You can feel free to contact me about any information in this talk or for references. Please be as specific as possible about any references you will request as I have used approximately forty references to back up this discussion today.
The outline for my discussion is as follows: Nonspecific plaque hypothesis – The idea is that all plaque is equally pathogenic. This is still taught in dental schools around the world. This idea was originated in the 1890s by Dr. Miller after his failure to isolate any specific bacteria from caries or periodontal lesions. I will discuss this theory simply to develop a historical perspective. Specific plaque hypothesis – new theory developed after 1975. 8 This theory was developed by Dr. Loesche and Dr. Keyes among others through their extensive research which continues to this day. 8,12-15,18-21,25,26,28-30,32 Without the research support for this theory developed by Dr. Keyes and Dr. Loesche, it would be difficult for dentists to use these ideas in clinical practice since the specific plaque hypothesis and the practitioners who use it have been under attack by the Luddites of our profession. The Luddites were craftsmen from the beginning of the Industrial Revolution who organized people to throw wrenches into the steam powered factory machinery in an attempt to stop the development of industry. Just as in the struggle for industrial development which was carried out at the expense of the craft industries of that era, the fact that treatments based on the specific plaque hypothesis are cheaper, less painful, more cosmetically pleasing and more effective 33 have caused continued improvement by clinicians and product development by companies to improve and support our methods. I believe our methods will ascend to become dominant in the future based on proven superior performance for patients and obvious economic benefits in a era of searching for more cost effective ways to deliver health care. Companies involved: Hydrofloss – irrigation equipment. Oratec - microscope supplies, support for education, irrigation supplies. Diamond General Probe- sulphur detection/periodontal probe detects anaerobic bacterial activity This probe has promising initial results.
Here is a section of mural from the Diego Rivera Court at the Detroit Institute of Arts which depicts the labor intensive nature of automobile production just after WWII. Auto manufacturers would never consider to produce automobiles in this manner today. It was the scientific development of materials sciences and computer controls of machinery which has caused the move away from these antiquated wasteful methods.
We stand now at the beginning of a new stage of development in our profession. This new period will be characterized by more attention to evidence based models of prevention, diagnosis and treatment with the goal of developing the most cost effective health care delivery to out public. There will be more emphasis on serving the public actively, assisting them to achieve their best health through preventive medicine. With improvements in preventive screening tests, computer modeling and predictions based on large database analysis, preventive medicine is becoming more predictable than ever. It is time to use the science developed by our researchers in our public research institutions to change clinical practice. We need to move away from antiquated, surgically oriented methods towards a brighter future of prevention. In the future we will do much more screening using some of the brilliantly conceived tests developed and we will reduce our reliance on surgery as well as improving outcomes. Good website for modern gum treatment http://loeschelabs.dent.umich.edu/ Treatment can be more effective, less painful and less costly. These advantages are a reality today in my practice and in the clinics of many dentists who have trained with the International Dental Health Foundation. WEBSITE http://members.aol.com/idhf/ Unfortunately, there are very few of us who practice in this modern manner so the vast majority of patients do not have access to these advanced methods. I believe as a profession we can change this reality and bring the advanced treatments to the entire public of the United States and the world.
The nonspecific plaque hypothesis maintains that all plaque has equal potential to cause destructive dental disease. This means one does not need to differentiate disease associated plaque from health associated plaque because no differences exist between the dental plaque present in healthy mouths and those present in the mouths with periodontitis and rampant caries. 8 Historically, periodontal treatment developed around the idea that caries and periodontitis was caused by nonspecific bacterial overgrowth. These ideas led to treatment protocols designed to suppress the entire flora by removing plaque from tooth surfaces as thoroughly as possible every day. When plaque control failed, surgical intervention allowed better plaque control. When surgery failed, broad spectrum antibiotics were used in attempts to suppress the entire plaque flora without regard to the possibility that only certain specific species were responsible for the infections. This idea was first forwarded by Miller in the 1890’s to explain the cause of caries. Miller developed his ideas after failing to isolate specific bacteria from carious lesions. We know now that the periodontal pathogens are anaerobic 8,15,17 and that it would have been impossible for Miller to isolate and grow these since he did not use anaerobic chambers.
Miller’s nonspecific plaque hypothesis was first invalidated by studies which demonstrated qualitative microbiologic species differences between health associated and disease associated dental plaques in animal experimental models. With references from studies conducted in the 1960’s and 1970’s, Loesche compiled a table of three broad types of plaque associated with health caries and periodontitis. 8 Keyes, Rams also demonstrated bacterial profiles associated with health and periodontal disease. They published these profiles in June 1983 in JADA in an article entitled, “A rationale for management of periodontal diseases: rapid identification of ‘therapeutic targets’ with phase contrast microscopy” Loesche has reported in a recent literature review work 37 that there have been over one hundred studies in the last twenty five years comparing periodontal disease associated microflora with health associated microflora. Loesche has summarized the results of these studies and identified three bacterial species which are consistently associated with periodontal infections. Treponema denticola, Porphyromonas gingivalis and Bacterioides forsythus have been statistically associated with Early onset Periodontitis, , Adult Periodontitis and Refractory Periodontitis. These three types of periodontitis represent the vast majority of treatment cases in general practice today.34 This has resulted in his development of the BANA assay which uses enzyme hydrolysis technology to identify these three types of bacteria. Though this test does not differentiate between species, it may not be necessary since they are all sensitive to metronidazole as a systemic agent and locally(topically) delivered iodine as well as other irrigation agents. 35
Since no difference in pathogenicity of plaque is recognized in the nonspecific model, no bacterial testing is considered necessary. Current standard diagnostic testing in the nonspecific model is limited to historical measurements such as radiographs, visual examination, probing depth and inflammation scores. These tests have been demonstrated to have little predictive value and limit the clinicians role to documenting continuing damage caused by anaerobic infections. Diagnosis in the nonspecific model consists chiefly of classification of severity of the historical anatomic damage to the patient such as Class II, localized Class III periodontitis meaning pocket depths 4-6mm throughout the mouth with localized greater than 6mm. There are no predictions for the future of this patient only advice and surgery prescriptions designed to improve plaque control.
The nonspecific plaque hypothesis proposes that in order to become healthy a patient must maintain perfect plaque control and that any development of gum disease results from the failure to remove plaque adequately. Periodontal disease is well known to result in loss of attachment of gingival tissues to the teeth causing periodontal pockets around the teeth. Following the development of pockets if the disease is not treated successfully, the pockets will increase in depth and loss of supporting bone will result. The nonspecific plaque hypothesis proposes that the destruction of tissue is caused by failure to remove plaque in pockets so surgery is prescribed to cut away excess tissue and allow the patient ability to more adequately clean the area surrounding the teeth. This surgery is quite invasive and causes postsurgical pain, sensitive teeth and causes permanent loss of attachment with each gum surgery of 1-2 mm. 26,27
Clinicians have noted for a long time that Certain patients cause problems for this model since they maintain healthy gingival tissues despite failure to clean plaque off their teeth. These people are considered fortunate to be ”genetically predisposed” to health. Today for example I saw two new patients – cohabiting spouses both whom had not had dental treatment of any kind for eight years and they do not floss. Neither had perfect plaque control and both had subgingival tartar deposits. Neither had any signs of periodontal disease. Their bacteriologic testing revealed absence of anaerobic bacteria in subgingival plaque. This first citation revealed some important contradictions in the current model which the researchers pointed out. The next few slides document some important clinical studies comparing the effects of nonsurgical vs. surgical treatment of gum disease. The first controlled clinical study comparing surgical and nonsurgical treatment was carried out at University of Michigan by Ramfjord and Nissle in 1968. No comparative treatment study could be found in the literature prior to that date. Treatments up to that date were conceived simply from clinical impressions about what worked. This study utilized subgingival curettage for its nonsurgical method and gingivectomy (pocket reduction surgery) for its surgical method. The study was of split mouth design and the results were as follows:
The most significant finding is the gain in attachment that occurred following curettage and periodic scaling in deep periodontal pockets (>6mm). Dr.Ramfjord wrote, “The statistically significant total gain of attachment following subgingival curettage compared with a slight loss following surgical pocket elimination obviously will call for revision of current practice if these results are confirmed by more extensive studies.” Our current standard of care would include modified Widman flap surgery and would not be characterized as pocket elimination and scaling and root planing which may be less invasive than gingival curettage. The results of this study held up well in the following two studies as we shall see.
This study is also split mouth design where half of the mouth is treated with scaling alone the other half with scaling followed by modified Widman flap surgery. No infection control methods were administered except local debridement followed by oral hygiene instructions and three month follow-up prophylaxis. The results were as follows: 1) Treatment results following scaling versus scaling plus modified Widman flap surgery were maintained over a 6-1/2 year period. 2) Pocket depth did not change in shallow pockets (1-3mm deep) over 6-1/2 years for either treatment. 3) For pockets 4-6mm deep, both treatments resulted in equally effective and sustained pocket reduction. 4)
The conclusions here are interesting. If there are no differences between effectiveness of procedures what patient would authorize surgery if they were informed that they could likely do just as well without it. Surgery is more painful, more expensive and more debilitating causing root sensitivity, clinically long crowns, etc. Yet scaling alone is equally effective at treating the disease. Though it is contradictory to the scientific evidence, periodontal surgery is still being prescribed for large percentages of patients when scaling alone will result in roughly equivalent results as scaling with surgery. Methods of intimidation have been utilized to turn dental students away from scientific evidence. For example one young woman related to me that the answer she received from clinical instructors at University of Michigan was that in Dr. Nissle’s hands those results will work but that most dentists lacked the expertise to carry out successful curettage and that they would be better off doing surgery. Just a word about our medico legal obligations here. A large majority of my patients who have been attracted to our office by the possibility that they do not need periodontal surgery have stated they were never informed by their previous dentist that there were alternatives to the surgery. Usually they were told they needed the surgery. It is part of the civil law governing medical practice that patients must be informed of risks benefits and alternatives to any treatment proposed to satisfy informed consent. However, it appears that this is rarely satisfied prior to periodontal treatment. Please note that the results reported by Dr Ramfjord and Nissle were indeed supported by this study as well. These studies should have resulted in significant changes in the clinical treatment standards in this country but these important changes in standard of care have yet to come about. The next study is virtually a repeat of the previous one. Both of these follow-up studies referred to the Ramfjord, Nissle study as they were designed to repeat the first study.
This last study in the series was done partly to determine if plaque control was important. The results which follow generally support the previous two similar studies. These studies are important because they document that patients generally do not have superior results of treatment following surgical intervention even though there was no infection control employed during treatment. After extensive clinical experience and more supportive research, we know that nonsurgical treatment of gum disease with the addition of infection control results in significant improvement in treatment results compared to current standards. 15,18,28-33
There was much confusion introduced by these comparison studies and there was great resistance to the idea that possibly surgery might not be necessary for adequate treatment of periodontal disease. A new rationale justifying periodontal surgery of “quality of debridement” was published with this study. IDEA: – clean the roots better by seeing them first. In my opinion this represented pure desperation trying to develop a new rationale to protect a profitable revenue stream that could only be scientifically supported in limited usage. The next topic is the Specific Plaque Hypothesis. This new theory promises to clear up a lot confusion for practitioners and take periodontal therapy to new success levels along with making it more comfortable for patients.
The concept of the Specific Plaque Hypothesis (SPH) has been advanced by Dr. Walter Loesche in 1976. 8 The significant statement is as follows: “only certain plaques cause infections, because of the presence of a pathogen(s) and/or a relative increase in the levels of certain indigenous plaque organisms. The SPH requires that a diagnosis of infection be made so that prompt mechanical and/or chemical therapy can be initiated in order to restore the normal plaque flora.” This hypothesis is currently accepted as fact and is used to guide the diagnosis and therapy by many clinicians. The requirement of bacteriologic diagnosis is one significant difference. When the clinician utilizes microbiologic testing, a measure of predictability of results is attained which was never before possible. Keyes etal demonstrated that certain plaques were associated with periodontal disease and others were associated with periodontal health. He demonstrated the usage of morphotype screening using phase contrast microscopy to differentiate between health associated and disease associated dental plaques.15 Loesche developed the BANA test to detect pathogenic microbes which were statistically associated with periodontal disease. Those bacteria detected are P. gingivalis, P. forsythus and Treponema denticola. This test is used at chairside and takes approximately 10 minutes to complete including the 5 minute incubation time determined to give the best results. I have personally completed over 5000 samples with this test and I can vouch for its ease of use and practicality. 35 After this slide show we will take a short break so I can bring up preliminary data in our clinical study which now has approximately 1000 patients who have had active and maintenance treatment over the last three years.
Diagnosis with SPH – screening guidelines There is a need to have high quality predictive tests in order to be able to detect those patients who have active disease. This will become increasingly important if the recent studies associating gum disease with heart disease are confirmed. This is because gum disease as a risk factor for heart disease is modifiable (i.e. the infections can be treated and cured potentially eliminating the risk factor for heart disease). How do we do it in our clinic? Take four samples, split between BANA and microscope slide wet mount preparation. IDHF and Oratec representatives can prepare you to do this technique properly. We do the bacteriology on all adult patients on their first visit. Children with gingivitis have bacteriologic screening on their first visit. The total time taken for this testing is 5 minutes with explanations to patients taking an additional 15 minutes. Diagnosis of anaerobic infection is critical to assess who needs treatment. The historical diagnostic tests have little or no prognostic value. Not all pockets are equivalent. A pocket with healthy plaque is OK since the disease will arrest when the pathogens are gone. For nonresponsive or “refractory” cases, it may be useful to use culture and sensitivity although I have found this to be an impractical path to take due to high cost to the patient and the fact that metronidazole will effectively treat most anaerobes. I would suggest utilizing culture and sensitivity only on refractory cases at the doctors discretion.
This is from Keyes Rams JADA 1983
Treatment protocols differ significantly with Specific Plaque Hypothesis. Diagnosis of periodontitis (the existence of the process of gum disease) is accomplished by of visual examination to detect signs of gingival inflammation, bleeding and damage to periodontal structures in the form of pockets around teeth and bone loss detected on radiographs. Diagnosis of anaerobic infection assesses who needs treatment. Treatment involves local debridement (scaling and root planing) followed by topical 0.5% iodine irrigation and/or systemic antibiotic treatment which helps select in favor of healthy bacteria and alters character of dental plaque to low risk profile. Recall the slide on infected vs. uninfected plaque. Debridement (scaling and root planing) should always precede the prescription of antibiotics as has been demonstrated by studies. The only time I will prescribe antibiotics prior to scaling is when the patient has acute periodontal abscess and the antibiotics serve to reduce the chance for bacteremia and/or acute exacerbation of infection. Infection control promotes excellent healing response and does not require surgery. Using these treatments virtually eliminates need for surgery. 33
The documentation of reduced need for surgery has been done by Dr. Loesche. His group documented a 93% reduction in the need for surgery about individual teeth and 81% reduction in the need for tooth extractions. 81% of patients went to maintenance phase without surgery. Conclusion: These findings indicate that a treatment paradigm based on the diagnosis and treatment of anaerobic infection is likely to be successful in those patients for who access surgery is recommended.
The references are repeated in Dental Care of the Future Parts 1 and 2. REFERENCES 1. Barnett ML, Baker RL, Olson JW: Material adherent to probes during a periodontal examination. J Periodontol, 1982,53(7): 446-448. 2. Watson MR, Lopatin DE, Bretz WA, Ertel IJ, Loesche WJ: Detection of two anaerobic periodontopathogens in children by means of the BANA and ELISA assays. J Dent Res 70(7):1052-1056, Jul, 1991. 3. Kononen E, Asikainen S, et al The early colonization of gram negative anaerobic bacteria in edentulous infants. Oral Microbiol Immunol 1992:7: 28-31. 4 Kononen E, Jousimies-Somer H, et al Relationship between oral gram-negative anaerobic bacteria in saliva of the mother and the colonization of her edentulous infant. Oral Microbiol Immunol 1992:7: 273-276. 5. Van Steenbergen TJM, Petit MDA, et al: Transmission of Porphyromonas gingivalis between spouses. J Clin Periodontol 1993: 20: 340-345. 6. Alaluusa S, Asikainen S, et al: Intrafamilial transmission of Actinobacillus actinomycetemcomitans. J Periodontol 1991: 62:207-210. 7. Offenbacher S, et al: The similarity of periodontal microorganisms between husband and wife cohabitants - association or transmission?: J Periodontol 1985: 56(6): 317-323. 8. Loesche WJ: Chemotherapy of dental plaque infections. Oral Sci Rev. 1976: 9: 63105. 9. Microbiology: Fundamentals and applications 2nd edition: Chap 21: Ronald Atlas: MacMillan Publishers, New York, c. 1988. 10. see reference 9, p.655. 11. On consultation with the ADA Council on Dental Practice Dr. Don Collins, it appears that the &quot;standard of care&quot; is decided in the courts on a county by county basis by testimony of expert witnesses in response to medical malpractice lawsuits. The profession has resisted efforts to develop set standards for itself. In my opinion, this is a potentially dangerous system by which to run health care for the public. It allows backward practitioners to continue to practice on humans for extended periods of time. In addition, since the &quot;standard of care&quot; varies from county to county, to attempt to control treatment outcomes and costs is impossible. 12. Keyes PH and Jordan HV: Periodontal lesions in the Syrian hamster. Arch Oral Biol. 1964 (9): 377-400 13. Keyes PH, et al: The use of phase-contrast microscopy and chemotherapy in the diagnosis and treatment of periodontal lesions-an initial report (I). Quintessence International 1/197B: 51-56. 14. Keyes PH, et al: The use of phase-contrast microscopy and chemotherapy in the diagnosis and treatment of periodontal lesions-an initial report (II). Quintessence International 2/1978: 69-76. 15. Keyes PH, Rams TE: A rationale for management of periodontal diseases: Rapid identification of therapeutic targets'with phase-contrast microscopy. JADA: 1983: 106: 803-812. 16. Vanooteghem R, HUtchens LH, et al: Subjective criteria and probing attachment loss to evaluate plaque control and root debridement. J Clin Periodontol: 1990: 17: 580-587. 17. Slots J: Bacterial specificity in aduit periodontitis. A summary of recent work. J Clin Periodontol: 1986: 13: 912-917. 18. Keyes PH: A treatment rationale for management of periodontal diseases. Alabama State Dent J: 1984: 68: 18-25. 19. Rams TE, Keyes PH and Wright WE: Treatment of juvenile periodontitis with microbiologically modulated periodontal therapy (Keyes Technique). Pediatric Dent:1985: 7: 259-270. 20. Rams TE and Keyes PH: Nonsurgical management of rapidly progressive periodontitis. Gen Dent: 1986: 34(1): 54-59. 21. Rams TE and Keyes PH: Treatment of periodontal patients with impaired manual dexterity - A case report. Gerodontics: 1987:3: 89-93. 22. Bragd L, et al: Clinical and microbiologic study of &quot;refractory&quot; adult periodontitis. J Dent Res (Special Issue): 1985:64:234 (#538). 23. Gordon J, et al: Efficacy of clindamycin hydrochloride in refractory periodontitis - 12 month results. J Periodontol (Supplement): 1985: 56: 75-80. 24. Slots J, Feik D, and rams TE: Prevalence and antimicrobial susceptibiiity of Enterobacteriaceae, Pseudomonadaceae, and Actinobacter in human periodontitis. Oral Microbiol Immunol: 1990:5: 149-154. 25. Keyes PH: Periodontists have limited success predicting disease activity. Annotations: 1991: 6(6). 26. Ramfjord SP, Nissle RR, et al: Subgingival curettage versus surgical elimination of periodontal pockets. J Periodontol: 1968: 3: 167-175. 27. Pihistrom BL, McHugh RB, et al: Comparison of surgical and nonsurgical treatment of periodontal disease - A review of current studies and additional results after 6 1/2 years. J Clin Periodontol: 1983: 10: 524-551. 28. Rams TE, Keyes PH, et al: Long-term effects of microbiologically modUIated periodontal therapy on advanced adult periodontitis. JADA: 1985:111(9): 429-441. 29. Loesche WJ, Syed SA. et al: Metronidazole in periodontitis 1. Clinical and bacteriologic results after 15-30 weeks. J Periodontol: 1984:6: 325-335. 30. Loesche WJ, Syed SA, et al: Treatment of periodontal infections due to anaerobic bacteria with short term treatment with metronidazole. J Clin Periodontol:1981 :8:29-44 31. Schmidt EF, Webber RL. et al: Effect of periodontal therapy on alveolar bone as measured by subtraction radiography. J Periodontol: 1988: 59 (10): 633-638. 32. Loesche WJ, Schmidt E, Smith BA, et al: Effect of metronidazole on periodontal treatment needs. J Periodontol 1991: 62(4): 247-257. 33. Loesche WJ. Giordano J. Soehren S. Hutchinson R. Rau CF. Walsh L. Schork MA. Nonsurgical treatment of patients with periodontal disease . Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, & Endodontics . 81(5):533-43, 1996 May. 34. Loesche WJ. The Antimicrobial Treatment of Periodontal Disease: Changing the Treatment Paradigm. Critical Reviews in Oral Biology & Medicin e. 1999; 10(3):245-275. 35 Loesche, Walter J., Kazor, Christopher E.; Taylor, George W. The optimization of the BANA test as a screening instrument for gingivitis among subjects seeking dental treatment. J Clin Periodontol Vol24(10) Oct 1997 pp718-726
Dental Care of the Future
Dental Care of the Future: Part I David J.Apsey, DDS www.futuredental.com 810-293-8750 Email: [email_address]
Periodontal Disease - Changing the Paradigm <ul><li>Historical perspective - nonspecific plaque hypothesis (NSPH) </li></ul><ul><li>Modern perspective - specific plaque hypothesis (SPH) </li></ul><ul><li>Infectious disease nature of dental diseases </li></ul>
Nonspecific Plaque Hypothesis <ul><li>All plaque is equally pathogenic - no qualitative differences in plaque exist </li></ul><ul><li>Proposed by Miller 1890s after failure to isolate specific bacteria in caries. </li></ul>
Nonspecific plaque hypothesis has been invalidated by data <ul><li>Invalidated by more than one hundred studies since 1970’s demonstrating microbiologic specificity of disease associated flora. </li></ul>
Diagnostic Parameters of NSPH <ul><li>No specificity of plaque is recognized therefore no need to differentiate between healthy or pathogenic plaque </li></ul><ul><li>Diagnostic testing is limited to historical factors such as examination, radiographs, probing depths and inflammation scores </li></ul><ul><li>Diagnosis consists exclusively of description of anatomic factors </li></ul>
Treatment According to NSPH <ul><li>Historically evolved standard of care. </li></ul><ul><li>Plaque must be thoroughly removed continuously to maintain healthy gums . </li></ul><ul><li>Failure to remove plaque will cause disease process to continue. </li></ul><ul><li>When disease causes bone loss and deep pockets around teeth, surgery is used to remove tissue to make hygiene easier. </li></ul>
Subgingival Curettage versus Surgical elimination of Periodontal Pockets Ramfjord, Nissle, etal J Periodontol v39 Issue 3 May 1968 167-175
1)A statistically significant gain in periodontal attachment occurred following curettage of deep periodontal pockets. 2) Subgingival curettage was followed by more favorable results than surgical elimination of periodontal pockets. 3) Slight loss of attachment followed surgical elimination of periodontal pockets.
Comparison of surgical and nonsurgical treatment of periodontal disease <ul><li>Pihlstrom, McHugh etal J Clin Periodontol 1983: 10: 524-541. </li></ul><ul><li>Pocket depth in shallow pockets (1-3mm) did not change for either treatment. </li></ul><ul><li>Pockets 4-6mm – both treatments resulted in sustained pocket reduction. </li></ul>
<ul><li>Deep pockets ( > 7mm) – no difference between treatments after two years. </li></ul><ul><li>Shallow pockets suffered sustained attachment loss following flap surgery. </li></ul><ul><li>Scaling alone resulted in sustained attachment gain in 4-6mm pockets. </li></ul><ul><li>Conclusions - scaling alone and scaling plus surgery were effective – decisions for or against surgery must be made on the basis of individual patient considerations. </li></ul>
Long term effects of surgical/nonsurgical treatment of periodontal disease J.Lindhe, E. Westfelt J Clin Periodontol 1984: 11: 448-458
Sites with initial pocket depths greater than 3mm responded equally well to nonsurgical and surgical treatments based on initial and multiple recall probing depth, attachment level measurements. It is suggested that the critical determinant in periodontal therapy is not the technique (surgical/nonsurgical) but the quality of debridement of the root surface.
Specific Plaque Hypothesis <ul><li>First scientifically developed standard of care in periodontics. </li></ul><ul><li>Only certain plaque causes infections. </li></ul><ul><li>Diagnosis of anaerobic infection is required. </li></ul><ul><li>Microscopic and BANA analysis can detect the statistical pathogens. </li></ul>
Diagnosis With SPH <ul><li>All patients are screened. </li></ul><ul><li>Pathogens are detected primarily with phase contrast microscope and BANA assay. </li></ul><ul><li>Anaerobic infection diagnosis is made. </li></ul><ul><li>Progress is documented with follow-up bacteriology. </li></ul><ul><li>Diagnostic testing including culture and sensitivity for nonresponsive patients “refractory cases”. </li></ul>
Why Do We Use Microscopy in Diagnosis? <ul><li>Provides qualitative analysis of bacterial types and WBC </li></ul><ul><li>Increases confidence and accuracy of predictive decisions </li></ul><ul><li>Establishes microbiologic end points of treatment </li></ul><ul><li>Enables formulation of custom recall intervals for maintaining treated patients </li></ul><ul><li>Microscopy provides quick, inexpensive results - up front cost high due to equipment cost </li></ul>
Treatment According to Specific Plaque Hypothesis <ul><li>Diagnosis of anaerobic infection is used to determine who needs treatment. </li></ul><ul><li>Treatment is targeted towards elimination of specific anaerobic bacteria from plaque - healthy types are selected by treatment. </li></ul><ul><li>Antibiotics are more successful when used after debridement. </li></ul><ul><li>Need for surgery is virtually eliminated. </li></ul>
Success of treatment assessed using bacteriology <ul><li>Progress is documented by repeated microbiologic screening. </li></ul><ul><li>If patient still harbors anaerobic bacteria, treatment is continued until they are reduced. </li></ul>
Nonsurgical treatment of patients with periodontal disease Loesche, Giordano Oral Surg Oral Med Oral Path Vol 81 No. 5 May 1996 pp533-542