The Relationship Between Periodontitis and Glycaemic Control in Type 2 Diabetes

Periodontitis is a bacteria-related, chronic inflammation that results in destruction of the bone and connective tissue support of teeth forming periodontal pockets between the tooth and gingival soft tissue.¹ It is initiated by inadequate oral hygiene and the development of a biofilm colonised with pathogenic bacteria on the tooth surface that results in direct damage to local tissues by bacterial virulence factors (see Figures 1 and 2).² The stimulation, an inflammatory/immune response to the offending bacteria, is further associated with indirect tissue damage
Periodontitis is a bacteria-related, chronic inflammation that results in destruction of the bone and connective tissue support of teeth forming periodontal pockets between the tooth and gingival soft tissue.¹ It is initiated by inadequate oral hygiene and the development of a biofilm colonised with pathogenic bacteria on the tooth surface that results in direct damage to local tissues by bacterial virulence factors (see Figures 1 and 2).² The stimulation, an inflammatory/immune response to the offending bacteria, is further associated with indirect tissue damage^3,4 mediated by cytokines including interleukin-1 beta (IL-1β), IL-6, tumour necrosis factor-alpha (TNF-α) prostaglandins and collagenolytic enzymes.^6,7 Oxidative damage to the tissues is also a feature of the periodontitis lesion,^8,9 thought to result from hyper-reactive neutrophils generating excessive reactive oxygen species (ROS) during bacterial phagocytosis¹⁰ causing both direct damage and stimulating redox-sensitive pro-inflammatory transcription factors. Individuals vary in their susceptibility to periodontitis and the key determinant appears to be a phenotype coding for a particularly exaggerated inflammatory and immune response to pathogenic bacteria.¹¹