Periodontal disease process is site specific and has multifactorial origin where periodontal pathogens, host response, genetic, systemic and behavioral risk factors interplay to develop the disease process. Hence, various measures have been taken to include microbial, immunologic, systemic, genetic and behavioral factors, in addition to traditional clinical and radiographic parameters, for assessing patient's periodontal status.
The activity of β-Glucuronidase is associated with severity of inflammation and also with the presence of putative pathogenic flora. This enzyme has been detected in GCF of patients with active site of periodontal disease, thus making β-Glucuronidase as an important biochemical marker for disease activity and for predicting future attachment loss.[3
Diabetes mellitus encompasses a heterogenous group of disorders with common characteristics of altered glucose tolerance and impaired lipid and carbohydrate metabolism. Diabetes develops from either deficiency in insulin production or an impaired utilization of insulin.
Diabetes is linked to severe periodontal destruction. Uncontrolled diabetic frequently show a combination of inflammatory and degenerative changes ranging from a mild gingivitis to advanced chronic periodontitis with a widened periodontal ligament, exudation from periodontal pockets, and/or multiple lateral periodontal abscesses. Although it may be more severe in nature, the periodontal disease of the diabetic seems to be clinically similar to that found in non-diabetic individuals. This suggests that the diabetic state serves as a predisposing factor which can accelerate periodontal destruction originated by microbial agents.
In the present study, we have attempted to test the hypothesis that ‘diabetics with chronic periodontitis have higher levels of disease activity markers in GCF as compared to non-diabetics with chronic periodontitis’. The probing pocket depth in chronic periodontitis patients with or without diabetes was standardized, so that these parameters did not have any bearing on the level of activity of GCF β-glucuronidase, thus allowing comparisons to be made between β-glucuronidase activity of diabetic and non-diabetic patients. Also, this study was aimed to determine β-glucuronidase activity in host tissues and not from the bacterial origin hence acidic pH was used to detect activity of enzyme.[6
In this study, plaque index, gingival index and probing pocket depth values were significantly lower in Group I, as compared to Group II and Group III patients. Though there was statistically non-significant difference in plaque index and gingival index in between Group II and Group III patients, the average probing pocket depth was significantly higher in Group III as compared to Group II. These findings are consistent with that of Oliver and Tervonen[5
] and Lamster et al
The relationship between oral hygiene to periodontal disease has long been well established in the dental literature. In this study, with respect to oral hygiene (Plaque Index) and gingival status (Gingival index), the values in diabetic and non-diabetic patients with chronic periodontitis (Group III and II) were statistically not significant. However, when compared with Group I patients, these values were significantly higher.
In Group I (periodontally healthy patients), low levels of β-glucuronidase activity could be demonstrated, similar to the findings of Lamster et al
] In their study they observed that even in periodontally healthy individuals, some amount of subclinical inflammation was always present. Hence, in the present study, the presence of low levels of β-glucuronidase in Group I patients also indicates the presence of subclinical gingival inflammation.
This study demonstrates that there is an increase in GCF β-glucuronidase level in Group II patients i.e. non diabetic with chronic periodontitis (t=6.92, P
< 0.001), as compared to healthy individuals, showing highly significant correlation between GCF β-glucuronidase level and probing pocket depth. These results are consistent with the findings of Bang et al.
] and Lamster et al
] These authors observed that β-glucuronidase increases with the development and severity of inflammation resulting into increased probing pocket depth and attachment loss. Also, the higher levels of β-glucuronidase can be predictive of attachment loss on a site specific and whole mouth basis with high levels of sensitivity and specificity.[10
The present study also demonstrates that there is higher level of GCF β-glucuronidase activity in patients of diabetes with chronic periodontitis as compared to non-diabetic with chronic periodontitis (t=2.09, P
< 0.05). This finding is in accordance with study by Bacic et al.
] who showed that periodontal disease is more frequent and severe in diabetics as compared to non-diabetics. Hayden and Bucklay[12
] demonstrated that in diabetics with periodonitis, other than impaired glucose metabolism, genetic predisposition plays an important role in the progression of disease.
Shlossman et al
] stated that diabetes is a risk factor for development of periodontal disease and there is a significant progressive periodontal destruction in diabetic patients. Cutler et al
] claimed that the increased susceptibility of diabetic patients to periodontal breakdown may be due to an abnormal PMN's function.
It is also observed that there was a significant positive correlation between GCF β-Glucuronidase and RBS levels, in diabetics with chronic periodontitis. This observation is comparable to the findings of Oliver et al
] who demonstrated increased β-glucuronidase levels in GCF in uncontrolled diabetics. It has been hypothesized that increased GCF β-glucuronidase activity may be due to hyperactivity and increased deregulation of lysosomes of polymorphonuclear leucocytes in diabetes mellitus. Though, Ginwala et al
] did not find any significant correlation between blood sugar level and β-glucurondiase levels. In their study, salivary and serum β-Glucuronidase levels were assessed rather than the GCF so, their results can not be correlated with the present one.
Another important observation made in the present study was that even with difference in clinical parameters between study groups, periodontitis patients irrespective of their diabetic status, showed an increased periodontal destruction with elevated β-Glucurondiase level than control. This suggests that β-Glucuronidase level can be used as a biochemical marker for chairside diagnostic kit, which can diagnose early phases of disease with reasonable confidence.