Background
Type 2 diabetes mellitus (T2DM) and periodontitis are chronic inflammatory diseases with a bidirectional relationship. The uncontrolled levels of glucose in T2DM patients change the pathophysiology and balance of inflammatory mediators. Matrix Metalloproteinase-2 (MMP-2) is a zinc-dependent endopeptidase that is responsible for tissue remodeling and degradation of the extracellular matrix in periodontal tissue. Therefore, the uncontrolled levels of glucose in T2DM could lead to an imbalance in MMP-2 activity in saliva, favoring the development of periodontitis.
Conclusions
T2DM with glycemic uncontrol conditions, distinct clinical alterations in periodontal tissue were identified, including a decrease in the gingival redness, increased the clinical attachment loss and imbalance of MMP-2/TIMP-1, as the possible causes of disorders promoting the progression of periodontitis. Accelerated periodontitis development with poor glycemic uncontrol likely results from the altered response of host defenses and decreased activity of polymorphonuclear cells. Taken together, these findings identify MMP-2 as a promising molecular market for periodontitis.
Methods
Ninety-seven T2DM patients from Hospital Dr. Donato Alarcon were included in the study. Following clinical examination, the patients were classified into four groups according to the presence and degree of periodontal disease and glycemic control. Blood and whole saliva samples (WSS) were collected from each patient. Blood samples were used for Hba1c and polymorphonuclear cells count determination, while WSS were used to determine MMP-2 activity, TIMP-1 and nitrite. MMP-2 activity was determined by zymography. TIMP-1 were determined by Western blotting, and nitric oxide (NO) levels were determined by the Griess method.
Results
Of the 97 patients with T2DM, 66 had periodontitis of different severities: 18 patients had mild periodontitis, 15 had moderate and 33 had severe. Salivary MMP-2 activity, HbA1c and TIMP-1 were positively correlated with the severity of periodontitis. On the other hand, the increase in HbA1c was negatively correlated with MMP-2 activity and quantity of TIMP-1 but was positively correlated with nitrite levels. Conclusions: T2DM with glycemic uncontrol conditions, distinct clinical alterations in periodontal tissue were identified, including a decrease in the gingival redness, increased the clinical attachment loss and imbalance of MMP-2/TIMP-1, as the possible causes of disorders promoting the progression of periodontitis. Accelerated periodontitis development with poor glycemic uncontrol likely results from the altered response of host defenses and decreased activity of polymorphonuclear cells. Taken together, these findings identify MMP-2 as a promising molecular market for periodontitis.