Periodontal Disease Management by Risk Assessment

4. 4 �A Real Wake-up Call !�Diane Sawyer & Tim Johnson, M.D. 64% increase risk for Pancreatic Cancer Inflammation & Bacteria that can get into your Blood Stream The One Symptom: Blood If you have Bleeding: a sign of of Serious Disease It IS a Disease See your dentist & hygienists twice per year or more Tx will require antibiotics: topically & systemically

5. 5  �The Silent Epidemic� U.S. Population 74% - Perio. Infection AGD 2002 80% - Mild to Moderate ADA 2006 90% - Age 55-64: M - S AAP J Perio. Aug. 2005, 1408 David Satcher, MD, Surgeon General

6. 6 NIH NEWS � Perio Pathogens, Stroke & Heart Attack �These data mark first report of a direct association between CVD and bacteria involved in periodontal disease.� �Older Americans with higher proportions of four periodontal disease causing bacteria (A.a, P.g., T.f., P.i.) tend to have thicker carotid arteries, a strong predictor of stroke and heart attack.� Feb. issue of Circulation & supported by four agencies of NIH. Feb.7, 2005

7. 7 Acute Coronary Syndrome �The presence of specific bacteria and combinations of bacteria in periodontal pockets �.the findings suggest that T. denticola, T. forsythia and streptococci spp are bacteria in a shared infectious etiology for periodontitis and Acute Coronary Syndrome (ACS).� �Bacterial Profile and Burden of Periodontal Infection in Subjects with a Diagnosis of Acute Coronary Syndrome� J Periodont Aug. 2006 Red Complex: �Consensus Pathogens�

8. 8 Oral / Systemic Connection Heart Disease: 700 % > risk Fatal CHD: 50% > risk Stroke: 300% > risk Pre-Term Birth: 700% > risk Diabetes: > risk Rheumatoid Arthritis: > risk Aspiration Pneumonia: > risk for death Organ transplants: > risk for failure Cancer: OSC & Pancreatic

9. Periodontal InflammationsSystemic Effects Myocardial Infarction Brit Med J 298:779, 1989

10. 10 Oral infections and systemic disease- an emerging problem in medicine Clin Microbiol Infect 2007 Nov;13(11):1041-7 �The relationship between oral health and general health has been increasingly recognised during the past two decades. Several epidemiological studies have linked poor oral health with cardiovascular disease, poor glycemic control in diabetics, low birth-weight pre-term babies, and a number of other conditions including rheumatoid arthritis and osteoporosis.�

11. 11 Anders Holmlund, Gunnar Holm, Lars Lind. Severity of Periodontal Disease and Number of Remaining Teeth Are Related to the Prevalence of Myocardial Infarction and Hypertension in a Study Based on 4,254 Subjects. Journal of Periodontology 2006, Vol. 77, No. 7, Pages 1173-1178

12. 12 American Heart Journal Volume 154, Issue 6, December 2007, Pages 1086-1094 The relationship between the initiation of antimicrobial therapy and the incidence of stroke in infective endocarditis: An analysis from the ICE Prospective Cohort Study (ICE-PCS)

13. 13 Inflammation Associate With Incident Cardiovascular Disease Events Pirkko J. Pussinen; Karolina Tuomisto; Pekka Jousilahti; Aki S. Havulinna; Jouko Sundvall; Veikko Salomaa Arteriosclerosis, Thrombosis, and Vascular Biology. 2007;27:1433.

14. 14 Inflammation, heat shock proteins and periodontal pathogens in atherosclerosis: an immunohistologic study. Ford PJ, Gemmell E, Chan A, Carter CL, Walker PJ, Bird PS, West MJ, Cullinan MP, Seymour GJ. Oral Biology and Pathology, School of Dentistry, The University of Queensland, Brisbane, Australia. p.ford@uq.edu.au

15. 15 Chronic Inflammatory Autoimmune Disorders and Atherosclerosis Authors: ABOU-RAYA, S.1; ABOU-RAYA, A.2; NAIM, A.3; ABUELKHEIR, H.4 Source: Annals of the New York Academy of Sciences, Volume 1107, Number 1, June 2007 , pp. 56-67(12)

16. 16 Prim Dent Care. 2007 Apr;14(2):59-66. Links Cardiovascular and oral disease interactions: what is the evidence? Ford PJ, Yamazaki K, Seymour GJ. Oral Biology and Pathology, University of Queensland, Brisbane, Australia. p.ford@uq.edu.au

17. 17 J Med Microbiol 54 (2005), 93-96; DOI: 10.1099/jmm.0.45845-0 Molecular detection of Treponema denticola and Porphyromonas gingivalis in carotid and aorticatheromatous plaques

18. 18 Ross R, Atherosclerosis: an inflammatory disease. N Engl J Med. 1999;340:115- 126 Ridker PM. Evaluating novel cardiovascular risk factors: can we better predict heart attacks? Ann Intern Med. 1999;130:933 937.

19. 19 Lagrand WK, Visser CA, Hermens WT, et al. C-reactive protein as a cardiovascular risk factor: more than an epiphenomenon? J Circulation. 1999;100:96 102.(Abstract)

20. 20 Tracy RP, Lemaitre RN, Psaty BM, et al. Relationship of C-reactive protein to risk of cardiovascular disease in the elderly: results from the Cardiovascular Health Study and the Rural Health Promotion Project. Arterioscler ThrombVasc Biol. 1997;17:1121 1127

21. 21 Partial Literature Source Summary Arteriosclerosis, Thrombosis, and Vascular Biology Journal Journal of Clinical Microbiology & Infection American Heart Journal Journal of Periodontology Annals of the NY Academy of Sciences Primary Dental Care Journal of Medical Microbiology New England Journal of Medicine Journal of Circulation American Journal of Epidemiology American Journal of Medicine British Medical Journal

22. 22 Thanks to Dr Bill Domb for his research

24. Traditional Assessment Can traditional tests detect pathogenic biofilms?

25. Traditional Diagnostic Tests Historical Legacy Techniques

26. Disclosing Solution & Plaque Indices Only measure supragingival plaque. (typically Gram (+) & aerobic ? i.e. health) Cannot differentiate between pathogenic & non-pathogenic biofilms Mostly useful for patient motivation

27. Radiographs Mostly ID historical damage Cannot identify pathogenic risk factors

28. Pocket Depth: The Bottom Line The pocket is not the disease. It is a result of disease, not the cause.

29. Bleeding on ProbingNot Correlated with Disease

30. BOP ? Common Drug Effects Hypertension ~ 25% of adults take Rx BP medications, most of which increase capillary fragility Aspirin 325 mg daily / 7 days 12.4% Increase in BOP 

31. Pocket Depth Review Cannot distinguish between high & low risk infections Not predictive Identifies historical disease sites Fraught with measurement error

33. New Diagnostic Paradigm Identify the presence of pathogenic bacteria in the sulcular fluid

34. New Treatment Paradigm Antimicrobial therapy specific for the identified pathogens

35. Phase Contrast Video Microscopy Chairside Fast: 2 minutes Cheap: 25� / test ID�s: Morphotypes Spirochetes WBC�s  Protozoans Antibiotic Verification (efficacy/compliance) Patient Motivation!

36. Phase Contrast Video Microscopy Disadvantages Initial cost: $3-7 K No antibiotic specificity Unfamiliar technology

37. What Microbiota is Consistent withPeriodontal ?

38. What Microbiota is Consistent withPeriodontal ?

39. Treponema (spirochetes)

40. Red group + 8 Additional Pathogens Antibiotic Specificity Diagrammatic Pt. Chart Independent Lab Micro-IDent Plus

41. Micro-IDent Plus Comparison of the two methods revealed that the Micro-IDent kit identified both P. gingivalis and B. forsythus more often than did the cultivation method.

42. Micro-IDent Plus Conclusions: Nucleic acid techniques should replace cultivation methods as the gold standard in microbiological diagnosis of progressive periodontitis.

43. PeriodontitisPredominant Microbial Species Gram-Negative Anaerobic Species

44. 44 DNA-PCR TESTING �

45. 45

46. 46

47. Micro-IDent (report detail)

48. 48 Do we really realize �.? The implications of the Oral/Systemic Connection for our patients The significant health impact that only WE can make The Financial Impact the Oral / Systemic Connection can have �

49. 49 �Clearly, it will be critical that medical students, dental students, nursing students and public health students be educated about the significance of oral disease as it relates to systemic disease and about some of the things we can do to intervene.� David Satcher, M.D.,2000:U.S. Surgeon General; Oral and Whole Body Health; 40

50. 50

51. 51 Periodontal Medicine How DNA is changing our paradigm

52. 52 An entirely new aspect of perio. is currently being born: the strong relation-ship between Oral status & Systemic health.

53. 53 Consequently, a new discipline, Periodontal Medicine has emerged in dentistry which seeks to further define these interrelationships � D.W. Paquette, DMD, MPH, DMSc, J of Cont Dent Pract, Vol. 1, 1-17, 2005

54. 54 * 32% traditional tx fails within 9 months � A. Haffejee,, J Clin Periodon 1997;24:324-334 * 64% Tx fails over time � Rosling B, J Clin Periodontol 2001;228:241-249

55. 55 �Keys� to FAILURE� �A poor treatment response �persistence of periodontopathogenic species� �After treatment, DNA extraction revealed: 86% of patients were positive for pathogenic microorganisms.� J Clin Perio Supp 7, Vol 33, 2006 >32% have Genetic Predisposition for inflammatory infections Korman; J of Period, 1997

56. 56 Something�s wrong with our present Oral Health System � We are treating �Plaque, Calculus & Pockets� While we should be treating �Wounds� caused by very toxic/virulent organisms In people that are often Genetically Predisposed and have high risk for Systemic Diseases

57. 57 �Pocket� vs. �Wound� � When the gingival attachment is lost due to the pathogenic bacterial invasion, the body has lost an important protective component. As a result, we have an open, infected wound all the way to bone level. (A true invasive infection) Why shouldn�t we treat this infected wound using the same medical concepts of other infected wounds?

58. 58 Important Information ��most patients receive essentially the same anti-infective therapy, despite the recognition that subjects differ in the composition of their subgingival microbiotas. The �standard� therapy may be appropriate for the subgingival microbiota in one individual, but not in another.� �Conceivably, when the most appropriate therapy is matched to a subject�s Specific Microbial Profile, the reductions in the individual's pathogenic complex will be greater and more reproducibly sustained, leading to long-term clinical stability.� Microbiological goals of periodontal therapy; Periodontol 2000; Vol. 42, 2006, 180-218: Teles, Haffajee, Socransky

59. Tissue Invasion Some Species invade gingiva to become partially independent of the original biofilm Life Below the Gum Line:Pathogenic mechanisms of Porphyromonas gingivalis. Lamont & JenkinsonMicrobiol & Molecular Biol Rev 62:1244-1263 1998 Ecosystems: Development, functions & consequences of disturbances with special reference to the oral cavity. Midtvedt, J Clin Periodontol 19: 348-356 1992

60. Periodontal InflammationsCardiovascular Risk �Why? Biofilm inflammations aresimilar to systemic infections

61. Microbiological AssessmentGenco Recommendations - 1986 Although all specific pathogens have not been defined,a sufficient number of important pathogens are knownand testing for these organisms is, therefore, indicated. Technologies have been developed to the point whererapid microbiological tests are feasible and practical. The rationale for (microbial) assessment and the present level of technology making such assessment feasible, strongly supports the use of microbiologic assays as adjuncts in the clinical management of periodontal disease.

62. Finally, in 2003AAP on Microbiological Diagnosis Plaque-induced periodontal diseases are mixed infections associated with relatively specific groups of indigenous oral bacteria. Susceptibility to these diseases is highly variable and depends on host responses to periodontal pathogens. Presently, the diagnosis & classification of periodontal diseases are almost entirely based on traditional clinical assessments. Supplemental quantitative & qualitative assessments of the subgingival microflora can potentially provide useful information about the patient�s periodontal disease [and] may be particularly valuable in establishing the endpoint of therapy.

63. Periodontology 2000 The vast majority of periodontal diseases are caused by microorganisms that reside at or below the gingival margin. The best way to control periodontal infections is to control the pathogenic species residing in these locations. Actinobacillus actinomycetemcomitans, P. gingivalis & Tannerella forsythia were designated periodontal pathogens at the 1996 World Workshop in Perio. Since then, evidence for a number of other species, including: Prevotella intermedia, Prevotella melanino-genica, Fusobacterium nucleatum, P. micros, Eubacterium spp., Eikenella corrodens, Prevotella nigrescens and Spirochetes has gotten stronger.

64. Microbial Testing A. actinomycetemcomitans and P. gingivalis cannot be removed from a significant part of deep periodontal lesions by mechanical therapy alone. Slots J, Ting M. Systemic antibiotics in the treatment of periodontal disease. Periodontol 2000 2002: 28: 106�176. The percentage of A. actinomycetemcomitans and P. gingivalis may even increase following scaling and root planing. Mombelli A, McNabb H, Lang NP. Black-pigmenting gramnegative bacteria in periodontal disease. II. Screening strategies for detection of P. gingivalis. J Periodontal Res 1991: 26: 308�313.

65. Diagnostic ? Diagnostic Consequences

66. Traditional Periodontal Assessment