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Periodontal Therapy & Maintenance – Part I

A 21st Century Perspective

Introduction

Data from 1988 to 1994 on the extent and prevalence of periodontal disease in the US population indicated that about 35% of people ages 30 to 90 had periodontal disease, with nearly 22% having a mild or moderate case and more than 12% experiencing a more severe form.1 Recently, a study found that these numbers might have been underestimated by as much as 50%. The new calculation used a full-mouth exam in contrast to a partial mouth evaluation, which had been used in past assessments. The findings led the researchers to speculate that more people than previously believed may suffer from moderate to severe periodontal disease.2

According to the American Academy of Periodontology, the majority of people can retain teeth over their lifetime with proper treatment, reasonable plaque/biofilm control, and regular care.3 As well, implants have become an ideal esthetic and functional option for the replacement of missing teeth even for people who have periodontal disease. Successful retention of teeth and implants is contingent upon regular periodontal maintenance. It is well established that patients who participate in routine periodontal maintenance visits can prevent or minimize the recurrence of periodontal disease. Dentists and dental hygienists from general and periodontal practices working in partnership with the patient are responsible for providing the care and support to meet this goal.

 

Periodontal Disease: Evolving Theories

Our understanding of the etiology of periodontal disease has progressed by leaps and bounds over the last 50 years. Early theories focused on plaque as the primary causative factor, often referred to as the non-specific plaque hypothesis. From this grew the specific plaque hypothesis, the understanding that specific types of bacteria caused the disease, not just plaque accumulation. Today, bacterial plaque has been redefined as biofilm, and periodontal disease is considered a biofilm-associated inflammatory disease caused by multiple etiologies.4

Research over the last 20 years has demonstrated that the susceptibility, extent, and severity of periodontal disease are influenced by multiple factors. These factors range from genetics to environmental and also include immunological and microbial influences. Because of this range of factors, etiology likely varies from one patient to another. This means that treatment can no longer be approached as “one-size-fits-all.” Instead, the approach should be tailored to the patient’s specific risk factors.4  

 

The Microbial Influence: Biofilm

Costerton and Schaudinn note that the constant temperature, permanent moisture, and abundant and diverse nutrient supply of the oral cavity provide ideal growth conditions for more than 500 species of bacteria. Within the oral cavity, the gingival sulcus creates the conditions for a protected microhabitat. It provides protection against the tongue, saliva, and mastication. Bacteria can cling to the hard, non-shedding surface of the root. The gingival crevicular fluid and human food provide a constant source of nutrition.5

Biofilm formation begins when bacteria attach and colonize a surface. They secrete a sticky, extracellular substance made up of polysaccharides, proteins, lipids, nucleic acid, and other polymers. This substance helps the bacteria stick to the surface and each other, allowing them to mature, grow, and thrive.4

One way biofilm thrives is through its unique ability to function as a coordinated, spatially organized, and metabolically integrated community.6 Biofilm can support a broad range of bacteria, allowing oxygen-consuming and oxygen-sensitive bacteria to co-exist in close proximity. The waste products of one type of bacteria are the food source of another. Bacteria within a biofilm exhibit resistance to antibiotics. Minimum inhibitory concentrations to kill bacteria in a biofilm are 100 to 200 times higher than for planktonic cultures. Antibiotics may have difficulty penetrating the sticky extracellular matrix. Subpopulations of bacteria in a biofilm grow slower and are less susceptible to antibiotics. Additionally, the synergistic nature of the biofilm community of bacteria is likely much more pathologically virulent than what a single bacterial species could achieve on its own.4,6 Periodontal disease has been associated with a progressive change in periodontal pathogens. “Orange complex” species like Provotella intermedia and Fusobacterium nucleatum are commonly found in people with periodontitis. As the disease worsens, it has been shown that there is a shift to “red complex” pathogens such as Porphyromonas gingivalis, Tannerella forsythia, and Treponema denticola. Yet research indicates that P. gingivalis is frequently present in the biofilm of healthy patients. Also confounding is the discovery that some gram-negative bacteria are associated with periodontal health while a gram-positive one may be linked with disease.4

An emerging theory in the etiology of chronic disease is the “microbial shift hypothesis.” This theory posits that disease is a result of a decrease in the number of beneficial bacteria and a proliferation in the number of pathogens. Great variation in oral microflora has been observed among patients with periodontal disease. Researchers are exploring the idea that the lack of beneficial organisms in the biofilm may be as important as the presence of pathogens.4 Perhaps this is why it is well established that the presence of biofilm alone is not sufficient to cause periodontal disease.7  

(Continued from page 1 )

Immunological Influences: Inflammation

The immune response to bacteria and/or infection is essential in fighting disease. The swelling, inflammation, and bleeding symptomatic of gingivitis are the hallmark of an acute inflammatory response to bacterial biofilm. Early gingivitis has been shown to develop within two to four days of new biofilm growth. From days four to ten, the immune response heightens, including loss of connective tissue collagen. Within two to three weeks, the lesion progresses with additional connective tissue loss and fibrosis but no attachment or bone loss. In some individuals, this stage of gingivitis may be present for years without developing into periodontitis.8

While most people develop some type of local or generalized gingivitis at some time during their lives, not everyone develops periodontal disease. The reason for this is not completely known. On the cellular level, there is some indication that bacteria evade the neutrophil challenge and stimulate the progression from an acute to a chronic inflammatory response.8 It is the chronic inflammatory process that ultimately drives connective tissue and bone loss. The expression of critical concentrations of pro-inflammatory cytokines, especially interleukin (IL)-1, 6, 11, 17; tumor necrosis factor-alpha (TNFa); and others in the gingival crevicular fluid (GCF), stimulate the chronic immune pathways.9 Of these, IL-1 has been shown to be a “master” or key cytokine mediating the production of other potent cytokines like prostaglandins. It affects many major immune processes, including cell recruitment, tissue destruction, and bone resorption.10

Another key player in the immune response is RANKL, a cytokine related to TNFa. The pro-inflammatory cytokines stimulate RANKL, which drives a process called osteoclastogenesis. In the chronic periodontal inflammatory state, RANKL enhances the production of osteoclasts while decreasing the production of osteoblasts. This process changes the balance of bone homeostasis and leads to pathological bone loss.9,11

There is great variation in the severity of bone loss among patients that is not explained by the amount or type of bacteria in the biofilm. This has led to the hypothesis that some individuals may be “high responders” to the periodontal infection because they produce higher levels of pro-inflammatory mediators. It has been demonstrated that patients with severe periodontal disease have higher levels of IL-1ß in all probing depth areas, including shallow pockets. This suggests that the expression of IL-1ß may be a host or genetic trait.12  

 

Genetic Influences

Not every individual is susceptible in the same way to the same amount of biofilm and/or bacteria. Experimental gingivitis studies from the 1970s found that even in the absence of oral hygiene for 21 days, some individuals did not develop gingivitis, while others had substantial inflammation within two weeks. The differences in gingivitis susceptibility were independent of both a quantitative difference in plaque accumulation and a qualitative difference in plaque content.13

A study of 117 pairs of adult identical (64) and fraternal (53) twins found that about 50% of the variability in disease expression had a genetic basis. The differences in probing depth and attachment loss were not attributable to behaviors such as smoking, oral hygiene habits, or utilization of dental services. Identical twins were more similar in disease expression than fraternal twins. This genetic variance was related to both severity and extent of disease. The researchers concluded that about half of the variance in disease expression in the population is based on heritability.14

In 1997, Korman and colleagues identified a genetic marker associated with the increased production of IL-1ß.15 During the next decade, researchers investigated the genetic nature of periodontitis. The IL-1ß polymorphism was found to be most prevalent in Caucasians and lower in those of Asian descent. Emerging work seems to indicate that periodontal disease is not a single but polygenetic disease with anywhere from 10 to 50 different genes affecting its development.16

In a study that examined the presence of periodontal pathogens and the consequent chronic inflammatory immune response, Offenbacher et al. found that individuals who had the deepest pockets and the most severe bleeding had higher levels of IL- ß in the GCF, but not higher microbial counts or biofilm scores compared to those with less bleeding. The investigators termed this an excessive or hyperinflammatory response relative to the microbial burden. They speculated that the excessive response could be related to genotype or to the presence of an unknown non-cultivable organism.17  

 

Environmental Influences: Smoking and Diabetes

An environmental influence is an externally acquired aspect of health or behavior that increases the risk of disease. In periodontal disease, smoking and the presence of diabetes are two of the strongest and most well-established risk factors to date. About half of periodontal cases are attributed to smoking: 41.9% in current smokers and 10.9% in former smokers.18 The American Diabetes Association lists periodontal disease as one of the complications of diabetes, noting that one-third of people with diabetes have severe attachment loss of 5 millimeters (mm) or more.19

A current cigarette smoker is four times more likely to have periodontal disease than an individual who has never smoked.18 Regular cigar and pipe smoking also have been shown to be detrimental to periodontal health.20 Studies indicate that smokers are more likely to have deeper probing depths, greater attachment loss, more bone loss, and fewer teeth. There is often more calculus but less inflammation. A dose-response relationship between smoking and periodontal disease has been observed, with the heaviest smokers having increased disease severity. Younger adult smokers (19-30 years) often have a higher prevalence and severity of periodontitis than young non-smokers. The “periodontal cost” of smoking has been calculated as 27 years of disease progression. This means that a 32-year-old smoker has similar periodontal attachment loss to a 59-year-old non-smoker.18

Smoking has been shown to impact the immune response. Systemically, nicotine impairs the function of neutrophils, including phagocytosis, and reduces salivary and serum IgG. Locally, GCF concentrations of nicotine have been shown to be 300 times that of plasma nicotine concentrations. Nicotine can bind to the root surface, altering fibroblast attachment while decreasing collagen and increasing collagenase production. Fibroblasts exposed to nicotine produce higher amounts of pro-inflammatory mediators, including IL-1 and IL-6.18

Not only does smoking increase the extent and severity of periodontal disease, it compromises the outcomes of surgical and non-surgical therapy. Overall, the data indicate that probing depth reduction and clinical attachment gain in smokers is 50%-75% of that observed in non-smokers. Smoking has also been associated with implant failure and impaired outcomes in regenerative therapy.18

When patients quit smoking, the rate of bone and attachment loss slows, and evidence indicates that disease severity is intermediate to that of current and non-smokers. Importantly, former smokers have been shown to respond to both surgical and non-surgical therapy similarly to never-smokers. Implant success rates are also similar to those of never-smokers.18

People who have diabetes are about three times more likely to have periodontal disease than people without diabetes. Glycemic control plays a large role, with adults who have the poorest control exhibiting a greater prevalence and severity of inflammation and attachment loss.21 Both adults and children with diabetes have been shown to exhibit more gingival inflammation than those without diabetes.22 Periodontal destruction may start early in life for children with diabetes and become more pronounced in adolescence.23 Data has shown that in children and young adults with diabetes, 13.6% of those aged 13-18 years and 39% of those aged 19-32 years have periodontitis.23

The way that diabetes impacts the periodontium is similar to the way it induces other diabetic complications. Diabetes has been shown to alter the immune response by impairing neutrophil adherence, chemotaxis, and phagocytosis. At the same time, there is evidence of a hyper-responsive monocyte/macrophage phenotype leading to increased production of pro-inflammatory mediators in the GCF.21 The level of cytokines in the GCF have been shown to correspond to glycemic control. Patients with poor control have been found to have GCF levels of IL-1ß twice the level of people with good glycemic control.21,22 It is believed this increased amount of IL-1ß may play a role in the increased inflammation, attachment, and bone loss observed in people with diabetes.21

The evidence on response to therapy for patients with diabetes is limited. It has been observed that, over a five year period, people with diabetes who have good or modest control responded to surgery and periodontal maintenance in a similar fashion to people without diabetes. Patients who have poor glycemic control seem to have a more rapid recurrence of periodontitis and less favorable long-term outcomes.22  

 

Conclusion

There are many competing theories about periodontal disease and its link to systemic health. Microbes such as biofilms can negatively affect both oral and systemic health if not treated properly, as can general inflammation and genetic factors. Smoking increases the risk of both periodontal disease and systemic health. This article is part I of our series about periodontal disease and management. For part II of this article, visit this link.

References:

  1. Albandar JM et al. Destructive periodontal disease in adults 30 years of age and older in the United States, 1988-1994. J Periodontol 1999; 70:13-29.
  2. Eke PJ et al. Accuracy of NHANES periodontal examination protocols. J Dent Res 2010; 89:1208-13.
  3. Comprehensive Periodontal Therapy: A statement by the American Academy of Periodontology, 2010. http://www.perio.org/resources-products/pdf/periodontaltherapy_statement.pdf Accessed 02-15-11.
  4. Berezow AB, Darveau RP. Microbial shift and periodontitis. Periodontology 2000, 2011;55:36-47.
  5. Costerton JW, Schaudinn C. The secret life of biofilm. Dimensions of Dental Hygiene Educational Supplement 2011; January:8-22.
  6. Marsh PD et al. Dental plaque biofilms: Communities, conflict, control. Periodontology 2000 2011; 55:16-35.
  7. Beikler T, Flemmig T. Oral biofilm-associated diseases: Trends and implications for quality of life, systemic health and expenditures. Periodontology 2000, 2011; 55:87-103.
  8. Van Dyke TE et al. What is gingivitis? Current understanding of prevention, treatment, measurement, pathogenesis, and relation to periodontitis. Int Acad Periodontol 1999;
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  10. Delaeu N, Bickel M. Interleukin-1and interleukin-; 18: Regulation and activity in local inflammation. Periodontology 2000 2004; 35:42-53.
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  12. Kinane DF et al. Human variability in innate immunity. Periodontology 2000, 2007;45:14-34.
  13. Kinane DF, Bartold M. Clinical relevance of the host responses of periodontitis. Periodontology 2000, 2007; 43:278-293.
  14. Michalowicz BS. Evidence of a substantial genetic basis for risk of adult periodontitis. J Periodontol 2000; 71:1699-1707.
  15. Kornman KS et al. The interleukin-1 genotype as a severity factor in adult periodontal disease. J Clin Periodontol 1997; 24:72-77.
  16. Yoshie H et al. The role of genetic polymorphisms in periodontitis. Periodontology 2000, 2007; 43:102-132.
  17. Offenbacher S et al. Periodontal disease at the biofilmgingival interface. J Periodontol 2007; 78:1911-1925.
  18. Johnson GK, Hill M. Cigarette smoking and the periodontal patient. J Periodontol 2004; 75:196-209.
  19. Centers for Disease Control and Prevention. National Diabetes Fact Sheet: National estimates and general information on diabetes and prediabetes in the United States, 2011. Atlanta, GA: US Department of Health and Human Services, Centers for Disease Control and Prevention, 2011.
  20. Albandar JM et al. Cigar, pipe, and cigarette smoking as risk factors for periodontal disease and tooth loss. J Periodontol 2000; 71:1874-1881.
  21. Mealey BL, Ocampo GL. Diabetes mellitus and periodontal disease. Periodontology 2000, 2007; 44:127-153.
  22. Mealey BL, Oates TW. Diabetes mellitus and periodontal diseases. J Periodontol 2006;77:1289-1303.
  23. Lalla E et al. Periodontal changes in children and adolescents with diabetes. Diabetes Care 2006; 29:295-299.
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