Management of defects produced by periodontitis.
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Biomedical subjects
Publications and source records attributed to J G Caton.
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The purpose of this chapter is to set the stage for the more detailed information to follow in the succeeding sections of this work. The reader will be familiarized with the terms and definitions commonly used in periodontal wound healing and the methods used to evaluate the results of periodontal therapy. A discussion of the effects of conventional periodontal therapy will then be followed by a review of biological factors that must be considered if periodontal therapy is to result in regeneration.
The classic periodontal diseases are gingivitis and periodontitis; there are, however, numerous and distinct types of both of these diseases. These types of diseases are distinguished by age of onset, clinical appearance, rate of disease progression, pathogenic microbial flora and systemic influences. Determining the type of periodontal disease a patient has requires a proper medical and dental history, a thorough periodontal examination and recording, and possible additional tests such as identification of subgingival flora and medical laboratory tests. Specific periodontal diagnosis will lead to more rational and efficient patient management.
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This investigation was undertaken to determine the intra- and inter-examiner reliability of the method of stimulation for bleeding used in the Eastman interdental bleeding index. 26 subjects were examined twice, 1 h apart, by either a single examiner or 2 examiners in each half of their mouths, for the presence bleeding after stimulation with a wooden interdental cleaner. Scores were tabulated and intra- and inter-examiner % agreements and kappa-coefficients calculated. Z-tests were performed on the pairs of agreement statistics to check for significant differences. Overall, intra-examiner agreement statistics were high (91.3% to 93.1% agreement; 0.79 to 0.86 kappa-coefficient). Further breakdowns of the data into facial and lingual sites by arch and location (anterior or posterior) resulted in similar levels of reliability, with no significant differences within examiners. The overall inter-examiner agreement statistics were good (82.8% to 87.6% agreement; 0.62-0.75 kappa coefficient). When inter-examiner data were analyzed at facial or lingual sites by arch and location, a significant difference existed in reliability for mandibular posterior lingual sites, but reliability was high in all other areas. These data demonstrate a high level of reproducibility for this method, which suggests that the Eastman interdental bleeding index is suitable for clinical trials and epidemiologic studies of interdental gingivitis.
The "gold standard" outcome measure for periodontal diseases is clinical loss of attachment measured with a periodontal probe. All risk factors for periodontal diseases must be estimated against this standard, which provides post hoc evidence of past disease activity. Measurement of clinical attachment level is crude; therefore, rather large changes must be recorded for specificity to be ensured. This apparently results in rather poor sensitivity, masking good predictors that could prove valuable on a population, individual, and site basis. If risk assessment for periodontal diseases is to advance, this problem must be solved.
Periodontal diseases are a series of complex, distinct, pathologic entities caused by the interaction of bacterial plaque and the host. This interaction results in destruction of the supporting alveolar bone and connective tissue. Although bacterial plaque has been implicated as the primary etiologic agent in most forms of periodontal disease, there are local and systemic factors which may modify both microbial and host components. Local factors may favor plaque accumulation and maturation, while systemic factors may modulate and decrease the host's protective response.
The purpose of this investigation was to determine the histogenesis of periodontal regeneration using the principle of selective and guided cell repopulation of the root surface. A fenestration model, developed in the squirrel monkey, made it possible to exclude gingival epithelium and connective tissue and promote cell repopulation of the denuded root surface from the periodontal ligament and alveolar bone. Experimental and sham-operated control sites were compared histometrically after 3, 7, 14 and 35 days of healing. The results indicated that new cementum, bone and periodontal ligament formation occurred by the 14th day and that regeneration of the fenestration wound was almost complete by Day 35. Root resorption and ankylosis were observed in both experimental and sham-operated controls. There was significantly more periodontal regeneration in the experimental sites, which favored cell repopulation of the root surface from the periodontal ligament and alveolar bone.
The purpose of this study was to characterize the cell populations of the mid-interproximal gingival tissue related to the presence or absence of bleeding. 15 bleeding and 15 non-bleeding interproximal gingival biopsies were obtained from 30 patients and processed for light microscopic evaluation. Morphometric analysis of tissue components revealed that bleeding was associated with an inflammatory lesion located in the mid-interproximal connective tissue. The inflammatory infiltrate was dominated by mononuclear cells of the lymphocyte/macrophage/monocyte group, and the proportions of plasma cells and polymorphonuclear leukocytes were relatively small. The results of this study indicated that interproximal bleeding can be associated with an inflammatory infiltrate not dominated by plasma cells. The rôle of gingival bleeding in the diagnosis of periodontal disease activity is discussed.
This study was undertaken to evaluate the effects of a commercially available tissue adhesive upon healing of the coronal periodontium. In four squirrel monkeys, 24 teeth were extracted, and the coronal third of the roots planed free of fibers and cementum. Eight teeth were replanted without further alteration and eight were coated with tissue adhesive prior to replantation. In the remaining eight teeth, the planed surface was decalcified, coated with tissue adhesive and replanted. Histological observations were made at 1 and 7 days after replantation. In the teeth replanted after root planing alone and root planing plus tissue adhesive, epithelium migrated apically and was within the ligament space lining the denuded root at 7 days. In contrast, those teeth which were decalcified prior to application of tissue adhesive demonstrated fiber attachment to the planed root surface and little or no epithelial downgrowth.
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The effect of overdenture abutment tooth contour on plaque retention and periodontal health was evaluated in four patients over a 1-year period. Each patient had mandibular canines with similar periodontal support; however, one abutment was dome shaped while the other had 2 mm of natural peripheral root contour coronal to the ginvival margin. Eight parameters of periodontal health were measured, and no significant differences between different contours were observed after 1 year. Furthermore, irrespective of overdenture abutment contour, no deterioration in periodontal status occurred. Two subjects had significant wear of the overdenture abutments after 1 year. Further evaluation of more subjects over a longer period of time is indicated.
The presence of crevicular bleeding after probing is an objective clinical sign of gingival inflammation. It has been associated with a plasma cell-dominated inflammatory infiltrate in deep pockets and has been suggested as an indication of active periodontitis. The purpose of this study was to characterize the cellular composition of gingival connective tissue associated with shallow pockets which bled after probing. Prior to biopsy, the mid-facial gingiva associated with 30 teeth from 26 patients was assessed for the presence or absence of visual inflammation, pocket depth and bleeding after probing with a standardized force of 25 g. A horizontal reference incision was made on the facial aspect of the gingiva to demarcate for histologic analysis the specific gingival area probed and evaluated for inflammation. Cell populations were determined from histological sections using morphometric point counting techniques in six standard fields at and coronal to the level of the reference incision. The percentage of cell types and the per cent volume densities of all tissue components were compared between clinically normal and inflamed gingiva. In clinically inflamed gingiva there was a significantly greater percentage of lymphocyte/macrophage/monocyte cells and a smaller percentage of fibroblast/endothelial cells. The percentage of plasma cells was only a fraction of that found for other inflammatory cells. The results of this study indicated that a lesion in the gingiva associated with bleeding after probing can consist of an inflammatory infiltrate which is not dominated by plasma cells.
The purpose of this investigation was to determine histologically the depth of probe tip penetration into the clinically healthy gingival sulcus of humans using a controlled inserton pressure of 25 g. The midfacial gingival units of 22 maxillary and mandibular incisor, canine and premolar teeth, displaying no visual signs of inflammation, were used for probing determinations. An electronic pressure-sensitive probe, with a terminal probe tip diameter of 0.35 mm, was used to standardize insertion pressures. After insertion of the probe into the sulcus, it was then aligned on the facial surface of the gingiva with the tip corresponding to the depth and location of probe insertion. A horizontal reference incision was made on the facial gingival surface which corresponded to the depth of the sulcus probed. This incision served as a histologic landmark of probe tip generation. Gingival biopsies were taken, and step-serial sections analyzed histologically and histometrically. Probe tip penetration was coronal to the apical end of the junctional epithelium in all cases (mean = 0.25 mm). In addition, probe tip penetration was always apical to the coronal end of the junctional epithelium (mean = 0.70 mm).
Utilizing a nonhuman primate model, a study was carried out to determine the nature of the attachment between the tooth and the gingival tissues following periodic root planing and soft tissue curettage. Under the conditions of this investigation, periodic root planing and soft tissue curettage combined with thrice weekly plaque control resulted in the formation of a long junctional epithelium with no new connective tissue attachment. In eight of the 22 experimental pockets, however, this procedure produced discontinuities or "windows" in the junctional epithelium. The coronal attachment of gingival tissues to the root surface (increased resistance to probing) commonly reported following root planing and soft tissue curettage appears to result from the formation of a long junctional epithelium rather than new connective tissue attachment.