Can chlorhexidine mouthwash twice daily ameliorate cyclosporine-induced gingival overgrowth?

BACKGROUND/PURPOSE: Gingival overgrowth can be induced in patients treated with cyclosporine-A (CsA), an immunosuppressant often used following organ transplantation. A pre-existing rat model designed to mimic CsA-induced gingival overgrowth in humans was used to test the effectiveness of frequent application of a chlorhexidine antiplaque solution in reducing the overgrowth. METHODS: Four groups of rats were fed CsA. One group received chlorhexidine mouthwash twice a day, the second group received chlorhexidine mouthwash once a day, the third group received chlorhexidine mouthwash every other day, and the fourth group did not receive chlorhexidine mouthwash all. A fifth negative control group received only mineral oil. Overgrowth was determined by measuring the changes in the gingival probing depth and the keratinized gingival width on molars. A gingival histological examination was performed. RESULTS: Rats treated with mouthwash twice daily exhibited decreased probing depths and gingival widths without statistical significance. Histological examination revealed that CsA treatment caused gingival enlargement, whereas chlorhexidine treatment twice a day diminished the enlargement. CONCLUSION: These findings suggest that chlorhexidine mouthwash used twice daily may reduce the severity of CsA-induced gingival overgrowth. Further research is warranted to determine the optimal dose and treatment regimen.

Cyanidin-3-O-glucoside downregulates ligation-activated endoplasmic reticulum stress and alleviates induced periodontal destruction in rats.

OBJECTIVE: Cyanidin-3-O-glucoside (C3G), a dietary anthocyanin, possesses various biological properties, including alleviating endoplasmic reticulum (ER) stress. This study examined the effect of C3G on periodontitis via ER stress in rats. DESIGN: Periodontitis was induced by placing silk sutures around maxillary second molars. C3G (0, 3, or 9 mg/kg) was fed on the day before ligation (10 rats/group). Further, 10 non-ligation control rats received deionized water. On day 8, gingivae were obtained to determine CCAAT/enhancer-binding protein homologous protein (CHOP), c-Jun N-terminal kinase (JNK), phospho-JNK (p-JNK), and nuclear factor-κB (NF-κB) by immunoblotting. Periodontal destruction was evaluated using micro-computed tomography (µCT) and histology. RESULTS: Gingival expression of CHOP, p-JNK/JNK, and NF-κB significantly increased in ligation rats (0 mg/kg C3G) than that in controls. However, protein expression in ligation groups presented a negative association with C3G concentration. By µCT, the distance of cemento-enamel junction to bone significantly increased in ligation groups; however, distances showed a negative association with C3G concentration. In the region of interest, bone volume and trabecular thickness and number significantly decreased in ligation groups but they were positively associated with C3G concentration. In terms of trabecular separation, opposite results were found. Histologically, infiltrated connective tissue (ICT) and periodontal destructions increased in ligation groups; however, they were negatively associated with C3G concentration. Moreover, ICT area is positively correlated with µCT- and histologically measured destructions and protein expression of CHOP, p-JNK/JNK, or NF-κB. CONCLUSION: C3G promotes favorable modulation of ER stress and alleviates destruction of periodontitis, which may imply a new strategy.

Gelatinases and extracellular matrix metalloproteinase inducer are associated with cyclosporin-A-induced attenuation of periodontal degradation in rats.

BACKGROUND: The present study aims to examine the inhibitory effect of cyclosporin-A (CsA) on periodontal breakdown and to further explore the correlations of CsA-induced attenuation of periodontal bone loss with the expressions of gelatinases (i.e., matrix metalloproteinase [MMP]-2 and MMP-9) and extracellular matrix metalloproteinase inducer (EMMPRIN). METHODS: Forty Sprague-Dawley rats were randomly divided into four groups: 1) control; 2) CsA; 3) ligature (Lig); and 4) ligature plus CsA (Lig + CsA). The CsA group received 10 mg ⋅ Kg(-1) ⋅ d(-1) CsA for 8 days. The Lig group received silk ligature on selected molars. The Lig + CsA group received silk ligature and CsA treatment. The inhibitory effects of CsA on the ligature-induced periodontal breakdown was examined with microcomputed tomography (micro-CT) and histometric analyses to analyze the amount of attachment loss, crestal bone loss, connective tissue attachment, and the surface area with inflammatory cell infiltration. The effects of CsA on ligature-induced expressions of gelatinases and EMMPRIN in gingival tissues were examined with Western blotting and zymography, respectively. RESULTS: By micro-CT and histology, the Lig + CsA group had significantly more periodontal breakdown than the control and CsA groups but less periodontal breakdown than the Lig group. Consistent results were found for the expressions of gelatinases and EMMPRIN among the groups demonstrating that the Lig + CsA group had significantly less gingival protein expression of gelatinases and EMMPRIN than the Lig group. CONCLUSIONS: CsA inhibited the expressions of gelatinase MMPs and EMMPRIN and partially prevented the periodontal breakdown in ligature-induced experimental periodontitis. The CsA-induced attenuation of periodontal bone loss was strongly correlated positively with the expressions of MMP-2, MMP-9, and EMMPRIN in gingiva.

Configuration and corticalization of the mandibular bifid canal in a Taiwanese adult population: a computed tomography study.

PURPOSE: The configuration and degree of corticalization of bifid mandibular canals were examined using medical computed tomography (CT) images from 170 hemimandibles obtained from 308 Taiwanese adults. MATERIALS AND METHODS: The configurations of the bifid canals were assessed according to their anatomical position in relation to the ramus, molars, premolars, and mental foramen; their course (anterior/posterior or superior/inferior); the presence or absence of confluence with the main mandibular canal; and the presence or absence of penetration through the mandible to form an accessory foramen. The percentage of the canal length that was corticalized was measured. Two different classifications of bifid canals were also briefly summarized and compared. RESULTS: When bifid canals are present (41.2% of patients; 27.6% of hemimandibles), the bifid canals were primarily located in the ramus and retromolar regions (67.7%) running anteriorly (95.9%) and superiorly (95.9%) without confluence with the main mandibular canal (91.1%). Up to 16.5% of bifid canals form accessory foramina on the cortical surface of the mandible. Approximately 78% of the bifid canals have varied degrees of corticalization around the bifid canals. CONCLUSION: The configuration and course of 170 mandibular bifid canals were evaluated with CT images. The bifid canals were primarily located in the ramus and retromolar regions; however, 32.4% of the bifid canals were located in potential positions for dental implant placement. Most of the bifid canals ran anteriorly superior to the main mandibular canal, did not rejoin with the main mandibular canal, and diminished within the mandibular body. Approximately half of the bifid canals (45%) were completely corticated.