Abstract
Periodontal disease (PD) is characterized by a deregulated inflammatory response which fails to resolve, activating bone resorption. The identification of the proteomes associated with PD has fuelled biomarker proposals; nevertheless, many questions remain. Biomarker selection should favour molecules representing an event which occurs throughout the disease progress. The analysis of proteome results and the information available for each protein, including its functional role, was accomplished using the OralOme database. The integrated analysis of this information ascertains if the suggested proteins reflect the cell and/or molecular mechanisms underlying the different forms of periodontal disease. The evaluation of the proteins present/absent or with very different concentrations in the proteome of each disease state was used for the identification of the mechanisms shared by different PD variants or specific to such state. The information presented is relevant for the adequate design of biomarker panels for PD. Furthermore, it will open new perspectives and help envisage future studies targeted to unveil the functional role of specific proteins and help clarify the deregulation process in the PD inflammatory response.
Highlights
The different forms of periodontal disease (PD) share four stages: (i) bacterial biofilm presence and accumulation in the gingival sulcus, (ii) bacterial penetration of epithelium and connective tissue in the gingiva adjacent to the tooth surface, (iii) stimulation of a host response involving activation of the innate and acquired immune response, and (iv) irreversible destruction of connective tissue attachment to the tooth surface and bone [1].Gingival epithelial cells and fibroblasts in PD respond to Gram-negative bacterial lipopolysaccharide (LPS) by the transient expression of cytokines playing an active role in the initiation and maintenance of gingival inflammation [2]
In order to obtain the list of proteins suggested as biomarkers in periodontal diseases, we queried the OralOme database using OralCard [15, 16] for the mesh terms “aggressive periodontitis,” “chronic periodontitis,” “gingivitis,” and “periimplantitis.” Each of the identified proteins was checked to confirm if it was suggested as a biomarker for periodontal diseases proteins > action view > biomarker and the information for each protein quantification and presence in the different PD variants was obtained
Osteoprotegerin (OPG) is downregulated 4x in Aggressive periodontitis CCL13 (AP), 2.28x in Chronic Periodontitis (CP), and 2.44x in PI. Together these 6 proteins, neutrophil gelatinase-associated lipocalin, neutrophil defensin 1, annexin A1, plastin, RANKL,and OPG, identify the following molecular mechanisms present in AP: (i) high number of neutrophils remaining in the tissue which leads to an exaggerated innate immune response and prevalence of the associated molecular mechanisms; (ii) decrease in the antimicrobial defence mechanisms; (iii) increase in the expression of proinflammatory cytokines due to a decrease in the concentration of the main anti-inflammatory molecules; (iv) the onset of the acquired immune response by the recruitment and activation of T lymphocytes; (v) strong activation of osteoclastogenesis by a great increase in the protein regulating the differentiation and activation of osteoclasts (RANKL) accompanied by a corresponding decrease in the OPG
Summary
The different forms of periodontal disease (PD) share four stages: (i) bacterial biofilm presence and accumulation in the gingival sulcus (colonization), (ii) bacterial penetration of epithelium and connective tissue in the gingiva adjacent to the tooth surface (invasion), (iii) stimulation of a host response involving activation of the innate and acquired immune response (inflammation), and (iv) irreversible destruction of connective tissue attachment to the tooth surface and bone (tissue loss) [1]. Macrophages phagocytose periodontal pathogens and orchestrate wound repair by functionally coordinating innate and adaptive immune responses This is achieved by the production of specific cytokines and chemokines which contribute to the attraction and activation of subsets of T cells. For each protein, the following data were recorded when available: the identification of the protein; the source of the sample; the disease (MeSH code) and the up-/downregulation (fold change calculations performed according to Chan et al [17]) compared to normal samples; sample donor data (age, gender, and social habits); methods of sampling and analysis; type of study (proteomics and nonproteomics); and posttranslation modifications and whether the protein had been proposed as a biomarker. From the 43 proteins proposed as biomarkers for PD, only 8 were identified as being exclusively present in one of the disease variants (Table 1)
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