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Wiley InterScience | |||||||||||
  Journal of Periodontal ResearchVolume 45 Issue 1, Pages 136 - 142 Published Online: 23 Sep 2009 © 2010 John Wiley & Sons A/S
Abstract | References | Full Text: HTML, PDF (Size: 698K) | Related Articles | Citation Tracking  Expression of receptor activator of nuclear factor κB ligand in ligature-induced periodontitis in osteoporotic and non-osteoporotic rats Copyright © 2010 John Wiley & Sons A/S KEYWORDS receptor activator of nuclear factor κB ligand • periodontitis • osteoporosis • immunohistochemistry ABSTRACTAllam E, Draz A, Hassan A, Neamat A, Galal M, Windsor LJ. Expression of receptor activator of nuclear factor κB ligand in ligature-induced periodontitis in osteoporotic and non-osteoporotic rats. J Periodont Res 2009; doi: 10.1111/j.1600-0765.2009.01210.x. © 2009 The Authors. Journal compilation © 2009 Blackwell Munksgaard Background and Objective: This study investigated the expression of a key mediator that regulates differentiation of osteoclasts, receptor activator of nuclear factor κB ligand (RANKL), in rats with or without osteoporosis and periodontitis, to provide a better understanding of the association between these two diseases. Material and Methods: Forty adult Albino rats were divided into four groups: (1) control group; (2) experimentally induced periodontitis group; (3) experimentally induced osteoporosis group; and (4) experimentally induced osteoporosis and periodontitis group. At the end of the experimental period, blood samples were obtained and animals were sacrificed. Serum alkaline phosphatase (ALP) activity levels were measured. Histological evaluation and immunohistochemical detection of RANKL in the periodontal ligament and bone tissues were performed. Results: There were significantly higher ALP levels in all of the experimental groups than in the control group. The pathology observed in the histological sections from group 4 was more severe than in either group 2 or group 3. The percentage of RANKL-immunoreactive cells in both the periodontal ligament and bone tissues in group 4 (16.8 ± 5.1 and 11.2 ± 5.2%, respectively) was significantly higher (p < 0.001) than in the other groups. In the periodontal ligament, the percentage of RANKL-immunoreactive cells in group 2 (10.1 ± 1.9%) was significantly higher (p < 0.001) than in group 3 (5.3 ± 2.7%) and the control group (4.12 ± 1.5%). Conclusion: The increased bone loss observed in group 4 compared with either group 2 or group 3 supports the existence of an additive pathological effect of the two disease conditions. This is consistent with the increased RANKL expression observed in group 4. Accepted for publication January 19, 2009 | 
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