Peripheral blood monocyte responses in periodontitis

Abstract

Periodontitis results from the interaction of bacteria on the tooth surfaces and the host immune response. Although periodontal pathogens are essential for the initiation and progression of the disease, the tissue damage in periodontitis is primarily mediated by the host immune response. Differences in the susceptibility to the disease and in the clinal outcome of the therapy seem to be less dependent on genetics but more on lifestyle factors, like smoking, overweight, stress and nutrition. It has been shown that these lifestyle factors may modulate the immune response and therefore influence the initiation and progression of the disease. To study the host immune response, whole blood cell cultures (WBCC) stimulated with lipopolysaccharide (LPS) have been widely used and they specifically reflect the behaviour of monocytes. It has been shown that peripheral blood monocytes in LPS-stimulated WBCC from non-smoking periodontitis patients display a T-helper 2 (Th2)-promoting phenotype in comparison with controls. After periodontal therapy, this phenotype reversed and was comparable with controls. However, in smoking but treated patients, the Th2-promoting phenotype of monocytes still remained. Therefore, the aberrant phenotype of monocytes in the peripheral blood from periodontitis patients is likely to be a systemic response to exogenous and endogenous danger molecules released or induced by the periodontal infection or by smoking. It can be concluded that periodontal therapy in non-smoking periodontitis patients has beneficial health effects and that smoking cessation should be an integral part of the therapy as well for general health reasons as for the clinical outcome.

The innate host response in caries and periodontitis

“…In this environment, monocytes may differentiate into osteoclasts and activate bone destruction (Di Benedetto, Gigante, Colucci, & Grano, ). During periodontitis, the peripheral blood monocyte Th1‐promoting phenotype can change to Th2 ex vivo in response to LPS (Fokkema, ). After periodontal treatment in non‐smokers, the Th2‐promoting cells appear to be replaced by Th1.…”

Candida albicans Shields the Periodontal Killer Porphyromonas gingivalis from Recognition by the Host Immune System and Supports the Bacterial Infection of Gingival Tissue

“…The monocytes and neutrophils found in abundance in the gingival tissue during periodontal disease respond to microbial stimuli, among others, via cytokine and chemokine production [44]. In our previous report [45], we used THP-1 cells to demonstrate the influence of mixed biofilm formation on host cell genetic responses.…”

OCT4B1 Regulates the Cellular Stress Response of Human Dental Pulp Cells with Inflammation

“…Exposure to LPS activates the cellular stress response, which results in apoptosis and cell death in dental pulp. Pathological alternations of DPCs caused by LPS could give rise to acute dental pain and adversely affect the repair process [8–10]. Therefore, it is of great importance to develop the anti-inflammatory strategy during dental regeneration.…”