Inflammation represents the central component of several chronic disorders, and seems that genetic variations of the inflammatory response can influence the future disease evolution in human. One of the most significant practical application of inflammatory disease modulation would reside in regulation of “key” gene expression, involved in these inflammatory disorder mediation. Periodontal alteration is the end result of immune inflammatory response, generated by bacterial accumulation upon dental surfaces adjacent to supra and subgingival tissues. There is an initial gingivitis-like bacterial-mediated inflammatory response, that can be held at this level, existing in some individuals as an independent, clinical condition, with no further progression. Development of periodontitis is plurifactorial, with several contributors: bacterial infection, genetic susceptibility, metabolic response and anatomic modifications in the oral tissues, all of which have to be considered whenever one can diagnose periodontal disease. It is so less probable that one sigle biochemical parameter can express solely the diagnostic of such disorder. Nevertheless, tissular markers of the connective tissue (collagen, MPS, osteocalcin, osteonectin, fibronectin, enzymes) have significant values in metabolic response evaluation during the active course of disease, many of which possessing an elevated expression within GCF (gingival crevicular fluid).