with nondiabetics.33 Similar findings were reported from an epidemiologic study of the same population, with diabetes increasing the risk for periodontal disease by three times.34
Treatment outcomes
On the other hand, prediabetics or well-controlled diabetics are not at additional risk for periodontal disease.35 The level of glycemic control has an impact on the outcome of the treatment. A favorable response is observed in well-controlled diabetics, similar to nondiabetic controls.36
The immunologic response of diabetics to bacterial plaque is similar to nondiabetics in terms of IgG levels, although differences can be observed in regard to the levels of E-selectin, vascular cell adhesion molecule-1 (VCAM-1), adiponectin, and plasminogen activator inhibitor-1.37
With regard to the effect of periodontal treatment on diabetic control, nonsurgical periodontal therapy can reduce the hemoglobin A1c (HbA1c) levels. However, this reduction may be considered insignificant, and it is not stable over time. The magnitude of the reduction is higher in Type 2 diabetics compared with Type 1 and when antibiotics were prescribed as an adjunct to nonsurgical treatment. Although the reduction of HbA1c following periodontal treatment reported from several studies can vary, based on the current evidence, it is anticipated to correspond to 0.3% to 0.4% less than the original value38,39 (Box 4-3).
BOX 4-3 Link between diabetes and periodontal status
PATHOGENIC BACTERIA
Groups of bacteria with specific characteristics have been shown to be implicated as primary etiologic factors in the pathogenesis of periodontal diseases. The classic 1998 study by Socransky et al,40 among others, investigated this association and identified specific bacterial complexes to be associated with increased PDs.
The qualitative and quantitative differences in the microflora of periodontitis and nonperiodontitis patients was also evidenced in a study by Listgarten and Hellden41 in 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.41 See chapter 3 for further considerations.
Risk Determinants
GENETICS
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,42 while 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.44 Furthermore, a specific genotype of interleukin 1 β (IL-1β) has been shown to be associated with increased disease severity45,46 and a 2.7-fold increase in risk of tooth loss.29
AGE
There have been studies connecting age with higher percentages of bone and attachment loss.9,47 It 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.48 In 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
SEX
Males have been identified as being in higher risk for attachment and bone loss (OR 1.36 and 1.29, respectively), in cross-sectional9 as well as longitudinal studies.50 The 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
RACE
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.47 Furthermore, 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
Risk Indicators
OBESITY
Adipose tissue secretes a number of proinflammatory cytokines and acute phase proteins, which can potentially affect the progression of periodontitis (among other possible mechanisms).54 Young 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.55 Gorman et al56 examined 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
OSTEOPOROSIS
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.57 A similar association was found between CALs and T scores, especially in women without subgingival calculus.58
STRESS
Genco et al59 evaluated 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).59 The 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
ALCOHOL
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 1.67.61 A smaller cross-sectional study reported similar conclusions, as alcohol dependence exhibited a linear relationship with CALs and PD.62
RHEUMATOID ARTHRITIS
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