MATERIALS AND METHODS: This was a randomised control clinical trial at the Faculty of Dentistry, University of Malaya. A total of 66 obese patients with chronic periodontitis were randomly allocated into the treatment group (n=33) who received NSPT, while the control group (n=33) received no treatment. Four participants (2 from each group) were non-contactable 12 weeks post intervention. Therefore, their data were removed from the final analysis. The protocol involved questionnaires (characteristics and OHRQoL (Oral Health Impact Profile-14; OHIP-14)) and a clinical examination.

RESULTS: The OHIP prevalence of impact (PI), overall mean OHIP severity score (SS) and mean OHIP Extent of Impact (EI) at baseline and at the 12-week follow up were almost similar between the two groups and statistically not significant at (p=0.618), (p=0.573), and (p=0.915), respectively. However, in a within-group comparison, OHIP PI, OHIP SS, and OHIP EI showed a significant improvement for both treatment and control groups and the p values were ((0.002), (0.008) for PI), ((0.006) and (0.004) for SS) and ((0.006) and (0.002) for EI) in-treatment and control groups, respectively.

CONCLUSION: NSPT did not significantly affect the OHRQoL among those obese with CP. Regardless, NSPT, functional limitation and psychological discomfort domains had significantly improved.

METHODOLOGY/PRINCIPAL FINDINGS: Sprague Dawley rats were separated into 7 groups. Groups 1-2 were orally challenged with carboxymethylcellulose (CMC); group 3 received 20 mg/kg omeprazole and groups 4-7 received 50, 100, 200 and 400 mg/kg of ethanolic leaf extract, respectively. After 1 h, CMC or absolute ethanol was given orally to groups 2-7. The rats were sacrificed after 1 h. Then, the injuries to the gastric mucosa were estimated through assessment of the gastric wall mucus, the gross appearance of ulcer areas, histology, immunohistochemistry and enzymatic assays. Group 2 exhibited significant mucosal injuries, with reduced gastric wall mucus and severe damage to the gastric mucosa, whereas reductions in mucosal injury were observed for groups 4-7. Groups 3-7 demonstrated a reversal in the decrease in Periodic acid-Schiff (PAS) staining induced by ethanol. No symptoms of toxicity or death were observed during the acute toxicity tests.

METHODS: The rats were divided into seven groups according to their pretreatment: an untreated control group, an ulcer control group, a reference control group (20 mg/kg omeprazole), and four experimental groups (50, 100, 200, or 400 mg/kg of extract). Carboxymethyl cellulose was the vehicle for the agents. Prior to the induction of gastric ulcers with absolute ethanol, the rats in each group were pretreated orally. An hour later, the rats were sacrificed, and gastric tissues were collected to evaluate the ulcers and to measure enzymatic activity. The tissues were subjected to histological and immunohistochemical evaluations.

RESULTS: Compared with the extensive mucosal damage in the ulcer control group, gross evaluation revealed a marked protection of the gastric mucosa in the experimental groups, with significantly preserved gastric wall mucus. In these groups, superoxide dismutase and malondialdehyde levels were significantly increased (P < 0.05) and reduced (P < 0.05), respectively. In addition to the histologic analyses (HE and periodic acid-Schiff staining), immunohistochemistry confirmed the protection through the upregulation of Hsp70 and the downregulation of Bax proteins. The gastroprotection of the experimental groups was comparable to that of the reference control medicine omeprazole.