RESUMO
Background: Periodontitis is the bacterial-induced inflammation of tooth-supporting structures. Local antibacterial agents are used as adjunctive therapy in the treatment of periodontitis. This study aimed to compare the effect of subgingivally delivered propolis extract (a resin produced by honey bees) with chlorhexidine (CHX) mouthwash on clinical parameters and salivary levels of matrix metalloproteinase 8 (MMP-8) in periodontitis patients. Methods: Twenty-eight periodontitis patients in stage II or III and grade B, who had deep periodontal pockets (≥4 mm) around at least three non-adjacent teeth, were divided into two groups. In the control group, patients were prescribed 0.2% CHX mouthwash twice a day for two weeks. In the 20% propolis hydroalcoholic group, subgingival irrigation was performed twice a week for two weeks. Clinical parameters were measured at baseline and after two months. Salivary samples were collected from the propolis and control groups at baseline and two months later to assess MMP-8 levels using the enzyme-linked immunosorbent assay. Additionally, salivary samples from 12 periodontally healthy subjects were used to determine the normal levels of MMP-8. The data were analyzed using SPSS. P<0.05 was considered the level of significance. Results: In the healthy group, the mean salivary levels of MMP-8 were significantly lower than that in the control and propolis groups at baseline (P<0.001). The results indicated a significant improvement in clinical parameters (P<0.001) in the propolis group compared to the control group, while MMP-8 levels decreased significantly in both groups (P<0.001). Conclusion: Propolis is recommended as adjunctive therapy for periodontitis patients. Clinical trials registration code: IRCT2016122030475N3.
RESUMO
BACKGROUND: Papillon-Lefèvre syndrome (PLS) is a rare autosomal recessive disorder characterized by hyperkeratosis involving the palms, soles, elbows, and knees followed by periodontitis, destruction of alveolar bone, and loss of primary and permanent teeth. Mutations of the lysosomal protease cathepsin C gene (CTSC) have been shown to be the genetic cause of PLS. This study analyzed CTSC mutations in five Iranian families with PLS and modeled the protein for mutations found in two of them. METHODS: DNA analysis was performed by direct automated sequencing of genomic DNA amplified from exonic regions and associated splice intron site junctions of CTSC. RFLP analyses were performed to investigate the presence of previously unidentified mutation(s) in control groups. Protein homology modeling of the deduced novel mutations (P35 delL and R272P) was performed using the online Swiss-Prot server for automated modeling and analyzed and tested with special bioinformatics tools to better understand the structural effects caused by mutations in cathepsin C protein (CTSC). RESULTS: Six Iranian patients with PLS experienced premature tooth loss and palm plantar hyperkeratosis. Sequence analysis of CTSC revealed a novel mutation (P35delL) in exon 1 of Patient 1, and four previously reported mutations; R210X in Patient 2, R272P in Patient 3, Q312R in two siblings of family 4 (Patients 4 and 5), and CS043636 in Patient 6. RFLP analyses revealed different restriction fragment patterns between 50 healthy controls and patients for the P35delL mutation. Modeling of the mutations found in CTSC, P35delL in Patient 1 and R272P in Patient 3 revealed structural effects, which caused the functional abnormalities of the mutated proteins. CONCLUSIONS: The presence of this mutation in these patients provides evidence for founder CTSC mutations in PLS. This newly identified P35delL mutation leads to the loss of a leucine residue in the protein. The result of this study indicates that the phenotypes observed in these two patients are likely due to CTSC mutations. Also, structural analyses of the altered proteins identified changes in energy and stereochemistry that likely alter protein function.
