Stemodia maritima L. Extract Decreases Inflammation, Oxidative Stress, and Alveolar Bone Loss in an Experimental Periodontitis Rat Model.

Periodontitis is very prevalent worldwide and is one of the major causes of tooth loss in adults. About 80% of the worldwide population use medicinal plants for their health care. Stemodia maritima L. (S. maritima) antioxidant and antimicrobial effects in vitro as well as anti-inflammatory properties. Herein, the potential therapeutic effect of S. maritima was assessed in rats subjected to experimental periodontitis (EP). EP was induced in female Wistar rats by nylon thread ligature around 2nd upper left molars for 11 days. Animals received (per os) S. maritima (0.2; 1 or 5 mg/kg) or vehicle (saline + DMSO) 1 h before ligature and then once daily for 11 days. The naive group had no manipulation. After this time-point, the animals were terminally anesthetized, and the maxillae were removed for morphometric and histological analyzes (HE). Gingival tissues were dissected to cytokine levels detection (TNF-α, IL1-ß, CINC-1, and IL-10), enzymes superoxide dismutase (SOD), and catalase (CAT) analysis, as well as gene expression (TNF-α, IL-1ß, RANK, and iNOS) by qRT-PCR. Systemic parameters (weight variation, plasma levels of hepatic enzymes aspartate aminotransferase (AST) and alanine aminotransferase (ALT), creatinine, total alkaline phosphatase (TALP), and bone alkaline phosphatase (BALP) were performed. Histological analysis of the stomach, liver, kidney, and heart was also performed. S. maritima (5 mg/kg) decreased alveolar bone loss, TNF-α and CINC-1 gingival levels, oxidative stress, and transcription of TNF-α, IL1-ß, RANK, and iNOS genes. It elevated both BALP activity and IL-10 gingival levels. The animals showed no any signs of toxicity. In conclusion, S. maritima reduced pro-inflammatory cytokine production, oxidative stress, and alveolar bone loss in a pre-clinical trial of periodontitis. S. maritima is a potential tool for controlling the development of periodontitis.

Correction: Topical HPMC/S-Nitrosoglutathione Solution Decreases Inflammation and Bone Resorption in Experimental Periodontal Disease in Rats.

[This corrects the article DOI: 10.1371/journal.pone.0153716.].

Topical HPMC/S-Nitrosoglutathione Solution Decreases Inflammation and Bone Resorption in Experimental Periodontal Disease in Rats.

S-nitrosoglutathione (GSNO) is a nitric oxide (NO) donor, which exerts antioxidant, anti-inflammatory, and microbicidal actions. Intragingival application of GSNO was already shown to decrease alveolar bone loss, inflammation and oxidative stress in an experimental periodontal disease (EPD) model. In the present study, we evaluated the potential therapeutic effect of topical applications of hydroxypropylmethylcellulose (HPMC)/GSNO solutions on EPD in Wistar rats. EPD was induced by placing a sterilized nylon (3.0) thread ligature around the cervix of the second left upper molar of the animals, which received topical applications of a HPMC solutions containing GSNO 2 or 10 mM or vehicle (HPMC solution), 1 h prior to the placement of the ligature and then twice daily until sacrifice on day 11. Treatment with HPMC/GSNO 10 mM solution significantly reduced alveolar bone loss, oxidative stress and TNF-α e IL-1ß levels in the surrounding gingival tissue, and led to a decreased transcription of RANK and TNF-α genes and elevated bone alkaline phosphatase, compared to the HPMC group. In conclusion, topical application of HPMC/GSNO solution is a potential treatment to reduce inflammation and bone loss in periodontal disease.

Effect of alendronate on bone-specific alkaline phosphatase on periodontal bone loss in rats.

OBJECTIVE: The study aims to evaluate the effect of alendronate (ALD) on bone-specific alkaline phosphatase (BALP) serum levels on periodontal bone loss in Wistar rats. DESIGN: Periodontitis was induced by ligature around the upper second molar in 36 male Wistar rats (± 200 g). Groups of six animals received 0.9% saline (SAL) or ALD (0.01; 0.05; 0.25 mgkg(-1), s.c.), over 11 days; then they were sacrificed and their maxillae were removed to be defleshed and stained for macroscopic or histopathological analysis. Blood samples were collected for BALP, transaminases and total alkaline phosphatase (TALP) serum dosage, and haematologic study. Rats were weighed daily. RESULTS: Periodontitis induction caused reduction of BALP, intense alveolar bone loss (ABL), cementum and periodontal ligament destructions and intense leucocyte infiltration seen microscopically. Systemically, periodontitis induced leucocytosis, weight loss and TALP reduction. ALD (0.25 mgkg(-1)) prevented BALP reduction (19.17 ± 1.36 Ul(-1)) when compared to SAL (13.6 ± 1.5), as well as prevented ABL, by 57.2%, when compared to SAL (4.80+0.18 mm(2)), which was corroborated by histological findings (ALD 0.25 mgkg(-1)=1.5 (1-2) and SAL=3 (2-3)) (p<0.05). ALD did not alter transaminases but reduced TALP levels (p<0.05). ALD 0.25 mgkg(-1) reduced 6th-h neutrophilia (2.50 ± 0.22cell × 10(3)mm(-3)) and 7th- (12.29 ± 0.66) and 11th-day lymphomonocytosis (15.74 ± 0.52) when compared to SAL (5.20 ± 0.28; 18.24 ± 1.05; and 23.21 ± 1.48, respectively). ALD did not alter the weight loss. CONCLUSION: ALD prevented BALP reduction and ABL and reduced inflammatory infiltrate, without causing systemic alterations.