Advanced Glycation End-products inNon-Diabetic Periodontal Disease

Objectives: A list of risk factors has been proposed for their occurrence. A potential addition to this list is the deposition of advanced glycation end-products (AGE).The reaction proceeds through a number of intermediate compounds leading to a variety of end-products that effectively modify or cross-link proteins. The consequence of these chemical modifications is impairment, both of function and turn-over, of the proteins. AGE accumulation has been implicated in the process of ageing as well as in the pathogenesis of several diseases, including: diabetes, atherosclerosis, Alzheimer’s disease, and in renal failure. The various pathologies associated with diabetes have been strongly linked to AGE deposition formed in response to hyperglycemia. The aim of the present study was to determine the role of AGE in chronic periodontal disease of non-diabetic subjects where sugars derived from bacterial plaque or from the inflamed periodontal connective tissues could drive the non-enzymatic glycosylation reaction.

 

Methods: AGE products share common properties of yellow-brown colour and characteristic fluorescence spectra that provide the opportunity to measure AGE levels in complex tissues.

Single biopsies from 18 patients with healthy periodontium and 17 patients with  chronic periodontitis were homogenised, then digested with collagenase and acid for fluorimetric determination of AGE.

To analyse this further, paired biopsies, comprising tissue from least diseased and most diseased sites, from 26 patients with chronic periodontitis were studied. A full suite of relevant criteria, including haemoglobin glycosylation values, were available for this group.

 

Results : There was no significant difference in AGE level between healthy and disease sites after adjustment for protein levels.

 

Conclusion: The results are indicating that levels of AGE are not correlated with disease status of the biopsy site in patients with chronic periodontitis. Accordingly, there is a lack of evidence to support a role for AGE deposition in the pathology of chronic periodontal disease.