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Proteinase-activated Receptor-2 (PAR₂) Agonist Causes Periodontitis in Rats

¹ Department of Pharmacology and Therapeutics, Faculty of Medicine, University of Calgary, Calgary, 3330 Hospital Drive, NW, Calgary, T2N 4N1, Alberta, Canada; and
² Department of Oral Pathology, Dental School of Araraquara, State University of São Paulo (UNESP), Araraquara, São Paulo, Brazil;

View larger version (30K): [in a new window]   Figure 1. Effects of topical gingival application of PAR2 agonist peptide (SLIGRL-NH2) control peptide (LRGILS-NH2), or saline, on radiographic alveolar bone loss (mm) (A) and granulocyte infiltration (B), at 3, 7, 15, and 30 days after treatment began. *Significant difference (P < 0.05) compared with saline group at the same time period (ANOVA). N = 8 animals/group/period; data expressed as means ± SEM. Representative digital radiograph of the mandibular area 30 days after daily treatment with control peptide LRGILS-NH2 (C) or PAR2-activating peptide SLIGRL-NH2 (D), showing preservation (C) or resorption (D) of bone crest at the mesial surface of the first molar and in the furcation area. In C and D, the upper lines represent the cemento-enamel junction, and the bottom lines represent the alveolar bone crest. The distance between these two reference points represents the alveolar bone loss at the mesial surface of the first mandibular molar.

View larger version (35K): [in a new window]   Figure 2. Ligature-induced periodontitis, effects of topical gingival application of PAR2 agonist peptide (SLIGRL-NH2), control peptide (LRGILS-NH2), or saline on radiographic alveolar bone loss (mm) (A) and granulocyte infiltration (B), at 3, 7, 15, and 30 days after ligature and the beginning of treatment. *Significant difference (P < 0.05) compared with the Ligature + Saline group at the same time period (ANOVA). N = 8 animals/group/period; data expressed as means ± SEM. Representative digital radiograph of the mandibular area 30 days after ligature placement and the beginning of daily treatment with control peptide LRGILS-NH2 (C) or PAR2-activating peptide SLIGRL-NH2 (D), showing resorption of bone crest at the mesial surface of the first molar and in the furcation area, due to the presence of ligature (C), and exacerbated resorption when ligature was combined with PAR2 agonist peptide treatment (D). In C and D, the upper lines represent the cemento-enamel junction, and the bottom lines represent the alveolar bone crest. The distance between these two reference points represents the alveolar bone loss at the mesial surface of the first mandibular molar.

View larger version (16K): [in a new window]   Figure 3. Effects of MMP inhibitor (MMPi), indomethacin (Indo), or their vehicle (V) treatments on PAR2 agonist peptide (SLIGRL)-induced alveolar bone loss (A) and granulocyte infiltration (B), at 7 days after the beginning of PAR2 agonist treatment. *Significant difference (P < 0.05) compared with the V + SLIGRL group at the same time period (ANOVA). N = 8 animals/group/period; data expressed as means ± SEM.

View larger version (35K): [in a new window]   Figure 4. Expression of MMPs and COX enzymes in gingival tissues of rats 7 days after the beginning of the PAR2 agonist (SLIGRL) or control peptide (LRGILS) daily topical treatment, analyzed by Western blot. Representative Western blots for MMPs and COX enzymes (A), each band corresponding to the tissues from one rat. Mean density of detected bands (B), N = 5 animals/group; data expressed as means ± SEM. *Significant differences (p < 0.05) when compared with the LRGILS group by unpaired t test.