%0 Journal Article
%T Effects of Gelam Honey (Melaleuca cajuputi) on Alveolar Bone Loss in Experimental Periodontitis
%A N. Hamzah
%A S. A. Aziz
%A A. R. Fauzi
%A Y. A. Mohd Yusof
%A M. Razali
%A N. Ibrahim
%A B. Baharin
%J Journal of Dental Surgery
%D 2014
%R 10.1155/2014/907970
%X Gelam honey has been shown to exhibit antioxidant and anti-inflammatory activities in animal model. The aim of this study was to determine the effects of Gelam honey (Melaleuca cajuputi) on alveolar bone level in experimental periodontitis. Thirty male Sprague-Dawley rats were used in this study and randomly divided into four groups: ligated saline (LS), ligated honey (LH), nonligated saline (NLS), and nonligated honey (NLH). Fifteen days after supplementation with Gelam honey (3£¿g/kg), the rats were sacrificed and alveolar bone level was determined by radiography and histomorphometry. The number of osteoclasts was also calculated for all groups. Both radiographic and histomorphometric analyses showed that alveolar bone resorption was severely induced around the ligated molar in the LS and LH groups. There was no significant difference in alveolar bone level between the LS and LH groups. However, there was a nonsignificant reduction of osteoclast number by 15.2% in LH group compared to LS group. In the NLH group, there was less alveolar bone resorption and the number of osteoclasts was reduced by 13.2% compared to NLS group. In conclusion, systemically supplemented Gelam honey was shown to have the potential of reducing osteoclast activity in the experimental periodontitis rats, even though the effect on alveolar bone level was not well demonstrated and it warrants further research. 1. Introduction Periodontitis is one of the most common chronic inflammatory diseases among adults worldwide. It is characterized by gingival inflammation, periodontal pocket formation, and bacterial plaque formation which lead to alveolar bone destruction and tooth loss. The pathogenesis of periodontitis involves the presence of plaque that may initiate local inflammatory reaction in a predisposed host, thus evoking edema, cell influx, and release of inflammatory mediators which ultimately leads to alveolar bone loss [1]. Among the inflammatory mediators, PGE2, Il-1, and TNF-¦Á seem to be the important mediators as causative agents of tissue destruction [2]. In periodontal disease, the response of bone to local factors, produced by the inflammatory process, changes the bone remodeling balance, with a net effect of alveolar bone resorption and loss of attachment [3]. Alveolar bone resorption can be measured using various methods, that is, radiograph [4], two-dimensional/three-dimensional imaging [5, 6], morphometric method [6], histomorphometric method, [7] and immunocytochemistry [8]. Radiographically, alveolar bone loss can be determined by the radiograph density changes
%U http://www.hindawi.com/journals/jds/2014/907970/