Your oral health: How periodontal inflammation is connected to disease

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How periodontal inflammation is connected to overall health -- you'd be surprised at the connection

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Your oral health: How periodontal inflammation is connected to disease

  1. 1. In fla m m a tio n a n dP e rio d o n ta l Dis e a s e sA paradigm shift in periodontology and what itmeans for patient care
  2. 2. Outline of Presentation All about inflammation: the paradigm shift in periodontology Inflammation, periodontal disease and cardiovascular disease Inflammation, periodontal disease and other disease states Risk factors for periodontal disease Treatment of periodontal inflammation Five Things to Remember Future Directions and Questions 2
  3. 3. Media Coverage Re ce n t Ne w s Co ve r a g eThe Bos ton Globe November 2, 2009 )Audience: 713,083) We bMD January 12, 2010 (Audience: 10,845,896) Ea ting We ll January 1, 2010 (Audience: 530,309) Me n’s He a lth January 1, 2010 (Audience: 7,438,572) Me dica l Ne ws Toda y February 20, 2010 (Audience: 1,800,000) 2
  4. 4. Periodontal Disease: A Quick Overview Periodontal disease is a chronic inflammatory disease that destroys the bone and gum tissues that support the teeth. The American Academy of Periodontology (AAP) estimates that 3 out of 4 Americans are affected by periodontal disease, ranging from mild gingivitis to more severe periodontitis. If left untreated, mild cases of gingivitis can lead to periodontitis.
  5. 5. Periodontal Disease However, the periodontal disease of yesterday is not the periodontal disease of today.  Yesterday: researchers believed that gum loss in periodontal disease was caused by the bacteria in plaque.  Today: researchers have determined that the gum loss in periodontal disease is caused by the inflammatory response to the bacteria in plaque. 5
  6. 6. J Periodontol 2008;79:1560-1568. 43
  7. 7. What is Inflammation? Inflammation is the body’s first response to an injury. The first phase (acute inflammation) includes redness, swelling, heat, and altered function. It is self-perpetuating. There are several biological markers of inflammation in your blood, including C-reactive protein (CRP).  CRP is a protein found in the blood which can rise in response to inflammation.  Acute inflammation often causes elevated C-reactive protein.  Elevated CRP is a risk factor for several chronic inflammatory diseases. Inflammation appears to be a common link between several common diseases of aging.  These diseases include heart disease, arthritis, and periodontitis. 6
  8. 8. Examples of Inflammation Sunburn Infection A cut on the skin 7
  9. 9. Inflammation’s Objective Inflammation tries to contain the injury to the local site. The body’s reaction is immediate (called the innate response). Its ultimate purpose is to protect the body from further damage. 8
  10. 10. Inflammation is Damaging when Uncontrolled Though inflammation can be helpful under certain conditions, uncontrolled inflammation, also called chronic inflammation, is harmful and causes tissue loss. Chronic inflammation occurs when there is a sustained infection, like periodontitis. Chronic inflammation involves more inflammatory mediators than the immediate innate response. 9
  11. 11. Chronic Inflammation Chronic inflammation can negatively affect all organs and tissues of the body. Chronic diseases of aging are connected through common chronic inflammatory mechanisms. 10
  12. 12. Periodontal Paradigm Shift: Because of this new focus on inflammation, there has been ashift in the way periodontists view periodontal disease and its relationship to other disease states. 11
  13. 13. Periodontitis is a Chronic Inflammatory Disease of Aging Periodontitis involves a microbial challenge to the gums which stimulates an inflammatory response Genetic and acquired risk factors lead to immuno-inflammatory response A prolonged immuno-inflammatory response leads to destruction of connective and bone tissues, which leads to the possible loss of teeth. Chronic inflammatory diseases, such as periodontitis, arise over decades. Periodontal disease is a significant contributor to the total inflammatory burden on your body and can adversely affect your systemic health. 12
  14. 14. “Inflammation and Periodontal Diseases: A Reappraisal” In January 2008 a workshop sponsored by the AAP brought together more than 80 leading experts:  Periodontists, cardiologists, diabetologists, geneticists, gerontologists, inflammation researchers This was an opportunity to engage in collaborative thinking and brainstorming across many different fields- using inflammation as a common finding. 13
  15. 15. Workshop, cont. The workshop was developed to expand and advance our understanding of inflammation and the role it plays in diseases of aging. The experts from the diverse fields addressed topics of inflammation:  What is inflammation?  What specific mechanisms constitute inflammation?  What factors regulate inflammation?  Why do individuals have different expression levels of inflammation?  Is the inflammation in one disease common to the inflammation in other diseases? 14
  16. 16. Workshop, cont. The experts engaged in discussion of the future of inflammation therapies and how they may change the future of periodontics. Proceedings from the Workshop were published in a supplement to the Journal of Periodontology in August 2008. (Available for free at: http://www.joponline.org/toc/jop/79/8s) 15
  17. 17. Workshop, cont. What we learned:  Periodontal disease is a bacterially-induced chronic inflammatory disease that does not resolve by itself.  The inflammatory response is extremely complex .  Environmental and genetic factors affect expression of inflammation in individuals .  The initiation and resolution of inflammation are well controlled processes.  Diabetes, CVD, and stroke all share common inflammatory processes similar to periodontal inflammation.  Resolution of any inflammation in the body is helpful for overall health. 16
  18. 18. The Workshop helped highlight the relationship between various disease states, and suggested that inflammation may be the basis for these relationships. 17
  19. 19. Perio-Cardio Link:The relationship between periodontaldisease and cardiovascular disease (CVD) 18
  20. 20. Cardiovascular Disease: A Quick Overview Cardiovascular disease generally refers to conditions that involve narrowed or blocked blood vessels that can lead to a heart attack, chest pain (angina), or stroke. The American Heart Association reports that cardiovascular disease is the leading killer of men and women in the United States.
  21. 21. Inflammation and CVD Inflammation contributes to heart attacks as much as or more than cholesterol.* Atherosclerosis always begins with injury to the endothelium of blood vessels.  Periodontal pathogens have been found in atherosclerotic lesions. 19*Ridker PM, et al. N Engl J Med. 2005 Jan 6;352(1):20-8.
  22. 22. Periodontal Disease and CVD Data derived from meta-analysis: meta-analysis combines the results of several studies that address a set of related research  Five prospective cohort studies hypotheses  Five cross sectional studies Ability to control for between-study variation  Five case control studies Subjects with periodontitis had a 1.14 - 1.59 fold greater risk for developing CVD compared to those without periodontitis.  Adjustments made for risk factors: smoking, diabetes, alcohol intake, obesity and blood pressureBahekar AA, Singh S, et al. Am Heart J 154:830-837, 2007 19
  23. 23. C-Reactive Protein (CRP) CRP is a protein found in the blood that reflects the amount of inflammation in your body. Periodontitis and other sources of inflammation elevate CRP levels. Elevated CRP is a direct risk factor for CVD. 20
  24. 24. AJC-JOP Consensus Paper The American Journal of Cardiology contacted the AAP after reading the August 2008 Journal of Periodontology supplement from the Workshop on Inflammation. A consensus paper was developed in collaboration with the American Academy of Periodontology and top cardiologists. The paper was published simultaneously in the Journal of Periodontology and the American Journal of Cardiology in June 2009. 21
  25. 25. AJC-JOP Consensus Paper, cont. The consensus paper is a summary of research that shows a connection between periodontal disease and CVD. It explains the underlying biologic and inflammatory mechanisms that may be the basis for the connection. Clinical recommendations for treating patients with cardiovascular disease and periodontal disease are also included. 22
  26. 26. CVD-PD Clinical Recommendations Examples of the clinical recommendations:  Dentists are asked to consider their patients’ heart health and risk for CVD.  Assess risk factors for CVD such as smoking and family history of CVD  Physicians are asked to consider their patients’ periodontal health and risk for periodontal disease.  Assess symptoms such as tooth loss or bleeding and swollen gum tissue  All health professionals are asked to educate patients on chronic inflammatory diseases and how they are related.  Health professionals are also asked to work together to ensure patients are in best health. 23
  27. 27. The Relationship of Periodontal Disease to Other Inflammatory Diseases Inflammation appears to be the basis for the association between oral and systemic disease. One chronic inflammatory disease potentially influences the expression of other diseases:  Tissue destruction is caused by prolonged inflammation.  Moderate/severe periodontitis increases systemic inflammation.  Systemic inflammation is associated with most chronic diseases of aging.  For example, periodontal disease influences diabetes and diabetes influences periodontal disease. 24
  28. 28. The Relationship of PeriodontalDisease to other Chronic InflammatoryDiseases of Aging  Cardiovascular disease  Arthritis  Diabetes  Alzheimer’s Disease  Cancers 25
  29. 29. Arthritis Arthritis (Rheumatoid arthritis and osteoarthritis) is an inflammation of the joints. Patients with arthritis have a higher incidence of periodontal disease compared to healthy controls.* Source: National Institutes of Health Periodontal treatment decreases arthritis parameters:**  Patients’ number of swollen and tender joints decreased following periodontal treatment.  Patients’ assessment of pain also decreased following periodontal treatment.*Pischon N, et al. J Periodontol. 2008 Jun;79(6):979-86.**Ortiz P, et al. J Periodontol. 2009 Apr;80(4):535-40. 26
  30. 30. Diabetes Worldwide incidence is expected to increase with increased prevalence of obesity. Major public health burden because of serious microvascular sequelae.  nephropathy  retinopathy  neuropathy  cardiovascular disease  periodontitis Total annual costs exceed $132 billion in US alone 28
  31. 31. Risk Factors for Diabetes Genetics Diet Sedentary lifestyle Perinatal environment Age Obesity Chronic Inflammation  Type I and Type II Diabetes 28
  32. 32. Diabetes Type I Diabetes  Adolescents and young adults  Autoimmune destruction of pancreatic islet cells that produce insulin  Increased CRP in patients with long termed type I diabetes Type II Diabetes  Occurs mainly in adults but prevalence among young people increasing due increase in childhood obesity  Characterized by increased cellular non responsiveness to insulin (insulin resistance)  Pancreatic beta cells do not secrete sufficient insulin 28
  33. 33. Diabetes Hyperglycemia inhibits the resolution of inflammation. High CRP and IL-6 promotes insulin resistance. Patients with diabetes are three times more likely to have periodontal disease. Controlling periodontal disease helps control blood sugar levels. Insulin 28
  34. 34. Obesity Patients with a higher body mass index (BMI) tend to have higher levels of CRP. Calorie reduction leads to decreased gingival bleeding and rate of periodontal disease progression.**Branch-Mays GL, et al. J Periodontol. 2008Jul;79(7):1184-91. 30
  35. 35. Alzheimer’s Disease Progressive intellectual failure and a major cause of dementia Pathologic hallmarks:  amyloid plaques and neurofibrillary tangles which are distributed in the frontal neocortex and limbic system Alzheimer’s Dz is an innate inflammatory response in an attempt to remove the amyloid deposits from the brain 27
  36. 36. Alzheimer’s Disease Antibodies and immune cells cross the blood brain barrier. Exposure to chronic periodontal disease quadruples an individuals risk of developing Alzheimers disease.**Watts A, et al. Neuropsychiatr Dis Treat.2008 Oct;4(5):865-76. © 2000 - 2009 American Health Assistance Foundation 27
  37. 37. Cancers Pancreatic cancer  Men with a history of gum disease are 54% more likely to develop pancreatic cancer than men with healthy gums.* Head and neck cancers  Chronic periodontitis is independently associated with the incidence of head and neck cancers.**  Smoking increases this association.*Michaud DS, et al. Lancet Oncol. 2008 Jun;9(6):550-8. Epub 2008 May 5.**Tezal M, et al. Cancer Epidemiol Biomarkers Prev. 2009 Sep;18(9):2406-12. 29
  38. 38. Other Inflammatory Diseases Asthma and other chronic respiratory diseases Osteoporosis Kidney disease Metabolic syndrome 31
  39. 39. Risk Factors for Periodontal Disease Genetic risk factors  Can be minimized with proper diet, exercise, and oral hygiene. Biological risk factors  Other systemic diseases of inflammation may increase the risk of periodontal disease.  Predisposition to inflammatory conditions such as obesity, diabetes, or CVD 32
  40. 40. Risk Factors for Periodontal Disease, cont. Behavioral risk factors Biologic Risk Factors  Poor oral hygiene  Smoking (specifically, nicotine intake)  Smokers have higher levels of CRP.  Stress  Sleep deprivation  Poor diet Behavioral Risk Genetic Risk Factors Factors 33
  41. 41. Treatment of Periodontitis Reduction of tissue inflammation Reducing one type of inflammation may reduce another:  Patients with periodontitis and rheumatoid arthritis who received periodontal treatment:  Reduced inflammation in periodontal tissues.  Reduced severity of RA symptoms.** Ortiz P, et al. J Periodontol. 2009 Apr;80(4):535-40. 35
  42. 42. The good news is that inflammation levels can be reduced.When chronic inflammation is controlled, the associated chronic inflammatory diseases may be controlled. 36
  43. 43. How to Reduce Inflammation: What does this mean for patients? Reduce direct sources of inflammation:  Visceral fat  Exercise  Reduce calories  Chronic infections  Periodontists can help reduce inflammation in the oral cavity. Have your teeth professionally examined and cleaned regularly. Stop smoking. Activate inflammation resolution systems:  Add Omega-3 fatty acids to your diet.  Take a daily low-dose aspirin. 37
  44. 44. J Periodontol 2008;79:1601- 1608. 43
  45. 45. Inflammation: 5 things to remember1. There has been a paradigm shift in the field of periodontology. Periodontal disease today is defined by the inflammatory response to the biologic components of plaque. 38
  46. 46. Inflammation: 5 things to remember2. The relationship between periodontal disease and other chronic inflammatory diseases of aging is better understood. These diseases include cardiovascular disease, respiratory diseases, diabetes and arthritis. 39
  47. 47. Inflammation: 5 things to remember3. Treatment of chronic oral inflammation should be done by trained dental professionals. Co-management with periodontal specialists to help in evaluating, diagnosing, and treating periodontal inflammation and disease. 40
  48. 48. Inflammation: 5 things to remember4. Reducing inflammation in the body can reduce the occurrence and severity of chronic inflammatory diseases. 41
  49. 49. Inflammation: 5 things to remember5. Dentists and physicians need to work together to ensure the best health of their patients. 42
  50. 50. Conclusions: Future Directions A paradigm shift is occurring in both medicine and dentistry in our understanding of preventing many of today’s systemic diseases. The incidence and amount of inflammation that patients experience may be critical to the onset and progression of certain systemic diseases. Prospective treatment studies are needed that define whether or not periodontal treatment makes a substantial difference in the expression of certain diseases. As we wait for such studies, we should educate our patients about what is known and to help them manage their own health by assisting in the reduction of inflammation. 43
  51. 51. Future Directions Significant clinical limitation in diagnosing and monitoring periodontal inflammation  gingival inflammation and bleeding  periodontal pocket depth  gingival attachment level Classical approaches to controlling periodontal inflammation rely on attempts to suppress bacteria that incite inflammatory response  Mechanical (SC/RP, flap surgery)  Chemical (antimicrobials, antibiotics) Emerging and future approaches need to rely more on  Modifying the inflammatory response itself  Limiting the activities of pro-inflammatory pathways, effector cells and mediators 43
  52. 52. Pathogenesis of Periodontal Disease P in k, He a lth y Tis s u e , No Clin ic a l S ig n s o f Dis e a s e Go o d Ora l Hyg ie n e Lo w S u s c e p tib ility He a lth No S ys te m ic Ris k Fa c to rs Na tu ra l En zym e In h ib ito rs Tis s u e De s tru c tive En zym e sBalance of Tissue Destruction in the Periodontium
  53. 53. J Periodontol 2008;79:1592-1600. 43
  54. 54. Pathogenesis of Periodontal Disease P o o r Ora l Hyg ie n e Dis e a s e S ys Hig hicSRisckeFatibto rs te m u s p ility cNa tu ra l En zym e In h ib ito rs • S m o kin g • Ge n e tic s • Dia b e te s Ove rp ro d u c tio n Tis s u e De s tru c tive En zym e s Imbalance of Tissue Destruction in the Periodontium
  55. 55. Pathogenesis of Periodontal Disease Na tu ra l En zym e In h ib ito rs Dis e a s e Ch ro n ic Ove rp ro d u c tio n Tis s u e De s tru c tive En zym e sS tudie s s how s moke rs (Bo n e Lo s s , De e p e r P o c ke ts Are ha ve a le s s fa vora ble Gre a tly Affe c te d )re s pons e to tra ditiona l Smokers mode s of pe riodonta l the ra py Imbalance of Tissue Destruction in the Periodontium
  56. 56. Pathogenesis of Periodontal Disease He a lth S RP + P e rio s ta t Dis e a s e S m o ke rs S m o kin g in c re a s e s le ve ls o f P ro -in fla m m a to ry m e d ia to rs ; in c re a s e re le a s e o f d e s tru c tive c o lla g e n a s e Na tu ra l En zym e In h ib ito rs Tis s u e De s tru c tive En zym e s P e rio s ta t® d e c re a s e s le ve ls o f P ro -in fla m m a to ry m e d ia to rs ; d e c re a s e o f c o lla g e n a s eAd d in g P e rio s ta t tip s th e b a la n c e to wa rd s p e rio d o n ta l h e a lth
  57. 57. The Future of Periodontal Diagnosis Traditional diagnostic (i.e. PD, AL, BOP, etc.) measures are informative to evaluate disease severity. We need diagnostic determinants of disease activity. Extensive research has been ongoing in this area since the 1990’s  Presence of biomarkers of measured with the gingival crevicular fluid (GCF)  Presence of biomarkers present within saliva 43
  58. 58. Gingival Crevicular Fluid Most appropriate analytical fluid of choice because it was specific to the periodontal tissues The three most promising biomarkers for predicting future disease activity  Beta-glucuronidase  Alkaline phosphatase  Cathepsin B Many diagnostic kits emerged based, many of which demonstrated high levels of sensitivity and specificity demonstrating disease activity at site level. 43
  59. 59. Gingival Crevicular Fluid Problems  Too time consuming to perform  Site specific - the choice of site was problematic  168 potential sites within the mouth to examine  Too costly for routine use  Results did not translate to changes in therapeutic intervention 43
  60. 60. Saliva Medium of choice in the 21st Century. Contains microbial and host response mediators. Simple to collect using non-invasive techniques. Provides whole mouth summary analysis. Already used as a diagnostic fluid for:  Determining hormone levels  Drug detection  Presence of HIV or Hep C virus 43
  61. 61. Saliva Problems  Assays need to be highly sensitive.  Biochemistry varies with its origin (whole saliva or specific gland secretions)  Not possible to fully quantify markers within saliva using chairside technologies. Qualitative analysis may be all that can be achieved  Saliva contains mucins and cell debris making it challenging to work with. 43
  62. 62. Saliva Identify the biomarkers for periodontitis - aid in diagnosis and therapeutic monitoring of disease activity. Difficult due to the complex nature op periodontal disease - no single etiology with multiple risk factors. Periodontal researchers do not fully understand the pathogenesis of periodontitis. However, identification of biomarkers the characterize periodontal tissue destruction will be attainable 43
  63. 63. Question? Can salivary testing for inflammatory biomarkers be a way for medical profession to screen patients for periodontal disease and the dental profession to screen patients for cardiovascular disease, diabetes and systemic diseases? 43
  64. 64. QuickTime™ and a decompressorare needed to see this picture. 43

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