Gum pockets and attachment
Gingival and periodontal inflammation↓
Also searched as Gingival and periodontal inflammation.
The most overlooked inflammatory load in the body. Treating it measurably lowers C-reactive protein in the blood — which means a dental problem is also a systemic one.
In depth
Chronic inflammation of the gum and the tissue holding the teeth, driven by periodontal bacteria.
What drives it
Pathogen tripwire increases it.
The gum lesion begins as a bacterial-pattern signal: lipopolysaccharide from Porphyromonas gingivalis — the principal periodontal pathogen — strongly induces IL-1β, IL-8 and TNF-α in human gingival epithelial cells, and siRNA knockdown of the mediating step reduces all three (PMC5608282). Periodontitis is a chronic inflammatory disease in which the inflammatory response, not the bacterium alone, does the structural damage. PMC5608282
What it drives
It increases Calms inflammation.
Gum inflammation does not stay in the mouth, and treating it lowers a systemic marker: a systematic review and meta-analysis of 26 randomized controlled trials in 2,579 participants found that treating periodontitis reduced C-reactive protein by 0.69 mg/L (95% CI −0.97 to −0.40) at six months (PMC10087558). Recurrent bacteremia with periodontal pathogens can damage vascular endothelium, and the landmark trial of intensive periodontal therapy improved brachial-artery endothelial function (Tonetti et al., N Engl J Med 2007;356:911). PMC10087558
Blends that modulate it
Each blend page names this pathway and carries the study behind its claim.
See it on the map
Open the causal map to follow this pathway upstream and downstream, arrow by arrow, each with its study.