Characterization of the soft-tissue wall lining residual periodontal pockets and implications in periodontal wound healing

AIM: To characterize the soft-tissue wall of remaining periodontal pockets for wound healing-related parameters versus healthy gingival crevices in the same individuals. MATERIALS AND METHODS: Gingival tissues collected from the diseased interface of pockets (GT biopsies) and from healthy gingival crevices (G biopsies) were subjected to RT(2)-profiler PCR Array for wound healing-related markers and network analysis of differentially expressed genes. Lymphangiogenesis-related gene expression was determined by qRT-PCR. The migration potential of mesenchymal stem cells isolated from GT biopsies (GT-MSCs) and G biopsies (G-MSCs) was evaluated by the scratch- and the transwell migration assays. The total collagen protein content was determined in GT-MSCs and G-MSCs homogenates. RESULTS: Gene-ontology analysis on significantly upregulated genes expressed in GT biopsies revealed enrichment of several genes involved in processes related to matrix remodeling, collagen deposition, and integrin signaling. No significantly expressed genes were seen in G biopsies. Regarding lymphangiogenesis-related genes, GT biopsies demonstrated greater expression for PROX1 than G biopsies (p = 0.05). Lower migration potential (p < 0.001), yet greater production of collagen protein (p = 0.05), was found for GT-MSCs over G-MSCs. CONCLUSION: Differential expression patterns of various molecular pathways in biopsies and cell cultures of diseased versus healthy gingival tissues indicate a potential of the former for tissue remodeling and repair. CLINICAL RELEVANCE: In the course of periodontitis, granulation tissue is formed within a periodontal defect in an attempt to reconstruct the site. Following treatment procedures periodontal granulation tissue remains inflamed but appears to retain healing potential. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s00784-023-05122-y.