Serum proteins associated with periodontitis relapse post-surgery: A pilot study.

2021 
BACKGROUND The knowledge of which genes and proteins that are connected to the susceptibility to gingivitis with subsequent local tissue degradation seen in periodontitis is insufficient. Changes of serum proteins associated with recurrence of bleeding on probing (BOP) and increased periodontal pocket depths (PPD) after surgical treatment of periodontitis could reveal molecules that could be early signals of tissue destruction and/or of importance for systemic effects in other tissues or organs. METHODS  We performed a longitudinal pilot study and followed 96 inflammation-related proteins over time in serum from patients who underwent surgical treatment of periodontitis (n = 21). The samples were taken before (time 0), and then at 3-, 6-, and 12-months after surgery. Changes in protein levels were analysed in relation to the clinical outcome measures, i.e. proportion of surfaces affected by BOP and PPD. RESULTS Changes in treatment outcomes with early signs of relapse in periodontitis after surgical treatment, e.g. increased BOP and PPDs, were during 12-months follow up associated with increased serum levels of high-sensitivity C-reactive protein (hs-CRP) and programmed death-ligand 1 (PD-L1), and reduced serum levels of cystatin-D protein. CONCLUSION This study shows that clinical signs of recurrence of periodontitis after surgery are reflected in serum, but larger studies are needed for verification. Our novel findings of an association between increased PD-L1- and decreased cystatin D-levels and recurrence in periodontitis are interesting because PD-L1 has been shown to facilitate bacterial infections and chronic inflammation and cystatin D to inhibit tissue destruction. Our results justify mechanistic studies regarding the role of these molecules in periodontitis. This article is protected by copyright. All rights reserved.
    • Correction
    • Source
    • Cite
    • Save
    • Machine Reading By IdeaReader
    40
    References
    0
    Citations
    NaN
    KQI
    []