Gingipains impair attachment of epithelial cell to dental titanium abutment surfaces

Eick, Sigrun; Gadzo, Naida; Tacchi, Manuel; Sculean, Anton; Potempa, Jan; Stavropoulos, Andreas

doi:10.1002/jbm.b.34345

Cited by 5 publications

(6 citation statements)

References 37 publications

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“…But also a cleavage of host cell receptors on membranes and of cell adhesion molecules enabling the contact between the cells can be suggested. E.g., P. gingivalis proteases affect cell adhesion capability of fibronectin and tenascin C to fibroblasts [25] and they are able to degrade adhesion molecules essential for epithelial integrity [26].…”

Section: Discussionmentioning

confidence: 99%

In-vitro antibiofilm activity of chlorhexidine digluconate on polylactide-based and collagen-based membranes

et al. 2019

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BackgroundIn Guided Tissue Regeneration (GTR), barrier membranes are used to allow selective cell populations to multiply and to promote periodontal regeneration. A frequent complication is membrane exposure to the oral cavity followed by bacterial colonization. The purpose of this in-vitro-study was to elucidate, if rinsing with a chlorhexidine digluconate solution (CHX) prevents bacterial adhesion, and whether it interferes with attachment of periodontal ligament (PDL) fibroblasts and epithelial cells to membrane surfaces.MethodsFirstly, two bioresorbable membranes (polylactide-based and collagen-based) were dipped into 0.06% CHX and 0.12% CHX, before biofilms (2-species representing periodontal health, 6-species representing a periodontitis) were formed for 2 h and 8 h. Subsequently, colony forming units (cfu) were counted. Secondly, the membranes were treated with CHX and inoculated in bacteria suspension two-time per day for 3 d before cfu were determined. In additional series, the influence of CHX and bacterial lysates on attachment of epithelial cells and PDL fibroblasts was determined. Parameter-free tests were applied for statistical analysis.ResultsCfu in “healthy” biofilms did not differ between the two membranes, more cfu were counted in “periodontitis” biofilm on collagen than on polylactide membranes. One-time dipping of membranes into CHX solutions did not markedly influence the cfu counts of both biofilms on polylactide membrane; those on collagen-based membrane were significantly reduced with being 0.12% CHX more active than 0.06% CHX. More-fold CHX dipping of membranes reduced concentration-dependent the cfu counts of both biofilms on both membranes. In general, the number of attached gingival epithelial cells and PDL fibroblasts was higher on collagen than on polylactide membrane. Lysates of the periodontopathogenic bacteria inhibited attachment of PDL fibroblasts to membranes. CHX decreased in a concentration-dependend manner the number of attached gingival epithelial cells and PDL fibroblasts.ConclusionsThe present in-vitro results appear to indicate that membranes in GTR should only be used when bacteria being associated with periodontal disease have been eliminated. An exposure of the membrane should be avoided. Rinsing with CHX may prevent or at least retard bacterial colonization on membrane exposed to the oral activity. However, a certain negative effect on wound healing cannot be excluded.

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Section: Discussionmentioning

confidence: 99%

In-vitro antibiofilm activity of chlorhexidine digluconate on polylactide-based and collagen-based membranes

et al. 2019

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“…This subject is also relevant regarding dental implants. As was shown for titanium-zirconium alloys, gingipain-mediated E-Cad degradation prevents GK adhesion to the implants, which hinders proper material incorporation into the dental alveolus [275].…”

Section: Porphyromonas Gingivalis-derived Proteases: a "Heavy Load" For The Periodontiummentioning

confidence: 92%

From the Matrix to the Nucleus and Back: Mechanobiology in the Light of Health, Pathologies, and Regeneration of Oral Periodontal Tissues

et al. 2021

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Among oral tissues, the periodontium is permanently subjected to mechanical forces resulting from chewing, mastication, or orthodontic appliances. Molecularly, these movements induce a series of subsequent signaling processes, which are embedded in the biological concept of cellular mechanotransduction (MT). Cell and tissue structures, ranging from the extracellular matrix (ECM) to the plasma membrane, the cytosol and the nucleus, are involved in MT. Dysregulation of the diverse, fine-tuned interaction of molecular players responsible for transmitting biophysical environmental information into the cell’s inner milieu can lead to and promote serious diseases, such as periodontitis or oral squamous cell carcinoma (OSCC). Therefore, periodontal integrity and regeneration is highly dependent on the proper integration and regulation of mechanobiological signals in the context of cell behavior. Recent experimental findings have increased the understanding of classical cellular mechanosensing mechanisms by both integrating exogenic factors such as bacterial gingipain proteases and newly discovered cell-inherent functions of mechanoresponsive co-transcriptional regulators such as the Yes-associated protein 1 (YAP1) or the nuclear cytoskeleton. Regarding periodontal MT research, this review offers insights into the current trends and open aspects. Concerning oral regenerative medicine or weakening of periodontal tissue diseases, perspectives on future applications of mechanobiological principles are discussed.

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“…Generally, gingipains support hemagglutination, modulate inflammatory cytokine activities, and can degrade host antibodies, features also relevant to periodontitis promotion. Since gingipains interfere with the natural barrier function of oral epithelia and induce matrix remodeling, they affect MT-related tissue homeostasis (Eick et al 2019; Fig. 3A).…”

Section: Gingipains and Ecm Homeostasis In The Periodontiummentioning

confidence: 99%

“…Synergistically with lipopolysaccharides, this enables further invasion of microbial pathogens, sustains inflammation through upregulation of reactive oxygen species and proinflammatory cytokines such as TNF-α (tumor necrosis factor α), and finally promotes the destruction of the periodontium (Abe-Yutori et al 2017). In the context of dental implants, gingipains can inhibit GKs' adhesion to titanium-zirconium alloys via E-cad degradation, which could prevent incorporation of the material into the periodontium (Eick et al 2019).…”

Section: Gingipains and Ecm Homeostasis In The Periodontiummentioning

confidence: 99%

Role of Mechanotransduction in Periodontal Homeostasis and Disease

et al. 2021

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Novel findings broaden the concept of mechanotransduction (MT) in biophysically stimulated tissues such as the periodontium by considering nuclear MT, convergence of intracellular MT pathways, and mechanoresponsive cotranscription factors such as Yes-associated protein 1 (YAP1). Regarding periodontal disease, recent studies have elucidated the role of bacterial gingipain proteases in disturbing the barrier function of cadherins, thereby promoting periodontal inflammation. This leads to dysregulation of extracellular matrix homeostasis via proteases and changes the cell’s biophysical environment, which leads to alterations in MT-induced cell behavior and loss of periodontal integrity. Newest experimental evidence from periodontal ligament cells suggests that the Hippo signaling protein YAP1, in addition to integrin-FAK (focal adhesion kinase) mechanosignaling, also regulates cell stemness. By addressing mechanosignaling-dependent transcription factors, YAP1 is involved in osteogenic and myofibroblast differentiation and influences core steps of autophagy. Recent in vivo evidence elucidates the decisive role of YAP1 in epithelial homeostasis and underlines its impact on oral pathologies, such as periodontitis-linked oral squamous cell carcinogenesis. Here, new insights reveal that YAP1 contributes to carcinogenesis via overexpression rather than mutation; promotes processes such as apoptosis resistance, epithelial-mesenchymal transition, or metastasis; and correlates with poor prognosis in oral squamous cell carcinoma. Furthermore, YAP1 has been shown to contribute to periodontitis-induced bone loss. Mechanistically, molecules identified to regulate YAP1-related periodontal homeostasis and disease include cellular key players such as MAPK (mitogen-activated protein kinase), JNK (c-Jun N-terminal kinase), Rho (Ras homologue) and ROCK (Rho kinase), Bcl-2 (B-cell lymphoma 2), AP-1 (activator protein 1), and c-myc (cellular myelocytomatosis). These findings qualify YAP1 as a master regulator of mechanobiology and cell behavior in human periodontal tissues. This review summarizes the most recent developments in MT-related periodontal research, thereby offering insights into outstanding research questions and potential applications of molecular or biophysical strategies aiming at periodontal disease mitigation or prevention.

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Gingipains impair attachment of epithelial cell to dental titanium abutment surfaces

Cited by 5 publications

References 37 publications

In-vitro antibiofilm activity of chlorhexidine digluconate on polylactide-based and collagen-based membranes

In-vitro antibiofilm activity of chlorhexidine digluconate on polylactide-based and collagen-based membranes

From the Matrix to the Nucleus and Back: Mechanobiology in the Light of Health, Pathologies, and Regeneration of Oral Periodontal Tissues

Role of Mechanotransduction in Periodontal Homeostasis and Disease

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