Non-surgical periodontal therapy for AIDS patient with periodontal involvement. A periodontal case management in a general practice.
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Little is known about the relationship of aging to periodontal disease. The immune response undergoes aging-related changes resulting in loss of functional capacity. The aim of this study was to investigate the relationship between levels of serum IgG antibodies against suspected periodontal pathogenic microorganisms to the presence or absence of periodontal disease in an elderly (65-75 yrs) population. From this study, we obtained information concerning: (1) the ability to differentiate elderly individuals without disease from those with disease by their levels of antibodies against periodontal pathogens and (2) which periodontal pathogen(s) triggered those responses. IgG anti- Porphyromonas gingivalis (strains W83 and 381) levels in the serum of elderly patients with severe periodontal disease were the only antibody responses measured which were elevated compared to the elderly control group of subjects with no periodontal disease. Anti- Prevotella intermedia IgG levels in both elderly patient groups were depressed compared to anti- P. intermedia levels in the young normal control subjects. Serum IgG antibody levels to six other plaque microorganisms did not differentiate between diseased and normal, elderly or young subjects. This data suggested that P. gingivalis was associated with periodontal disease in this elderly group of individuals and that those elderly individuals were able to respond with a normal IgG immune response.
Suspected periodontal pathogens can be transmitted between spouses. The treatment response may be unsuccessful in periodontitis patients, if the spouse harbors these bacteria. The aim of the present 6-month follow-up study was to clarify whether the microbiological treatment outcome of periodontitis patients is related to the detection of suspected periodontal pathogens in the saliva of the spouse. 10 patients with advanced periodontitis and their spouses were included in the study. The patients received mechanical periodontal treatment and 500 mg metronidazole systemically 2x a day for 7 days. The presence of visible plaque, gingival bleeding after probing, suppuration, supragingival and subgingival calculus and pocket depths were assessed at baseline and 1 and 6 months after treatment. Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Prevotella intermedia/Prevotella nigrescens, Campylobacter rectus and Peptostreptococcus micros were cultured from pooled subgingival samples from the patients and from salivary samples from the spouses at corresponding occasions. Periodontal conditions in the patients improved after treatment as determined by the significantly lower values of clinical variables 1 and 6 months after treatment compared to those at baseline. However, the re-emergence of periodontal bacteria after treatment of the patients was not related to the concurrent detection of the respective bacteria in the saliva of the spouses. In this study design, it seemed that the salivary bacterial load in the spouse was of minor importance for the microbiological treatment outcome of the patient.
692 dental adults in the age ranges, 15-19, 20-29, and 35-44 yr, were assessed for their periodontal conditions and treatment needs using the Periodontal Index (PI) and Community Periodontal Index of Treatment Needs (CPITN). The relative advantages and disadvantages of the two indices were evaluated as epidemiological screening procedures. The CPITN (which calls for examination of only 10 selected teeth) identified higher proportions of adults and teeth with a healthy periodontal condition and also those with periodontitis than the PI (which requires examination of all teeth). The proportion of adults and teeth with gingivitis as the worst condition was greater than when assessed by the PI. Evaluation of individual adult scores by PI and CPITN suggested that the CPITN, despite being a partial recording index only, is more sensitive in identifying existing periodontal conditions and treatment needs than the PI. This is explained by the clinical criteria and periodontal probe utilized in the CPITN. Although the original purposes of the PI and CPITN differ, it is proposed that as a epidemiological screening procedure for assessing periodontal treatment needs the CPITN is to be preferred to the PI.
OBJECTIVE: The aim of this study was to determine whether there was any change in T-lymphocyte subsets in patients with chronic periodontitis after applying different periodontal treatment methods. PATIENTS AND METHODS: Twenty-four patients with chronic periodontitis were included in the study. In every phase of the treatment (pretreatment, initial treatment, curettage and flap operations) the biopsy samples were taken from the gingival tissues at sites of chronic periodontitis. Then CD4(+) and CD8(+) lymphocyte and CD4(+)/CD8(+) ratio values were determined using flow cytometry in the biopsy samples. At the same time, gingival pocket depth, Löe-Silness gingival index, and Silness-Löe plaque index scores were recorded to assess the periodontal status in patients. To determine the correlation between the clinical measurements and the laboratory results obtained before the treatment, after initial treatment, after curettage and after flap operations, we conducted an analysis using a paired t-test. RESULTS: Flow cytometry findings in the patients with chronic periodontitis showed that CD4(+) and CD8(+) lymphocyte values before treatment were under the normal value and the CD4(+)/CD8(+) ratio was within the normal distribution interval. The CD4(+)/CD8(+) ratio decreased postcurettage and postflap operation. This decrease was statistically significant (p < 0.001). The CD4(+) and CD8(+) lymphocyte values were increased postcurettage and postflap operation. This increase was also statistically significant (p < 0.001). CONCLUSIONS: These findings suggest that local immune response was poor in the patients with chronic periodontitis. CD4(+) and CD8(+) T-lymphocytes could play a significant role in chronic periodontitis pathobiology.
OBJECTIVE: Periodontitis is a disease showing differences in disease progression between patients and between sites within a patient. Routine clinical examinations today are not useful enough to distinguish susceptible patients and active lesions from resistant patients and chronic lesions. Diagnostic markers should be pathogenic and inflammatory factors participating in periodontal tissue destruction. These are both local and systemic factors. MATERIALS AND METHODS: First of all, pathogenic factors and proinflammatory cytokines or mediators in gingival crevicular fluid (GCF) were examined and the difference was found between active and inactive periodontitis lesions distinguished by attachment loss. Active lesions were detected by discriminant-function analysis of these examinations, although the sensitivity of differential diagnosis was low. Then, we established a novel needle biopsy for understanding the pathophysiological conditions elicited in active and chronic inflammatory processes of periodontal tissue destruction. A variety of cytokines and mediators were detected in biopsied specimens by reversed transcription polymerase chain reactions (RT-PCR). Cytokine profiles were varied in inflammed periodontal biopsies. As IFN gamma mRNA expression was enhanced in inflamed gingiva, antigen-presenting-cell (APC) functions of human gingival fibroblasts (HGF) were examined. RESULTS: Despite the phenotypical resemblance of IFN gamma-treated HGF to so-called APC, HLA-DR positive HGF could not induce proliferation but suppressed proliferation of alloreactive peripheral blood T cells (PBT). However, HLA-DR positive HGF stimulated the proliferative responses of PBT which had been primed with allo-APC. Regulatory immune responses by IFN gamma were different in T cell conditions. CONCLUSIONS: Various kinds of cytokines participated in periodontal inflammation, and every cytokine is multi-functional. Complex and compound inflammatory processes can be clarified by examining cytokine networks and the precise effects of each cytokine on each of the cell types comprising periodontal tissue. It is, therefore, necessary for establishing diagnostic strategies to integrate pathogenic and inflammatory factors in periodontal tissue destruction.
BACKGROUND: The perceptions that patients have of periodontal therapy have not been extensively studied and are not well understood. The purpose of this study was to assess the degree of discomfort associated with periodontal therapy carried out in a specialist practice. METHODS: A consecutive group of 150 patients (90 females, 60 males; mean age 54.5 years) who had completed periodontal therapy, which included surgery, in a periodontal practice in Norway was studied. The patients indicated the discomfort they had experienced with periodontal therapy on a visual analog scale (VAS). Other factors associated with postoperative discomfort such as the use of analgesics were recorded. RESULTS: The mean VAS scores were low for all procedures investigated. The highest mean score was recorded for anesthesia in the upper anterior region. There were small differences between the levels of discomfort reported by males compared to females. The VAS scores decreased with increasing age for anesthesia in the lower arch (P = 0.004) and surgery in the lower arch (P = 0.003). Virtually all (97%) of the patients perceived periodontal treatment to be associated with no more discomfort than conventional dental treatment. CONCLUSIONS: Very low reported levels of discomfort were associated with both non-surgical and surgical periodontal therapy by Norwegian patients treated in a specialist periodontal practice.
BACKGROUND: Smoking is a well-known risk factor for destructive periodontal disease, but its relationship with periodontal status and subgingival microbiota remains unclear. Inherent limitations of microbiological methods previously used may partly explain these mixed results, and real-time polymerase chain reaction (PCR) has been presented as a valid alternative. The aim of the present study was to investigate the clinical condition and microbiological profile of patients with chronic periodontitis as related to the habit of smoking. METHODS: Fifty patients (33 to 59 years old), 25 smokers and 25 never-smokers, constituted the sample. The visible plaque index (VPI), gingival bleeding index (GBI), bleeding on probing (BOP), periodontal probing depth (PD), clinical attachment loss (CAL), and gingival crevicular fluid (GCF) volume were recorded. Real-time PCR quantified Porphyromonas gingivalis, Micromonas micros, Dialister pneumosintes, Actinobacillus actinomycetemcomitans and total bacteria in subgingival samples. RESULTS: Smokers and never-smokers showed similar values for VPI, GBI, and BOP. Smokers had deeper PD in buccal/lingual sites and higher CAL independently of the tooth surface. The GCF volume was smaller in smokers, independent of the PD. Similar amounts of total bacteria and P. gingivalis were observed for both groups. Significantly higher numbers of D. pneumosintes and M. micros were present in smokers and associated with moderate and deep pockets. When heavy smokers were considered, higher counts of total bacteria, M. micros, and D. pneumosintes were observed. CONCLUSIONS: Smoking seems to have a detrimental impact on the periodontal status and microbiological profile of patients with periodontitis. Compared to never-smokers, smokers had deeper pockets, greater periodontal destruction, and higher counts of some putative periodontal pathogens.
Our objective was to investigate the presence of periodontal pathogens in comparison with the total degree of microorganisms after non-surgical periodontal therapy. The study material consisted of microbiological samples from periodontal pockets originating from 140 consecutive patients with chronic generalized severe periodontitis. The subgingival samples from periodontal pockets were obtained by a sterile curette, placed into 2 ml of the VMGA III medium, homogenized and serially diluted in the Brucella broth. 100 microl aliquots from the dilutions were inoculated onto the Brucella and the TSBV agar. The plates were incubated in an anaerobic chamber and under microaerobic conditions. The isolates were identified according to colonial and cellular morphology, the potency disk pattern, and the biochemical profiles. After instrumentation, no periodontal pathogens were isolated in 46 (33%) patients, while 94 patients (67%) were infected with one to five different periodontal pathogens. However, higher degree of the total microflora was positively correlated with number of isolated pathogens, a putative indicator of their presence. Therefore, due to the occurrence of residual microorganisms after non-surgical mechanical treatment, information about the pattern of these pathogens is needed for application of antimicrobial therapy. The level of microbial load in gingival pockets, including both pathogenic and non-pathogenic species, is one of the determinants of presence of residual pathogens after non-surgical periodontal therapy.
The purpose of the present study was to compare the width of the periodontal space following two different marginal periodontal healing reactions (long epithelial junction and connective tissue healing involving formation of reparative cementum) with the width of normal periodontium, either intact or following reattachment. Twelve permanent lateral incisors in monkeys from a previous experimental study on periodontal wound healing on denuded surfaces were selected based on strict healing criteria. The periodontal width was measured histomorphometrically and compared to the periodontal width on the contra lateral side of the same root where reattachment had taken place and with the width of normal periodontal space of neighbouring untreated teeth. The mean periodontal width for both after formation of a long junctional epithelium and reparative cementum were significantly larger than the control width, approximately 290%. This may be taken as evidence of an impaired functional adaptation of the reparative tissue compared to a reestablished or normal periodontal membrane.
There are several discrepancies with respect to the composition of subgingival plaque in gingivitis and in inactive adult periodontitis (AP). In this study we compared subgingival plaque samples taken from gingivitis sites to those from inactive periodontitis sites of the same patients. Of 44 patients plaque samples from 86 gingivitis sites and 92 periodontitis sites were analysed. Darkfield microscopy showed a higher proportion of spirochetes and mobile rods in the periodontitis sites. Analysis of cultures revealed a higher and statistically significant number of anaerobes in the periodontitis sites (1.7 x 10(7) vs 3 x 10(6), p = 0.006). The following bacterial species were isolated more frequently from periodontitis sites than from gingivitis sites: Actinobacillus actinomycetemcomitans (18% vs 10%), as well as the black-pigmented Prevotella intermedia (68% vs 48%) and Porphyromonas gingivalis (48% vs 28%). On the one hand, these small differences in the bacteriological parameters can be explained by the fact that both gingivitis and periodontitis plaque samples were taken from the same periodontitis patients. An infection of the gingivitis sites from the parodontitis sites within the same patient could not be excluded. On the other hand, the mean probing depth of the gingivitis sites was relatively high, 3.6 mm (measuring point interdental plus pseudo-pocket) which may favor the growth of anaerobic bacteria.
Recent microbiological studies support the concept that specific gram negative bacteria play a major role in the etiology and pathogenesis of human chronic inflammatory periodontal disease. Actinobacillus actinomycetemcomitans has been isolated frequently from juvenile periodontitis and Porphyromonas gingivalis has been shown to be a prominent species in adult periodontitis in humans. The purpose of this study was to determine levels of the specific antibodies to A.actinomycetemcomitans and P.gingivalis in 17 patients with juvenile and 15 patients with adult periodontitis and 24 healthy subjects. IgG and IgM antibody titers against these antigens were determined by enzyme-linked immunosorbent assay (ELISA). The levels of antibodies against A.actinomycetemcomitans were significantly higher in the juvenile periodontitis compared to the adult periodontitis patients and controls. Anti-P.gingivalis antibodies were elevated in adult periodontitis compared to juvenile periodontitis patients and controls.
BACKGROUND: The purpose of this study was to compare 12-month clinical responses to mechanical periodontal treatment in Chinese chronic periodontitis patients at sites with and without Actinobacillus actinomycetemcomitans at baseline, and to investigate the ability of mechanical periodontal treatment to eliminate A. actinomycetemcomitans. METHODS: Nineteen patients and a total of 76 selected sites with a mean probing depth (PD) of > or = 7 mm were studied. Whole mouth presence or absence of supragingival plaque (PI%), bleeding on probing (BOP%), probing depth (PD), and probing attachment level (PAL) were recorded at six sites per tooth at baseline and after 3, 9, and 12 months. Baseline subgingival plaque samples were taken from the deepest PD site in each quadrant using sterile paper points and were cultured on TSBV plates for 5 days in a 5% CO2-air incubator. All sites received mechanical periodontal treatment, which included oral hygiene instructions and supragingival and subgingival instrumentation with or without surgical access, with maintenance care being provided once every 3 months thereafter. RESULTS: At baseline, A. actinomycetemcomitans was isolated in 13 of the 19 subjects (68%) and in 29 out of the 76 sampled sites (38%). At the end of 12 months, in three of the initially A. actinomycetemcomitans-positive subjects, A. actinomycetemcomitans was not detected in the sampled sites, while one subject, in whom A. actinomycetemcomitans was not initially found at the sampled sites was A. actinomycetemcomitans-positive at 12 months. Multi-level variance component models showed there was no statistically significant difference in all clinical parameters between A. actinomycetemcomitans-positive and -negative subjects (P > 0.05). In the sampled sites of the initially A. actinomycetemcomitans-positive subjects, the mean PD was reduced from 7.6 +/- 1.6 mm to 3.2 +/- 1.8 mm, the mean PAL gain was 1.4 +/- 2.0 mm, and the mean recession was 3.0 +/- 2.3 mm. The corresponding figures in the sampled sites of the initially A. actinomycetemcomitans-negative subjects were 7.5 +/- 1.6 mm to 2.7 +/- 1.0 mm, 2.3 +/- 2.6 mm and 2.4 +/- 2.2 mm for mean PD changes, PAL gain, and mean recession, respectively. CONCLUSIONS: Favorable clinical responses to mechanical periodontal therapy may occur in Chinese chronic periodontitis patients at sites infected with A. actinomycetemcomitans. The mere detection of subgignival A. actinomycetemcomitans does not necessarily imply poorer treatment outcomes in the control of chronic periodontitis.
BACKGROUND: Because epidemiological studies provide evidence that periodontal infections are associated with an increased risk of progression of cardiovascular and cerebrovascular disease, we postulated that endothelial dysfunction, a critical element in the pathogenesis of atherosclerosis, would be present in patients with periodontal disease. METHODS: We tested endothelial function in 30 patients with severe periodontitis and 31 control subjects using flow-mediated dilation (FMD) of the brachial artery. The groups were matched for age, sex, and cardiovascular risk factors. Three months after periodontal treatment, including both mechanical and pharmacological therapy, endothelial function was reassessed by brachial artery FMD. Markers of systemic inflammation were measured at baseline and at follow up. RESULTS: Flow-mediated dilation was significantly lower in patients with periodontitis than in control subjects (6.1% +/- 4.4% vs 8.5% +/- 3.4%, P = .002). Successful periodontal treatment resulted in a significant improvement in FMD (9.8% +/- 5.7%; P = .003 compared to baseline) accompanied by a significant decrease in C-reactive protein concentrations (1.1 +/- 1.9 vs 0.8 +/- 0.8 at baseline, P = .026). Endothelium-independent nitro-induced vasodilation did not differ between the study groups at baseline or after periodontal therapy. CONCLUSION: These results indicate that treatment of severe periodontitis reverses endothelial dysfunction. Whether improved endothelial function will translate into a beneficial effect on atherogenesis and cardiovascular events needs further investigation.
STATEMENT OF PROBLEM: The fibroblast is considered an important cellular component in periodontitis because it is the predominant cell type in periodontal connective tissue. PURPOSE: The purpose of this study was to test whether gingival fibroblasts (GF) and periodontal ligament fibroblasts (PDLF) are heterogeneous in their production of inflammatory mediators associated with bone resorption in response to lipopolysaccharides from the gram-negative bacterium Porphyromonas gingivalis. To test this hypothesis, we (1) compared interleukin-6 production by cultured human PDLF and GF isolated from the same individual when exposed to P. gingivalis lipopolysaccharide; and (2) compared prostaglandin-E2 production by cultured human PDLF and GF isolated from the same individual when exposed to P. gingivalis lipopolysaccharide. MATERIAL AND METHODS: Human periodontal ligament and gingival fibroblasts were cultured from biopsies and exposed to P. gingivalis lipopolysaccharide. Levels of interleukin-6 and prostaglandin-E2 secreted into culture supernatant were measured by enzyme-linked immunosorbent assay and the data analyzed. Gingival fibroblasts secreted similar interleukin-6 and elevated prostaglandin-E2 levels compared with unstimulated cells. Periodontal ligament fibroblasts secreted elevated levels of both mediators compared with unstimulated cells. Secreted levels of interleukin-6 and prostaglandin-E2 by primary gingival and periodontal ligament fibroblast cultures appear to differ when stimulated with a periodontal pathogen-related virulence factor. CONCLUSION: The fibroblast of the periodontal ligament and the fibroblast of the gingiva may represent different phenotypes that play unique roles in tissue responses to implants.
By using a sensitive enzyme-linked immunosorbent assay, 200 randomly selected sera from Red Cross blood donors were screened for immunoglobulin G (IgG), IgA, and IgM levels against Actinobacillus actinomycetemcomitans, Bacteroides gingivalis, and Bacteroides intermedius. A subgroup of 79 blood donors was clinically examined for type and extent of periodontal destruction, and serological and clinical data were subjected in all possible dual combinations to correlation analyses. The results revealed that the majority of the blood donors suffered from moderate to severe adult periodontitis, often coupled with severe gingival inflammation. No cases of localized juvenile periodontitis or rapidly progressive periodontitis were observed. The extent of periodontal destruction proved to be significantly correlated only to the IgG response levels against B. gingivalis. Corresponding correlation tests assessing the relationships of loss of attachment, bone loss, pocket depth, and papillary bleeding index with the IgG responses to A. actinomycetemcomitans were of marginal significance, while the IgG responses to B. intermedius revealed no relationship to the periodontal health status. The specific IgM responses proved to be unrelated to the clinical parameters, but interestingly, they were found to be highly correlated with each other. Specific IgA levels were frequently too low for enzyme-linked immunosorbent assay testing and, therefore, had to be exempted from statistical analyses. Assessments of the serotype specificity of strongly elevated IgG responses to A. actinomycetemcomitans disclosed no evidence for an association of a particular serotype-specific IgG response with the occurrence of adult periodontal destruction. In contrast to results of earlier studies, a number of sera were found to contain strongly elevated IgG levels against two or even all three serotypes. Although derived by an alternative approach, the reported results largely corroborate earlier observations linking only the occurrence of elevated anti-B. gingivalis IgG responses to the presence of marked periodontal lesions in adults.
Studies of blastogenic responsiveness induced in peripheral blood lymphocytes (PBL) from periodontally healthy subjects by periodontal bacteria have conflicted. This study was undertaken to examine the blastogenic response of periodontally healthy subjects under experimental conditions which provide improved control of laboratory variables. By using cryopreserved PBL the responses of all subjects in an experiment were determined on the same day under identical conditions. The periodontally healthy populations consisted of subjects of the same age range and sex matched to three distinct groups of periodontally diseased subjects (i.e., juvenile (JP), severe (SP), and moderate (MP) periodontitis). The bacterial stimulants tested were chosen on the basis of known association with and isolation from persons fitting the disease classifications. If PBL response differences between periodontally healthy and diseased subjects exist they should be most obvious in response to predominant organisms associated with the disease states. PBL cultures were harvested after a 4 hour pulse with 3H-thymidine on days 4 and 6 of culture. Three separate experiments were conducted comparing one healthy group and one diseased group. In all three experiments subjects in the healthy group responded as frequently as did those in the diseased group, the dose-response distribution was indistinguishable, and the magnitude of the responses was not substantially different between groups. These results suggest nonspecific activation as the major determinant in the blastogenic response, rather than specific sensitization occurring during initiation or progression of periodontitis.
The purpose of this investigation was to determine whether the presence of disease-associated bacteria in health-associated plaque correlated with susceptibility to periodontitis over time. Sites of periodontal health were identified in 65 adults. Six months later (recall 1), plaque was collected from sites that remained in periodontal health, and specific bacteria were detected using monoclonal antibodies in a microscopic assay. The spirochete morphogroup was identified by phase contrast microscopy. The relationship between detection at recall 1 and development of periodontitis over two successive 6-month intervals (recalls 2 and 3) was evaluated by means of logistic regression using generalized estimating equations (GEE), from which odds ratios (OR) were estimated and tested for significance. Significant relationships were defined as those having ORs with P < 0.05. Ninety-three of 1,032 sites developed signs of early periodontitis over the 12-month interval between recall 1 and recall 3. The spirochete morphogroup (OR = 3.13, P < 0.001) and pathogen-related oral spirochetes (PROS) (OR = 3.68, P < 0.001) were significantly associated with healthy sites that developed periodontitis. The association of Treponema socranskii was not significant (OR = 3.62, P = 0.0918). Odds ratios for Campylobacter rectus, Eikenella corrodens, and Porphyromonas gingivalis were less than 2.0 and not significant. Treponema denticola was not detected in health-associated plaque from stable health sites and was detected in only three sites that progressed to periodontitis. These findings indicate that the presence of PROS and some unidentified spirochetes in health-associated plaque is associated with increased susceptibility to periodontitis.