Fernando Suarez - Periodontics

The qualitative and quantitative differences in the microflora of periodontitis and nonperiodontitis patients was also evidenced in a study by Listgarten and Hellden 41in 1978. A significant increase in motile rods and a decrease in coccoid cells was observed in diseased sites (PD > 5 mm) compared with healthy sites. 41See chapter 3for further considerations.

The degree that periodontitis is influenced by genetics has been investigated in a number of studies. The role of genetics appears to be more significant in specific categories of periodontitis with rapid progression (previously known as aggressive periodontitis ). The mode of transmission, however, remains unclear. The majority of the studies point toward autosomal dominant mode, 42while others report X-linked or autosomal recessive. 43

For the majority of the rest of the phenotypic expressions of periodontitis (chronic periodontitis), evidence from cross-sectional studies in twins suggest that genetics (heritability) are responsible for up to 50% of the manifestation of the disease. 44Furthermore, a specific genotype of interleukin 1 β (IL-1β) has been shown to be associated with increased disease severity 45,46and a 2.7-fold increase in risk of tooth loss. 29

There have been studies connecting age with higher percentages of bone and attachment loss. 9,47It is debatable, however, if the increased attachment loss observed with aging is representative of increased susceptibility to periodontal disease. Studies in different populations (Japanese and Swedish) concluded that periodontal stability can be observed over time. 48In fact, recent evidence from epidemiologic studies supports the idea that the observed increase in clinical attachment loss is a result of changes accumulating over the years, rather than the result of periodontitis. These changes in CALs are mainly attributed to recession because PDs remain relatively stable over time. 49

Males have been identified as being in higher risk for attachment and bone loss (OR 1.36 and 1.29, respectively), in cross-sectional 9as well as longitudinal studies. 50The clinical signs of gingival inflammation may be more severe in females during periods associated with hormonal changes, such as pregnancy or menstrual cycles. 51,52

National Health and Nutrition Examination Survey (NHANES) data from the 2009–2010 period indicate that periodontitis is more prevalent among Mexican Americans, followed by non-Hispanic Black individuals, while non-Hispanic White individuals had the lowest prevalence among the three groups. 47Furthermore, disease entities that were classified as “aggressive periodontitis” according to the 1999 classification of periodontal diseases were found to be more prevalent among African-American and Hispanic children and adolescents (OR 15.1 and 2.4, respectively). 53

Adipose tissue secretes a number of proinflammatory cytokines and acute phase proteins, which can potentially affect the progression of periodontitis (among other possible mechanisms). 54Young females who are overweight or obese also have increased risk of being diagnosed with periodontitis. The same population, however, did not demonstrate altered bacterial plaque composition compared with nonobese individuals, with the exception of increased levels of T forsythia . 55Gorman et al 56examined male subjects over a period of more than 25 years. The participants in this study who showed increase in waist circumference–to-height ratio and were obese were more likely to demonstrate signs of periodontal disease progression. 56

Cross-sectional data suggest that there is an association in postmenopausal women between alveolar bone loss and osteopenia (T score between –2.5 and –1.0) as well as osteoporosis (T score < –2.5). This association is stronger in those 70 years old and above with worsening T scores. This subset of the population was 2.5 to 4.6 times more likely to present with loss of alveolar bone compared with subjects with normal bone scores. 57A similar association was found between CALs and T scores, especially in women without subgingival calculus. 58

Genco et al 59evaluated the association between periodontal disease and stress, distress, and inadequate coping behaviors. Analysis of questionnaires completed by more than 1,400 participants indicated that there was an association between bone loss and financial strain. This association, however, was altered depending on the approach the subjects demonstrated when coping with stress (emotional-based or problem-based). 59The mechanisms behind these associations are not fully understood. Behavioral changes as a result of stress as well as alterations in host’s immune function have been reported as possible mechanisms. 60

A NHANES study indicated that there appears to be a dose-dependent relationship between alcohol consumption and prevalence of periodontal disease. As the number of drinks per week increases from 5 to more than 20, the odds ratio also increases from 1.22 to 1.67. 61A smaller cross-sectional study reported similar conclusions, as alcohol dependence exhibited a linear relationship with CALs and PD. 62

Although there is only a low level of evidence, findings from a systematic review on the association between rheumatoid arthritis (RA) and periodontal disease indicate that patients with RA present with greater clinical attachment loss and increased tooth loss compared with individuals without RA. In the majority of cases, periodontitis precedes the manifestation of RA, but due to the quality of the existing studies, causality cannot be supported at this time. 63

Background characteristics, such as behavioral changes, socioeconomic status, and education level are frequently important when evaluating the associations between specific risk predictors and periodontal disease.

BOP has been thoroughly investigated in a number of longitudinal studies of periodontitis patients enrolled in maintenance programs. The high negative predictive value of this index makes it valuable in identifying the absence of clinical inflammation with high accuracy. 64However, the presence of BOP does not necessarily indicate disease progression. Consequently, BOP presents with high specificity but low sensitivity. As demonstrated by Lang et al 65in 1986 over a period of four consecutive maintenance appointments, a specific site may present with BOP in every maintenance visit, but there is still a 70% chance that this site will not lose attachment.

Another retrospective study evaluating patients in periodontal maintenance (for more than 11 years on average) showed that PDs of 5 mm and above following active periodontal therapy indicate increased risk for tooth loss. More specifically, the ORs of teeth with a deepest PD of 5, 6, or 7 mm to be extracted during the periodontal maintenance phase were 7.7, 11, and 64.2. 66

Several longitudinal studies in patients undergoing supportive periodontal treatment have demonstrated the association between furcation involvement and tooth loss. See chapter 5for further considerations.

A 3-year study by Rams et al 67concluded that the presence of radiographic crestal lamina dura is positively associated with clinically stable periodontal status in interproximal sites. On the other hand, the absence of crestal lamina dura cannot be used as a predictor for periodontal disease recurrence due to its low positive predictive value. 67Greenstein et al 68performed a cross-sectional study to investigate the potential relationship between the crestal lamina dura and clinical signs of inflammation, PD, BOP, and attachment loss. No association could be established based on the study findings. 68