Polymorphic Genetic Markers in Patients with Chronic Periodontitis.
Chronic periodontitis is an inflammatory disease caused by the interaction
among dental plaque, periodontal tissues, and host immune responses, which causes bone resorption. Interleukin and matrix metalloproteinase plays an important role
in the periodontium destruction. Some authors have studied polymorphisms in these genes but
the results were controversial.
Periodontitis is a chronic inflammatory disease caused by the interaction among biofilm, periodontal tissue, and host vascular and cellular responses, which leads to bone tissue resorption.1
Chronic periodontitis prevalence ranges from 40% to 80% in general population, which
is due to regional differences and methodological variations in the studies.2
CP affects the periodontium, and although bacteria are essential for the disease initiation, bacteria number and type are not sufficient to explain the differences in their severity.
Besides the pathogenesis of chronic lesions is associated with the interaction among
biofilm, host response and influences of secondary factors, genetic polymorphism may be determinant of certain immunological aspects of the disease.
Smoking is an important epidemiological factor associated with CP5 as well as some
systemic conditions such as diabetes and cardiovascular disease, especially hypertension. Periodontal disease is considered the 6th complication of diabetes.6 A longitudinal study demonstrates an increased risk of 50% to 100% of having oral conditions prior to the occurrence of
Interleukin is a multifunctional cytokine with a central role in host defense.
However, it also stimulates osteoclast activity, making it a potent inducer of alveolar bone resorption.
Matrix metalloproteinases are families of metal dependent proteolytic enzymes, which are capable of degrade all components of the extracellular matrix, including various types
of collagens and basement membrane components.
MMPs also actively participate in bone resorption that occurs in periodontitis.
Dent Open J. 2016; 2(5): 142-147. doi: 10.17140/DOJ-2-126