Bone loss in smoker-related periodontitis patients may be partially explained by suppression of OPG production.

Salivary RANKL and OPG concentrations are suggested to be affected by smoking as not only the untreated but also the treated smokers exhibited higher RANKL and lower OPG concentrations than non-smokers.

Elevated salivary TLR stimulants may represent a novel mechanism by which periodontitis increases the risk of developing cardiovascular disease and insulin resistance.

TNFSF cytokines correlate with periodontitis disease severity. However, only TNF, sRANKL and OPG levels were altered by cigarette smoking. APRIL and BAFF appear as good indicators of disease severity.

Plasma CXCL5/ENA-78 concentrations are a good systemic indicator of the inflammatory process and disease severity in subjects with periodontitis and in addition are potential indicator of inflammatory effects of cigarette smoking. Further studies are required to elucidate the biological mechanisms underlining this increase in CXCL5/ENA-78.