The Journal
Recent studies confirm participation of the genetic factors also in the pathogenesis of dental caries .[ 32 ] Data analyzing the coexistence of the two diseases in the present investigation suggested that periodontal disease and dental caries tend to accumulate in the same subjects . The prevalence of dental caries in the subjects having periodontal disease was 91.2 %. It increased with the severity of periodontal disease i . e . 90 % of the subjects with mild PD , 89 % with moderate and 94 % with severe PD had dental caries . This was observed in all subjects irrespective of age or sex . Similar investigations has been previously done with varying results .[ 5 , 7 , 20 , 34-40 ] The most striking finding in the current investigation was that all the subjects in the absence of periodontal disease had dental caries , which could be traced to be rooted in the complexity of the shared etiologic and risk factors . After analyzing all these contributory factors , we propose that the amount and nature of contribution from various background factors may differ between patients due to varying combinations of the host response pathways . It is conceivable that inherited genetic variation could also enhance these potential mechanisms . In Fig . 3 below , the proposed mechanistic links are summarized .
Figure 3
* Host associated factors affecting quality and quantity of plaque are : Intrinsic factors- genetics , systemic diseases , salivary quality and quantity etc .
Extrinsic-overhanging of restorations , habits , smoking etc .
Now , since the biofilm is the common denominator to initiate both the pathologies , it is imperative to understand that the kind and timing of ecologic shifts , and the unique interplay of all factors affecting such shifts for an individual host becomes a determinant of the clinical outcome . The ecological plaque hypothesis suggests that changes in the environment in the vicinity of the dental plaque biofilm could lead to either dental caries and periodontal diseases .[ 22 ] It is generally assumed that dental plaque biofilm matures by 72 hours , although this timing could be altered by factors such as dietery intake or immunity of the host .[ 22 , 41 ] So , for the patients whose dietary habits include frequent sugar intake , greater are the chances for an ecologic shift in bioflm , conducive to cariogenicity . For cariesactive patients , frequent sucrose consumption may be especially associated with the ecological emergence of the mutans streptococci and of the lactobacilli and caries activity .[ 42-45 ] Recent studies of S . mutans biofilms have shown that the biofilm mode of growth has greater tolerance of acidic stress , which could be as high as six orders of magnitude higher compared with the planktonic form of bacteria . Mature S . mutans biofilm down regulates the main energy generating glycolytic pathway in order to be acid tolerant .[ 22 , 32 , 46 ] Depending on the supply of nutrients , Streptococcus mutans can alter its patterns of acid production via the glycolytic pathway . For example , plaque which has formed in a highly cariogenic environment produces large quantities of lactate , formate and pyruvate , stronger organic acids that can more readily demineralize dental enamel .[ 41 ] Environmental acidification of the tooth , affects not only the number and species of bacteria , but also the release rate , viscosity and buffer capacity of saliva , fluoride levels in enamel and plaque and further regulates acidinduced adaptation through induction of proteins / enzymes .[ 32 , 41 , 46 ]
71 9 Vol . 12 No . 23 May-August Sept-Dec 2016