Clinical Update quiz
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May Clinical Update
A study into systemic and oral levels of proinflammatory biomarkers associated with endpoints after active non-surgical periodontal therapy
Werner N, Frasheri I, Heck K, Scalia C, Pitchika V, Summer B, Ern C, Heym R, Schwendicke F, Bumm CB, Folwaczny M
J Clin Periodontol 2025; 52:188–198. https://doi.org/10.1111/jcpe.14089
Compiled by Dr Sarah Chin
This article was originally published by Journal of Clinical Periodontology and has been edited for brevity and clarity.
Introduction
Periodontitis results from inflammation within the gingival tissues due to the presence of dysbiotic microbiota. The degree of immune response is influenced by genetic and epigenetic factors, as well as intrinsic and extrinsic exposures such as systemic disease. The majority of periodontitis associated biomarkers are cytokines and chemokines expressed by endothelia, epithelial cells, fibroblasts, macrophages and T-lymphocytes in response to the dysbiotic microbiota. Bacterial antigens (Pathogen associated molecular patterns - PAMPs), such as lipopolysaccharides, induce bioactive substance expression and can be detected in the serum (SE) and plasma (PL) of venous blood as well as gingival crevicular fluid (GCF).
Matrix metalloprotinease-8 (MMP-8) and prostaglandin E2 (PGE2) have been used as diagnostic marker molecules demonstrating inflammation levels and severity of periodontitis. Surfactant protein D (SP-D) is an innate immune scavenger receptor that binds to various PAMPs. It is present in plasma and has been shown to have antimicrobial and anti-inflammatory effects in cardiovascular and metabolic diseases. It also has been shown to reduce systemic inflammation in mouse models. Increased plasma concentration has been seen in periodontitis.
The current classification suggests the use of biomarkers to improve diagnostic accuracy. As there is insufficient evidence in the literature, this retrospective study was designed to assess the level of biomarkers - active MMP-8 (aMMP-8), PGE2 and SP-D in periodontitis patients and to analyse their association with the response to step I (preventive and health promotion) and II (cause-related therapy- elimination of subgingival biofilm and calculus) periodontal therapy and non- surgical re-instrumentation (NSRI).
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