (version 1.48, USA). In addition to treatment with water and Losartan (AT1 receptor antagonist; 50mg/kg/day) on the same day of PD induction, groups of animals were previously treated with the same drug and at the same dosage for 30 days. Therefore, the present study comprised 4 groups with 5 rats per group: G1 - control without PD; G2 - animals with PD and treated with water; G3 – Losartan-treated animals (treatment started at the same day of PD induction) and G4 - animals previously treated with Losartan for 30 days followed by induction of PD and continuity of treatment.
Results: Water-treated animals (G2) had greater bone loss after 14 days of PD compared with control group (G1) and with Losartan-treated rats (G3 and G4). Moreover, PD promoted ACE, AT1a and AT1b receptors increased expression, but Losartan treatment did not modulate this response. On the other hand, PD alone did not influence the expression of ECA-2 and MAS receptor; however Losartan treatment promoted an increase in the expressions of these two genes, which may explain the blockade of bone loss observed in the animals treated with Losartan, since ECA-2 enzyme is capable of cleaving Angiotensin (Ang)-II into Ang 1-7, which in turn promotes anti-inflammatory actions when bound to MAS receptor. The results of bone formation/absorption markers also help to explain the blockade of bone loss in Losartan-treated rats, as it was possible to observe that treatment promoted increased expression of OPG, ALP, PHEX and RUNX2. RANK and RANKL levels increased with PD and were not modulated with Losartan.
Conclusions: Losartan attenuates bone loss possibly through modulation of gene expression of RAS components and bone markers metabolism in experimentally-induced periodontal disease in rats.