Abstract
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.
Highlights
Periodontitis is one of the most common chronic inflammatory diseases among adults worldwide
The rats were divided into four groups (N = 7): ligated rats fed with saline (LS), ligated rats fed with Gelam honey (LH), nonligated rats fed with saline (NLS), and nonligated rats fed with Gelam honey (NLH)
Gelam honey given to the ligated honey (LH) and nonligated honey (NLH) groups was diluted according to the body weight
Summary
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, evoking edema, cell influx, and release of inflammatory mediators which leads to alveolar bone loss [1]. 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].
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
