This review addresses commonalities in specific biomarkers of chronic inflammatory diseases such as diabetes mellitus, rheumatoid arthritis and periodontal diseases, which could retrace common origins of susceptibility. Oxidative stress and free radical damage play an important role in the pathogenesis of diabetes mellitus, rheumatoid arthritis and periodontal diseases. There are aggravating and attenuating factors such as cigarette smoking and hormone replacement therapy, which contribute to disease aggression or alleviation respectively. A common locus of disease activity has implications for the co-existence of genetic susceptibility of more than one disease in an individual. Current concepts on aetiopathogenesis include single nucleotide polymorphisms (SNPs) for cytokines associated with free radical release. The association between local cytokine production and disease progression is common to systemic and periodontal diseases. Over-expression of these cytokines could lead to oxidative stress and its sequelae in selected individuals. The influence of phenotype over genotype and the presence of multiple polymorphisms contribute to difficulties in interpreting genetics in the context of clinical parameters. New knowledge in the area could lead to improved management strategies.