An economic evaluation of a chlorhexidine chip for treating chronic periodontitis: the CHIP (chlorhexidine in periodontitis) study.

BACKGROUND: The authors previously suggested that an adjunctive, controlled-release chlorhexidine, or CHX, chip may reduce periodontal surgical needs at little additional cost. This article presents an economic analysis of the CHX chip in general dental practice. METHODS: In a one-year prospective clinical trial, 484 chronic periodontitis patients in 52 general practices across the United States were treated with either scaling and root planing, or SRP, plus any therapy prescribed by treating, unblinded dentists; or SRP plus other therapy as above but including the CHX chip. Economic data were collected from bills, case report forms and 12-month treatment recommendations from blinded periodontist evaluators. RESULTS: Total dental charges were higher for SRP + CHX chip patients vs. SRP patients when CHX chip costs were included (P = .027) but lower when CHX chip costs were excluded (P = .012). About one-half of the CHX chip acquisition cost was offset by savings in other charges. SRP + CHX chip patients were about 50 percent less likely to undergo surgical procedures than were SRP patients (P = .021). At the end of the trial, periodontist evaluators recommended similar additional procedures for both groups: SRP, about 46 percent; maintenance, about 37 percent; surgery, 56 percent for SRP alone and 63 percent for SRP + CHX chip. CONCLUSIONS: Adjunctive CHX chip use for general-practice patients with periodontitis increased costs but reduced surgeries over one year. At study's end, periodontists recommended similar additional surgical treatment for both groups. CLINICAL IMPLICATIONS: In general practice, routine use of the CHX chip suggests that costs will be partially offset by reduced surgery over at least one year.

Dental implant outcomes in postmenopausal women undergoing hormone replacement.

To determine if hormone supplementation reduces the risk of failure for osseointegration of dental implants in postmenopausal women, the treatment outcomes of 116 women older than age 50, treated with 450 endosseous dental implants, were analyzed in this retrospective study. The findings indicated that hormone replacement therapy may not be linked with improved outcomes of endosseous dental implant treatment in postmenopausal women. Smoking, however, appears to significantly increase the implant failure rate in the group observed in this study.

Outcome failures of endosseous implants from a clinical training center.

In an effort to provide realistic clinical information from a "real-world" environment, the present retrospective study was undertaken to assess outcome failures after implant placement in a dental school clinical training center. A database was kept of the clinical information and was analyzed according to established parameters for implant outcomes. The demographics showed that over a period of 6 years, 80 different operators with a wide range of clinical experience had inserted 1,263 implants in a diverse patient pool of 380 individuals. Analysis of the outcomes showed a cumulative survival rate of 91.3%. The time of explantation, the type, size, and location of implants lost, and failure rates in smoking patients were also analyzed. The results indicated that the use of implants by operators with different levels of experience did not affect favorable outcomes.

Periodontal healing after guided tissue regeneration with Atrisorb barriers in beagle dogs.

Periodontal healing after use of Atrisorb barrier material (polylactic acid) for guided tissue regeneration was studied in the premolar and molar teeth of six beagle dogs. Defects studied were surgically induced or were caused by naturally occurring periodontitis. Barriers fragmented and became displaced in 2 to 5 weeks after application. Granulation tissue was sometimes present between the barrier and root surface at 10 days to 4 weeks. Several sites were surgically reentered at 4 months, and new bone covered 60% to 100% of the formerly exposed furcations and root surfaces. Sites obtained for histologic evaluation 9 to 12 months after the baseline surgery showed new connective tissue attachment, cementum, and alveolar bone. Histomorphometric analyses quantitated these tissue changes, and new connective tissue attachment covered 72% of surgically exposed root surfaces and 77% of periodontitis-exposed root surfaces. It was concluded that new periodontal supporting tissues became reconstituted on root and furcation surfaces after use of the Atrisorb barrier material for GTR.

Oriented cell and fiber attachment systems in vivo.

This investigation was undertaken to evaluate whether an oriented cell and fiber attachment system would develop if demineralized dentin surfaces were approximated in vivo. The approximated surfaces consisted of the internal, parallel surfaces of dentin cylinders. The experimental group was demineralized on both the external and internal surfaces of the dentin cylinder with citric acid, pH 1.0, for 3 minutes, but only the external surface of the control dentin cylinder was demineralized. Specimens were implanted transcutaneously into the backs of rats with one end protruding through the surface of the skin. Three specimens in each group were available for analysis at 1 and 10 days after implantation. The groups were compared using histologic and histometric analysis and the following conclusions were made. There were marked differences in the initial cellular response between the groups, and demineralization with citric acid prior to implantation predisposed towards a greater cell attachment at 1 and 10 days. An oriented fiber attachment developed between the demineralized approximated surfaces by 10 days, but did not develop between nondemineralized approximated surfaces. The morphology of the fiber attachment system was structurally similar to a periodontal ligament, with inserting fibers perpendicular to the implant surface. The findings of this study suggest that spatial approximation of appropriate substrates facilitates development of cell and fiber orientation. Thus, to regenerate a functionally oriented attachment system in the clinical setting, it may be beneficial to provide substrates that are appropriately approximated.

Effect of metronidazole on experimental periodontitis: cell population characteristics.

Systemic administration of metronidazole during an experimental periodontitis resulted in significantly less active tissue destruction compared to drug-free animals. However, the size of the inflammatory infiltrates in both groups was similar. The present study assessed cell populations within the infiltrates of metronidazole receiving and drug-free animals. In the experimental group, metronidazole was administered orally to 4 squirrel monkeys (100 mg/kg body weight per day) for 17 days. After 3 days, marginal periodontitis was induced around maxillary and mandibular bicuspids and molars by tying silk ligatures at the gingival margins. In 4 monkeys of the drug-free control group, periodontitis was induced around similar teeth. Biopsies of the gingiva representing 3, 7 and 14 days of experimental periodontitis were taken in both groups. The total number of cells and the number of polymorphonuclear leucocytes (PMN's) were counted on one-micron sections. At 3 days after ligature placement, there were numerically less total cells and PMN's in the metronidazole receiving experimental group. At 7 and 14 days the total number of cells and the number of PMN's was significantly greater in the drug-free control group, where more active periodontal breakdown had occurred. These results emphasize the potentially destructive role of PMN's in acute bursts of tissue destruction.

Histologic studies on the extension of the inflammatory infiltrate in human periodontitis.

This study was undertaken to re-examine early and recent morphologic descriptions of gingival and periodontal inflammation based on a study of gingival biopsies and block sections of human jaws. A collection of 350 autopsy and surgically retrieved jaw sections containing multiple teeth and displaying various stages of periodontal inflammation were subjected to routine histologic preparation and analyzed with step serial sections. 105 gingival biopsies, serially sectioned, including 15 clinically normal specimens, were also studied. The results of these investigations suggest that the inflammatory lesion extends into the alveolar process and elicits a response, often before evidence of crestal resorption or connective tissue attachment loss has occurred. Similarly, deep penetrations of inflammatory cells into the alveolar bone, periodontal ligament and periapical tissues, along with fibrosis and enlargement of the marrow spaces, were common findings with advancing disease. More widespread distributions of inflammatory cells than previously described were found in clinically normal gingiva, while in more inflamed gingiva, the inflammatory cell types found and their pattern of distribution varied greatly from individual to individual. These observations cast doubt on the perception of human periodontitis as a localized and marginal disease and suggest that its effects may be much more pervasive than previously thought.

Cell and fiber attachment to demineralized cementum from normal root surfaces.

The purpose of this study was to assess connective tissue and epithelial responses to cementum (from normal human root surfaces covered by periodontal ligament) after surface demineralization with citric acid. Each rectangular specimen had a face of cementum and an opposite surface composed of pulpal dentin. One half of the specimens were treated with citric acid (experimental group), while the remainder served as untreated control specimens. Specimens were implanted vertically into incisional wounds on the dorsal surface of rats with one end of the implant protruding through the skin. Four specimens in each group were available for examination 1, 3, 5, and 10 days after implantation. Histologic and histometric analyses of the implants included counts of adhering cells, evaluation of attached connective tissue fiber density and diameter, and assessment of epithelial migration. At day 1, a distinct lighter staining zone was present on the surface of both cementum and dentin in the experimental group which corresponded to a zone of surface demineralization produced by the acid treatment. Histometric comparisons between experimental and control groups at 10 days showed a greater number of cells attached to demineralized cementum surfaces. Also, a connective tissue fiber attachment system had developed on these experimental surfaces, but which differed morphologically from periodontal ligament fiber attachment to normal cementum. It was concluded that citric acid treatment can surface demineralize cementum from normal roots, and that the surface demineralization of this cementum facilitated a cell and fiber attachment to the cementum surface.

Tetracycline therapy in patients with early juvenile periodontitis.

Tetracycline therapy, when used in conjunction with surgery or root planing, has been shown to be effective in controlling the progression of juvenile periodontitis. However, the ability of tetracycline alone to control the disease has not been assessed. The present study evaluated the effects of tetracycline therapy, with supragingival plaque control, on clinical attachment levels and radiographic bone height in patients with clinical and radiographic evidence of juvenile periodontitis. The four patients (mean age 15.2 +/- 0.3 yrs) each demonstrated loss of attachment of greater than or equal to 2 mm at one or more probing sites and had accompanying radiographic evidence of early localized bone loss. Following an initial clinical evaluation consisting of pocket depths, attachment levels and standardized radiographs, the patients received systemic tetracycline therapy (1 gm/day for three to six weeks) and oral hygiene instruction. At the completion of antibiotic therapy, patients received a supragingival professional prophylaxis every two weeks for three months, whereupon the initial evaluation was repeated. On comparing the initial and three-month clinical and radiographic data, there were significant decreases in clinical and radiographic measurements. For a total of 85 affected probing sites around 26 teeth, 79% decreased in pocket depth by greater than or equal to 2 mm (with no sites increasing in pocket depth) and 69% gained clinical attachment (with only one site losing attachment of 1 mm). Radiographic measurements revealed an increase in both the height and area of coronal alveolar bone. The findings indicated that six weeks of systemic tetracycline therapy combined with supragingival plaque control was effective in the initial control of early juvenile periodontitis.

Gingival wound healing in the presence of plaque-induced inflammation.

An accelerated loss of connective tissue attachment has been reported following surgery in plaque-infected dentitions. It was the purpose of the present study to evaluate histologically the healing of incisional wounds in the gingival supracrestal region in the presence and absence of bacterially induced inflammation. In the experimental group, marginal periodontitis was induced around the teeth by tying plaque-retentive ligatures at the gingival margins and 10 weeks later an incisional wound was made from within the gingival sulcus to the crest of the bone. In the control group, similar incisional wounds were made in normal gingiva. In each group, three specimens were available for histologic and histometric analysis 1, 3, 7 and 21 days after wounding. In the control group, the wound healing sequence in the supracrestal region was similar to that reported following incisional cutaneous wounds. In the experimental group, epithelial continuity across the wound was re-established earlier, and marked invagination of epithelium occurred into the incision. This invagination was significantly greater than in control specimens at all time points. In addition, within the experimental group a second significant epithelial migration into the wound occurred between 7 and 21 days. The epithelial invagination extended through the major portion of the supracrestal area and terminated near the cementum surface. It is conceivable that marked epithelial invagination into a supracrestal wound may predispose to an accelerated loss of connective tissue attachment.

Effects of gold salts on experimental periodontitis. III. Ultrastructural observations.

Previous studies showed that the systemic administration of soluble gold salts resulted in significantly less periodontal destruction after 2 weeks of experimentally induced periodontitis. The present study compared the ultrastructural characteristics of the inflammatory lesion in animals receiving gold salts (experimental) with those in animals that had not received gold salts (control). Maxillary gingival biopsy specimens were obtained from the buccal aspect of ligatured teeth after 2 weeks of experimental periodontitis. A cellular and extracellular ultrastructural characterization was done in an "epithelial and superficial connective-tissue zone," and a "deep connective-tissue zone." Experimental (gold-receiving) specimens had an intact sulcular epithelium with narrow intercellular spaces overlying a collagen dense connective tissue. Control specimens had a degenerating disrupted epithelium overlying a collagen-poor connective tissue in which polymorphonuclear leucocytes predominated and often were closely apposed to morphologically altered fibroblasts. The cellular distribution of electron-dense deposits of gold salts was demonstrated, and their possible role in modulating mechanisms of cell cytotoxicity and collagen turnover is discussed.

Effects of gold salts on experimental periodontitis. II. Cell population characteristics.

A previous study showed that the systemic administration of soluble gold salts (gold sodium thiomalate) resulted in significantly less periodontal destruction after 2 weeks of experimentally induced periodontitis. In order to provide information on the possible mechanisms of action of gold salts in the experimental periodontitis situation, the present study analyzed and compared the characteristics of the inflammatory cell populations in animals receiving gold salts with those present in animals which had not received gold salts. Maxillary gingival biopsy specimens were obtained from the buccal aspect of ligatured teeth after 2 weeks of experimental periodontitis. Cell populations were characterized and enumerated, on 1-micron sections, in an epithelial and superficial connective tissue zone, and a deep connective tissue zone. Significantly fewer inflammatory cells were present in experimental (gold receiving) specimens, and this reduction was due primarily to fewer polymorphonuclear leucocytes (PMNs). No significant reduction occurred in any other inflammatory cell-type. The reduction in number of PMNs in experimental specimens was associated with a decreased number of morphologically altered, degenerating fibroblasts in the connective tissue compared to the PMN-dominated lesion of control specimens. Mechanisms whereby gold salts can reduce chemotaxis and functional capabilities of inflammatory cells are discussed.

Cell populations associated with gingival bleeding.

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.

Relationships between epithelium and connective tissue in inflamed gingiva.

Since chronic inflammation has been associated with degenerative and proliferative responses in connective tissue and epithelium, it was decided to investigate quantitatively the proportions of epithelium and connective tissue in inflamed gingiva. Forty-five midfacial gingival sites were assessed prior to biopsy for the presence or absence of bleeding after probing using a controlled insertion force fo 25 g. In order to delineate the corresponding area for histologic analysis, a reference incision was made on the facial surface of the gingiva which demarcated the depth and mesio-distal extent of the area probed. Step-serial bucco-lingual sections were morphometrically analyzed to determine the percentages of epithelium, inflamed, and noninflamed connective tissues coronal to the reference incision. The data was compared with respect to the presence or absence of bleeding after probing. Specimens which bled after probing had significantly less epithelium and more connective tissue. The increase in overall connective tissue was due to a significant increase in the inflamed component, and it appeared that the decrease in epithelium corresponded to the increase in inflamed connective tissue. The findings of diminished epithelium overlying inflamed connective tissue reinforces the concept that connective tissue status is important for determining structure and function of epithelium.

Depth of periodontal probe penetration related to clinical and histologic signs of gingival inflammation.

The purpose of this study was to determine if the depth of periodontal probe penetration into the gingival sulcus was related to bleeding after probing with a standardized force, visual signs of gingival inflammation, and histological parameters of gingival inflammation. Sixty midfacial gingival sites in 26 persons were evaluated for presence or absence of visible inflammation and bleeding after probing using a controlled insertion pressure of 25 gm. In order to delineate the area for histologic analysis, a reference incision was made on the facial surface of the gingiva which corresponded to the depth and mesio-distal extent of the area probed and evaluated for visual signs of inflammation. Gingival biopsy specimens were histometrically analyzed to determine the depth of probe penetration and percentage of inflamed connective tissue. Statistical analysis of the data demonstrated that probe penetration was significantly greater in the presence of visible inflammation, but not with bleeding after probing. Furthermore, only a weak correlation existed between depth of probe penetration and percentage of inflamed connective tissue adjacent to the area probed.

Histologic characteristics associated with bleeding after probing and visual signs of inflammation.

This study was designed to characterize histologically the gingival lesion associated with visual signs of inflammation and bleeding after probing. Sixty midfacial gingival sites in 26 persons were evaluated for visual presence of absence of inflammation and bleeding after probing using a controlled insertion pressure of 25 gm. In order to delineate the area for histologic analysis, a reference incision was made on the facial surface of the gingiva which corresponded to the depth and mesio-distal extent of the area probed and evaluated for signs of inflammation. Gingival biopsy specimens were morphometrically analyzed to determine the percentages of cell rich--collagen poor connective tissue and blood vessel lumens. Histometric data were grouped and compared with respect to the presence or absence of inflammation and bleeding. Specimens associated visually with inflammation had significantly greater percentages of both cell rich--collagen poor connective tissue and blood vessel lumens. Bleeding upon probing was associated with a significantly greater percentage of cell rich--collagen poor connective tissue without an increase of blood vessel lumens. It was concluded that both observed signs of inflammation and bleeding after probing can be used to detect inflammatory lesions in the gingiva. However, in areas inaccessible for evaluation of inflammation, bleeding determinations using controlled insertion pressures provided an objective diagnostic method for detecting the presence of an inflammatory lesion.

Interproximal and buccal cell populations apical to the sulcus before and during experimental periodontitis in squirrel monkeys.

The purpose of this investigation was to study inflammatory cell populations apical to the buccal and interproximal gingival sulcus during destructive experimental marginal periodontitis in squirrel monkeys. Specimens were obtained of the clinically healthy periodontium, and (after 2 and 10 weeks) of experimental periodontitis induced by the placement of plaque-retentive silk ligatures at the gingival margin. Cell populations were characterized and quantitated in a standard area of connective tissue immediately subjacent to the most apical cells of the junctional epithelium in buccal and interproximal locations. Comparisons of periodontitis cell populations showed there were no differences between the regions in relation to either total numbers of cells, or in the percentages of inflammatory cell types. The inflammatory cells consisted primarily of granulocytes and macrophages, with only small percentages of lymphoid and plasma cells. Mechanisms and consequences of these cell types relative to periodontal tissue destruction are discussed.

Cell populations in the transseptal fiber region before, during and after experimental periodontitis in squirrel monkeys.

A study was designed to enumerate cell populations before, during and after experimentally induced periodontitis in squirrel monkeys. The clinically healthy gingival connective tissue adjacent to the sulcus contained populations of macrophages, plasma cells, lymphoid cells, and granulocytes, indicating that immune responses were probably in operation. Although these cell populations have been associated with tissue destruction, it is possible that they may serve to confine the antigens to the tissue adjacent to the sulcus, and reduce their spread apically. Active periodontitis was associated with the presence of granulocytes and macrophages in the transseptal fiber region. These cells are capable of causing the localized collagen degradation and bone resorption that occur during the destructive phase of the disease. Eight weeks after etiologic agents were removed, the cell populations in the transseptal fiber area returned to a level comparable with those in the pre-experimental, clinically healthy. This indicates that active periodontitis within the transseptal fiber region had ceased and repair had occurred.

Osseous repair in infrabony periodontal defects.

The present investigation was undertaken to quantitate the osseous changes which occur throughout the entire circumferential extent of infrabony periodontal defects in patients with optimal plaque control. Fifteen defects were selected in nine patients. Periodontal surgery was scheduled after each patient had shown an ability to practice efficient plaque removal. Muco-periosteal flaps were raised and the osseous defects debrided. The dimensions of each defect were measured at several specific location points within the defect. The flaps were replaced at their original location and, post-operatively, optimal plaque control was maintained in the area (Mean Plaque Index 0.04). Six to 8 months after the initial surgery all areas were re-operated and the osseous defects were remeasured at the same specific location points. Each defect showed osseous regeneration at every location point. The mean initial osseous defect depth at a location point was 3.5 mm and the mean amount of bone regeneration which occurred was 2.5 mm. Crestal alveolar bone resorption occurred at almost half of the location points and averaged 0.7 mm. Eleven of the 15 defects had resolved completely. There were isolated areas where a shallow defect persisted in the remaining four defects. The behavior of an osseous defect throughout its circumferential extent was characterized by a combination of coronal bone regeneration (mean 77%) and marginal bone resorption (mean 18%). Infrabony periodontal defects may predictably remodel after surgical debridement and establishment of optimal plaque control.