Microbial etiological agents of destructive periodontal diseases

Specific risk indicators associated with either susceptibility or resistance to severe forms of periodontal disease were evaluated in a cross-section of 1,426 subjects, 25 to 74 years of age, mostly metropolitan dwellers, residing in Erie County, New York, and surrounding areas. The study sample exhibited a wide range of periodontal disease experience defined by different levels of attachment loss. Therefore, it was possible to accurately assess associations between the extent of periodontal disease and patient characteristics including age, smoking, systemic diseases, exposure to occupational hazards, and subgingival microbial flora. Age was the factor most strongly associated with attachment loss, with odds ratios for subjects 35 to 44 years old ranging from 1.72 (95% CI: 1.18 to 2.49) to 9.01 (5.86 to 13.89) for subjects 65 to 74 years old. Diabetes mellitus was the only systemic disease positively associated with attachment loss with an odds ratio of 2.32 (95% CI: 1.17–4.60). Smoking had relative risk...

Assessment of risk for periodontal disease. I. Risk indicators for attachment loss.

Apical periodontitis is a chronic inflammatory disorder of periradicular tissues caused by aetiological agents of endodontic origin. Persistent apical periodontitis occurs when root canal treatment of apical periodontitis has not adequately eliminated intraradicular infection. Problems that lead to persistent apical periodontitis include: inadequate aseptic control, poor access cavity design, missed canals, inadequate instrumentation, debridement and leaking temporary or permanent restorations. Even when the most stringent procedures are followed, apical periodontitis may still persist as asymptomatic radiolucencies, because of the complexity of the root canal system formed by the main and accessory canals, their ramifications and anastomoses where residual infection can persist. Further, there are extraradicular factors -- located within the inflamed periapical tissue -- that can interfere with post-treatment healing of apical periodontitis. The causes of apical periodontitis persisting after root canal treatment have not been well characterized. During the 1990s, a series of investigations have shown that there are six biological factors that lead to asymptomatic radiolucencies persisting after root canal treatment. These are: (i) intraradicular infection persisting in the complex apical root canal system; (ii) extraradicular infection, generally in the form of periapical actinomycosis; (iii) extruded root canal filling or other exogenous materials that cause a foreign body reaction; (iv) accumulation of endogenous cholesterol crystals that irritate periapical tissues; (v) true cystic lesions, and (vi) scar tissue healing of the lesion. This article provides a comprehensive overview of the causative factors of non-resolving periapical lesions that are seen as asymptomatic radiolucencies post-treatment.

https://onlinelibrary.wiley.com/doi/epdf/10.1111/j.1365-2591.2006.01099.x

On the causes of persistent apical periodontitis: a review.

The aim of the present study was to evaluate whether a regenerative surgical procedure, based on guided tissue regeneration, could predictably result in the formation of a new attachment in human teeth. The material included 12 teeth in 10 patients with advanced periodontal disease. Following flap elevation, scaling, root planing and removal of granulation tissue, a teflon membrane was placed over the denuded root surface in such a way that the epithelium and the gingival connective tissue were prevented from reaching contact with the root during healing. The flap was replaced on the outer surface of the membrane and secured with interdental sutures. This design of wound preparation gives preference to the cells originating from the periodontal ligament (PDL-cells) to repopulate the wound area adjacent to the root. Histologic analysis of the result of treatment was made in 5 of the 12 teeth scheduled for extraction. In the remaining 7 teeth, the result was evaluated using clinical measurements. The result of healing disclosed that in all teeth treated, substantial amounts of new attachment had formed. This suggests that predictable restitution of the attachment apparatus can be accomplished by using a method of treatment which is based on the principle of guided tissue regeneration.

New attachment formation in the human periodontium by guided tissue regeneration. Case reports.

Background: The purpose of this review is to provide the reader with practical knowledge concerning the relationship between diabetes mellitus and periodontal diseases. Over 200 articles have been published in the English literature over the past 50 years examining the relationship between these two chronic diseases. Data interpretation is often confounded by varying definitions of diabetes and periodontitis and different clinical criteria applied to prevalence, extent, and severity of periodontal diseases, levels of glycemic control, and complications associated with diabetes. Methods: This article provides a broad overview of the predominant findings from research published in English over the past 20 years, with reference to certain ‘‘classic’’ articles published prior to that time. Results: This article describes current diagnostic and classification criteria for diabetes and answers the following questions: 1) Does diabetes affect the risk of periodontitis, and does the level of metabolic control of diabetes have an impact on this relationship? 2) Do periodontal diseases affect the pathophysiology of diabetes mellitus or the metabolic control of diabetes? 3) What are the mechanisms by which these two diseases interrelate? and 4) How do people with diabetes and periodontal disease respond to periodontal treatment? Conclusions: Diabetes increases the risk of periodontal diseases, and biologically plausible mechanisms have been demonstrated in abundance. Less clear is the impact of periodontal diseases on glycemic control of diabetes and the mechanisms through which this occurs. Inflammatory periodontal diseases may increase insulin resistance in a way similar to obesity, thereby aggravating glycemic control. Further research is needed to clarify this aspect of the relationship between periodontal diseases and diabetes. J Periodontol 2006;77:12891303.

https://aap.onlinelibrary.wiley.com/doi/pdf/10.1902/jop.2006.050459

Diabetes mellitus and periodontal diseases.

The present experiment was undertaken to test the hypothesis that new connective tissue attachment may form on a previously periodontitis involved root surface provided cells originating from the periodontal ligament are enabled to repopulate the root surface during healing. A mandibular incisor with advanced periodontal disease of long standing (the distance between the cemento-enamel junction and the alveolar bone crest was 9 mm) was subjected to periodontal surgery using a technique which during healing prevented the dentogingival epithelium and the gingival connective tissue from reaching contact with the curetted root surface. Preference was hereby given to the periodontal ligament cells to repopulate the previously diseased root surface. After 3 months of healing a block biopsy containing the incisor and surrounding tissue was sampled. The histological analysis revealed that new cementum with inserting principal fibers had formed on the previously diseased root surface. This new attachment extended in coronal direction to a level 5 mm coronal to the alveolar bone crest. This finding suggests that new attachment can be achieved by cells originating from the periodontal ligament and demonstrates that the concept that the periodontitis affected root surface is a major preventive factor for new attachment is invalid.

New attachment following surgical treatment of human periodontal disease.

The present investigation was performed to study the frequency of recurrence of periodontitis in diabetic subjects, who, prior to the initiation of a 5-year period of monitoring, were treated for moderate to advanced periodontal disease. 20 patients with diabetes, type 1 (IDDM) or type 2 (NIDDM) and 20, sex and age matched, controls with similar amounts of periodontal tissue destruction, were selected for the study. Following a screening examination, all patients were subjected to non-surgical periodontal therapy (oral hygiene instruction, supra- and subgingival scaling). 3 months later, the baseline examination for the study was performed. This included assessments of several parameters such as: number of teeth, plaque, gingivitis, probing pocket depth and probing attachment level. 6 months after the baseline examination, all 40 subjects were recalled for a 2nd examination. Sites which at this 6-month examination exhibited bleeding on probing, and had probing depth > 5 mm, were scheduled for additional surgical therapy (modified Widman flap). Following this selective additional therapy, the main period of monitoring was initiated. During this period, a plaque control program was repeated every 3 months. Re-examinations regarding plaque, gingivitis, probing depth and probing attachment level were performed 12, 24 and 60 months after the baseline examination. The findings from the examinations disclosed that diabetics and non-diabetics alike, treated for moderately to advanced forms of adult periodontitis, during a subsequent 5-year period, were able to maintain healthy periodontal conditions. Thus, the frequency of sites which exhibited signs of recurrent disease was similar in the 2 study groups.

The effect of periodontal therapy in diabetics. Results after 5 years.

The aim of the present trial was to study the effect of meticulous supragingival plaque control on (i) the subgingival microbiota, and (ii) the rate of progression of attachment loss in subjects with advanced periodontal disease. An intra-individual group of sites exposed to non-surgical periodontal therapy served as controls. 12 patients with advanced periodontal disease were subjected to a baseline examination (BL) including assessments of oral hygiene status, gingival condition (BoP), probing depth, clinical attachment level and subgingival microbiota from pooled samples from each quadrant. The assessments were repeated after 12, 24 and 36 months. Following BL, a split mouth study was initiated. The patients received oral hygiene instruction, supragingival scaling and case presentation. 2 quadrants in each patient were identified as "test" and the remaining 2 as "control" quadrants. Subgingival therapy was performed in all bleeding sites in the control quadrants. Oral hygiene instructions and plaque control exercises were repeated once every 2 weeks during the initial 3 months of the study. Thereafter the plaque control program was repeated once every 3 months for the duration of the 3 years. Sites demonstrating loss of clinical attachment > or =2 mm in the test quadrants were treated subgingivally. The results showed that in both test and control quadrants repeated oral hygiene instructions and supragingival plaque removal procedures resulted in low plaque scores throughout the study. The gingival bleeding scores and the frequency of periodontal pockets > or =4 mm was, however, significantly higher in the test quadrants than in the control quadrants. At the end of the 3 year study, the control quadrants showed significantly more reduced (> or =2 mm) pockets than the test quadrants, 265 versus 96. The number of sites in the test quadrants showing probing attachment loss > or =2 mm was more than 4x greater than in the control quadrants (59 versus 13). The microbiological findings indicate a more pronounced reduction only for P. gingivalis in the control quadrants. None of the other 4 marker bacteria consistently reflected or predicted the clinical parameters. The present study shows that only supragingival plaque control fails to prevent further periodontal tissue destruction in subjects with advanced periodontal disease.

The effect of supragingival plaque control on the progression of advanced periodontal disease

In the present study, the frequency of sites exhibiting gingival inflammation and periodontal tissue breakdown was assessed in one group of 46 individuals (19-25 years old; test group T) who had suffered from diabetes mellitus (Type 1) for 10 years or more, and in another group of 41 non-diabetic controls (18-26 years old; control group C). Each individual was examined regarding oral hygiene status, gingival conditions, probing depths, probing attachment levels and gingival recessions. The interproximal marginal bone level was assessed in bitewing radiographs. No significant differences were found between the 2 groups regarding their oral hygiene status, frequency of sites with probing depths of greater than 3 mm and the position of the interproximal alveolar bone margin. The mean distance between the cemento-enamel junction (CEJ) and the interproximal bone crest was in group T, 0.91 +/- 0.14 (SD) mm and in group C, 0.95 +/- 0.18 (SD) mm. About 80% of the individuals in both groups were free from signs of marginal bone loss and only 1 subject in each group had greater than 6 sites with definitive bone loss. The group of diabetic patients had higher frequencies of inflamed buccal/lingual gingival units, gingival recessions and sites with attachment loss of greater than or equal to 2 mm. Most of the sites (85%) with attachment loss were located at the buccal and lingual surfaces. There were no significant correlations between the periodontal variables and the duration of diabetes, insulin dosage and HbA1 level. Individuals with both retinopathy and nephropathy had significantly more gingival inflammation than diabetic individuals without complications.

Prevalence of periodontal disease in young diabetics.

The aim of the present study was to analyze and express in quantitative terms some of the structural alterations which develop in an initially normal gingiva during a phase of continuous plaque accumulation. Four beagle dogs were used. The animals had from birth been twice daily subjected to meticulous mechanical tooth cleaning. When the dogs were 10 months of age their gingiva were in excellent health as evaluated by Gingival Index and Gingival Exudate measurements. Gingival tissues were harvested from the premolar and molar regions in the right jaws. The tooth cleanings were then terminated and plaque allowed to accumulate. Clinical examinations were performed and gingival biopsies sampled after 4, 7, 14, 21 and 28 d. The composition of the gingival biopsies was analyzed in a sampling microscope. After 4 d of plaque accumulation significant amounts of gingival exudate could be sampled. The exudation then gradually increased during the following weeks. Biopsies representing day zero did not contain any inflammatory cell infiltrates. However, after 4 d of the experiment leukocytes were found in the collagen-poor connective tissue immediately beneath the junctional epithelium. The size of the infiltrated connective tissue (ICT) gradually increased during the experiment. The volumetric density of collagen in the noninfiltrated connective tissue (NCT) was always much higher than in ICT. In ICT, however, this density parameter remained rather constant throughout the study. On days 4 and 7 neutrophilic granulocytes constituted 60-70% of the leukocyte population. On day 28, however, the infiltrate comprised mainly mononuclear leukocytes, especially plasma cells, neutrophils at that time occupying only a small fraction of the infiltrate.

Harald Rylander

Papers

New attachment following surgical treatment of human periodontal disease.

The effect of periodontal therapy in diabetics. Results after 5 years.

The effect of supragingival plaque control on the progression of advanced periodontal disease

Prevalence of periodontal disease in young diabetics.

Experimental gingivitis in young dogs.