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PubMed1985

Periodontal ligament areas and occlusal forces in dentitions restored with cross-arch bilateral end abutment bridges.

The aim of the present investigation was to find out to what extent the magnitudes of chewing and biting forces in dentitions restored with cross-arch bilateral end abutment bridges are correlated to the areas of the periodontal ligament supporting the abutment teeth. 12 subjects whose dentitions had been periodontally treated and prosthetically restored participated in the study. The chewing and biting forces were measured in various parts of as well as over the entire dentition simultaneously using 4 strain gauge transducers bilaterally placed in pontics of the posterior (first molar/second premolar) and anterior regions. Based on calculations of the periodontal ligament areas, a new periodontal support index, PSIL, is introduced. This index expresses the relation between the total remaining periodontal ligament area supporting the bridge abutments and total maximal periodontal ligament area if all teeth were preserved as abutments. It is compared with the index of Ante, PSIA, which expresses the relation between the total remaining periodontal ligament area of all abutments and the total maximal periodontal ligament area of all replaced teeth. Within the present group of subjects, PSIL varied from 10 to 44% and PSIA from 17 to 118%. Based on the results of the correlation analyses, it is suggested that in dentitions restored with cross-arch bilateral end abutment bridges, the magnitude of the chewing forces is positively correlated to the areas of the periodontal ligament supporting the bridge abutments, whereas the periodontal ligament areas have no influence on the comparatively larger biting forces. The relevance of the 2 periodontal support indices and the clinical implications of the results of the study are discussed.

Adult↗
PubMed1991

Microbiology in the management of destructive periodontal disease.

This paper summarizes the rationale for the application of microbiology in the management of destructive periodontal diseases. The subgingival microbiota in patients with severe periodontitis is complex and contains high numbers of obligate anaerobic bacteria as well as facultative micro-organisms. It has become clear that major differences exist in the composition of the subgingival microflora. These differences are not only quantitative but also qualitative. Difference in plaque composition is the basis for the application of clinical microbiology in the management of periodontal disease. Several bacterial species have emerged as useful indicators for progressive periodontitis. In this respect, the importance of Actinobacillus actinomycetemcomitans, Bacteroides gingivalis and Bacteroides intermedius has been shown in a number of studies. It has become clear that A. actinomycetemcomitans is not specifically associated with the local form of juvenile periodontitis, but this micro-organism is probably also of importance in severe periodontitis in adult patients. Selection of individuals with an A. actinomycetemcomitans associated periodontitis is essential since successful treatment in these patients needs an adjunctive antibiotic therapy. Microbiological testing can be useful in patients showing a poor response to periodontal treatment (refractory periodontitis). Factors which may be responsible include poor oral hygiene, poor subgingival debridement, the patient's susceptibility and a subgingival microflora resistant to therapy. In this patient category, microbiological testing is capable of diverting continuing periodontal treatment. Furthermore, microbiology can be useful in evaluating periodontal treatment. Successful elimination of specific periodontopathic microorganisms can be used to determine recall intervals.

Bacteria↗
PubMed2006

Tooth loss in well-maintained patients with chronic periodontitis during long-term supportive therapy in Brazil.

AIM: The objective of this retrospective study was to assess the reasons for tooth loss in a sample of patients who underwent periodontal therapy and supportive periodontal therapy (SPT) in a Brazilian private periodontal practice. MATERIAL AND METHODS: A sample of 120 subjects who had been treated and maintained for 10 years or longer was selected from patients attending a periodontal practice. All patients followed a similar treatment: basic procedures, re-evaluation and periodontal surgery where indicated. Reasons for tooth loss were categorized as periodontal, caries, endodontal, root fractures and extraction of retained or partially erupted third molars. RESULTS: Of the 2927 teeth present at the completion of active periodontal treatment, 53 (1.8%) were lost due to periodontal disease, 16 (0.5%) for root fracture, six (0.2%) to caries, five (0.2%) for endodontic reasons and 31 (1.0%) were lost to extraction of retained or partially erupted third molars. Logistic regression analysis was performed to investigate the association between five independent variables with tooth loss due to periodontitis. Only age (> 60 years) and smoking were statistically significant (p < 0.05). CONCLUSION: The findings of this survey were consistent with previous studies. Older subjects and smokers were more susceptible to periodontal tooth loss. In addition, patients with generalized chronic periodontitis were treated and maintained for long-term periods with low rates of tooth loss.

Adult↗
PubMed1997

Expression of T-cell receptor Vbeta2, 6 and 8 gene families in chronic adult periodontal disease.

Substantial evidence exists to suggest a role for T-cells in periodontal disease. As yet, however, the T-cell receptors remain to be characterised at the molecular level. The expression and the nucleotide sequence of genes from the T-cell receptor beta variable (TCRBV) gene families 2, 6 and 8 were analyzed in periodontal tissue from 24 patients with chronic adult periodontal disease (CAPD) and peripheral blood lymphocytes (PBL) of 16 of these patients. A restriction in the expression of these TCRBV gene families was detected in periodontal tissue from 14/24 patients with CAPD, and the pattern of gene expression was often different between individual patients; however there was no restriction in TCRBV gene expression in matched PBL samples from 8 of these 14 patients. Quantitative RT PCR analysis of samples from 5 CAPD patients who expressed all 3 TCRBV gene families in their periodontal tissues did not reveal any significant differences in the levels of gene expression in periodontal tissue and PBL. In contrast to the findings with some CAPD patients, genes from all 3 TCRBV families were always expressed in periodontal tissue and PBL from disease-free control subjects. PCR products from both the PBL and periodontal tissue of CAPD patients were cloned and sequenced; analysis of the nucleotide sequence revealed diversity with respect to the expression of TCRB joining (TCRBJ) and TCRB diversity (TCRBD) genes and the sequence of the junctional region in all samples analysed. In conclusion, in CAPD, the pattern of TCRBV gene expression in periodontal tissue is often but not always different from that in PBL and healthy periodontal tissue, which may indicate, in some cases, a local influence on particular T-cell subsets which is relevant to the pathogenesis of periodontal disease. However, the expressed TCRB genes are heterogeneous at the nucleotide level, emphasising the underlying complexity at the molecular level in the local T-cell response in CAPD.

Adult↗
PubMed1992

A re-evaluation of the distribution of the elastic meshwork within the periodontal ligament of the mouse.

The elastic properties of the periodontal ligament have been attributed, in part, to oxytalan fibers, as no other types of elastic fibers are described there. It has been difficult to study the periodontal elastic meshwork by standard microscopic techniques because it is partially obscured by the adjacent periodontal ligament collagen fibers. Our study employed methods which either completely or partially removed mandibular molar periodontal ligament collagen fibers, exposing a previously undescribed periodontal elastic meshwork. The periodontal elastic meshwork was composed of many elastin lamellae containing both peripheral microfibrils of regular arrangement and central microfibrils of irregular arrangement, which could only be demonstrated in oxidized tissues. Peripheral, regularly arranged bundles of microfibrils resembled oxytalan fibers, which were often adherent to the border of the elastin lamella. Elastin lamellae containing irregular microfibrils resembled elaunin fibers. These fibers probably enclosed either blood vessels, nerves or collagen fiber bundles. Peripheral microfibrils attached elaunin to cementum, alveolar bone, blood vessels, and principal periodontal collagen fibers. Thus, the periodontal elastic meshwork is composed of both oxytalan and elaunin fibers. Microfibrils attach elaunin fibers to the adjacent non-elastic tissue and also form bundles which traverse the periodontal ligament space and are probably the oxytalan fibers demonstrable by light microscopic techniques. This meshwork of oxytalan and elaunin fibers probably contributes to tooth support and maintenance of periodontal homeostasis by dissipating chewing forces and maintaining patency of periodontal blood vessels.

Animals↗
PubMed1993

Immunohistological analysis of memory T lymphocytes and activated B lymphocytes in tissues with periodontal disease.

Memory T-cells and activated B-cells were identified in cryostat sections of adult periodontitis (AP) lesions and categorized in terms of frequency and distribution. Nineteen periodontitis biopsies were obtained at the time of periodontal surgery to remove residual periodontal pockets following the completion of initial preparation. Gingival tissues exhibited various degree of inflammation (GI of 0-2) but probing depths of > 4 mm and > 5 mm loss of attachment. As a control, 5 gingivitis specimens (GI of 1, probing depth and loss of attachment of < or = 3 mm) were obtained from premolar and third molar sites requiring extraction for either orthodontic treatment or pericoronitis. Serial cryostat sections (6 microns in thickness) were prepared from each biopsy, on which a double staining avidin-biotin immunoperoxidase and avidin-biotin alkaline phosphatase technique was used to identify CD4+, CD45RO+ memory T-cells and activated CD19+ B-cells expressing CD23 or CD25. In periodontitis lesions, the mean percentage of CD4+ cells expressing CD45RO was consistently high (65.9% in the crevicular (C) one-third (1/3), 61.2% in the middle (M) 1/3 and 62.5% in the oral (O) 1/3). This contrasts with the low mean percentage of CD4+, CD45RA+ naive T-cells (17.1% in the C 1/3, 14.8% in the M 1/3 and 12.4% in the O 1/3). In gingivitis specimens, the incidence of CD4+, CD45RO+ was 81.9% in the C 1/3, 81.1% in the M 1/3 and 89.0% in the O 1/3. This was higher than that of periodontitis biopsies. With CD4+, CD45RA+ the incidence was 10.0% in the C 1/3, 8.0% in the M 1/3, and 6.6% in the O 1/3 and the relationship to the periodontitis biopsies was reversed. However, the percentage of CD23+ and CD25+, CD19+ B-cells which were identified in 13 out of 19 samples from periodontitis varied significantly (0-100% for CD23, 0-36.2% for CD25) in spite of similar clinical status. The frequency of B-cells and activated B-cells in the gingivitis was much lower than that of periodontitis. These results indicate that both T-cells and B-cells were in active stage in periodontitis lesions. Differences of immunohistological features between gingivitis and periodontitis may be attributable to the heterogeneity of profiles of cytokine production by CD4+, CD45RO+ "memory' cells.

Adult↗
PubMed2005

In vitro cell-type specific biological response of human periodontally related cells to platelet-rich plasma.

OBJECTIVES: Platelet-rich plasma is a blood-derived fraction containing high concentrations of platelets and growth factors. Applied in the form of a gel on surgical wounds, it is able to stimulate hard and soft tissue repair and has been proposed for use in the field of periodontal regeneration. However to date, little is known about the biological interactions between platelet-rich plasma and periodontally related cells. In this study, we investigated the effects between platelet-rich plasma and cell populations involved in periodontal regeneration, namely primary human periodontal ligament cells, gingival fibroblasts and keratinocytes. MATERIAL AND METHODS: The proliferation of human periodontal ligament cells, gingival fibroblasts and keratinocytes by [3H]thymidine incorporation was assessed. The alkaline phosphatase activity and type I collagen levels of human periodontal ligament cells were also evaluated by a spectrophotometric assay and western blot analysis, respectively. RESULTS: Incubation of human periodontal ligament cells with platelet-rich plasma resulted in time-dependent growth stimulation (up to fourfold of control at 72 h). Likewise, an increase in the specific activity of alkaline phosphatase (fourfold at 6 days) and collagen (twofold at 7 days) was observed. Platelet-rich plasma also enhanced human gingival fibroblasts proliferation by twofold, whereas it inhibited human keratinocytes growth by 40%, with respect to their own controls at 72 h. CONCLUSION: Cell populations related to periodontal tissue were differently affected by platelet-rich plasma. In fact, a strong stimulation of human periodontal ligament cells proliferation, a minor increase in the growth rate of human gingival fibroblasts and a marked decrease of human keratinocytes proliferation were evident. In addition, in human periodontal ligament cells increased collagen and alkaline phosphatase activity levels were observed. These findings appear interesting in view of platelet-rich plasma utilization in periodontal regeneration.

Alkaline Phosphatase↗
PubMed1980

Neutrophil chemotaxis dysfunction in human periodontitis.

Polymorphonuclear leukocyte (PMNL) chemotaxis studies of 32 patients with localized juvenile periodontitis (periodontosis or LJP), 10 adult patients with a history of LJP (post-LJP), 8 patients with generalized juvenile periodontitis (GJP), and 23 adults with moderate to severe periodontitis were performed: (i) to determine the prevalence of a PMNL chemotaxis defect in a large group of LJP patients; (ii) to study PMNL chemotaxis in patients with other forms of severe periodontal disease; and (iii) to determine if the PMNL chemotaxis defect seen in LJP patients is a cell-associated defect or is mediated by humoral factors. The effect of periodontal treatment on PMNL chemotaxis was studied in nine LJP patients. The chemotactic response was measured with the Boyden chamber procedure, and patient's peripheral PMNL were compared with those of control subjects, using endotoxin-activated serum, bacterial factor, N-formylmethionyl-leucylphenylalanine, and leukocyte-derived chemotactic factor as the standard chemoattractants. Based upon statistical analysis of chemotaxis assays, most carried out on at least two and often three or more separate occasions, 26 of 32 LJP patients, 7 of 10 post-LJP patients, and 5 of 8 GJP patients exhibited cellular defects of chemotaxis, whereas only 2 of 23 of the patients with adult periodontitis exhibited depressed chemotaxis. Elevated PMNL chemotaxis was occasionally found in subjects with juvenile periodontitis (2 of 32 with LJP and two of eight with GJP); however, it was found in a significant number (10 of 23) of patients with adult periodontitis. In eight of nine LJP patients, depressed PMNL chemotaxis was observed before and after periodontal therapy. The results indicate that the PMNL chemotaxis defect observed in juvenile periodontitis is due to a cell-associated defect of long duration. These studies suggest that the PMNL plays a major protective role against periodontal infection and that the cellular chemotactic defects and may predispose subjects to LJP.

Adolescent↗
PubMed1998

Prevalence of Porphyromonas gingivalis and periodontal health status.

Periodontitis is a common, progressive disease that eventually affects the majority of the population. The local destruction of periodontitis is believed to result from a bacterial infection of the gingival sulcus, and several clinical studies have provided evidence to implicate Porphyromonas gingivalis. If P. gingivalis is a periodontal pathogen, it would be expected to be present in most subjects with disease and rarely detected in subjects with good periodontal health. However, in most previous studies, P. gingivalis has not been detected in the majority of subjects with disease, and age-matched, periodontally healthy controls were not included for comparison. The purpose of the study reported here was to compare the prevalence of P. gingivalis in a group with periodontitis to that of a group that is periodontally healthy. A comprehensive sampling strategy and a sensitive PCR assay were used to maximize the likelihood of detection. The target sequence for P. gingivalis-specific amplification was the transcribed spacer region within the ribosomal operon. P. gingivalis was detected in only 25% (46 of 181) of the healthy subjects but was detected in 79% (103 of 130) of the periodontitis group (P < 0.0001). The odds ratio for being infected with P. gingivalis was 11.2 times greater in the periodontitis group than in the healthy group (95% confidence interval, 6.5 to 19.2). These data implicate P. gingivalis in the pathogenesis of periodontitis and suggest that P. gingivalis may not be a normal inhabitant of a periodontally healthy dentition.

Adult↗
PubMed1999

Chief complaints of patients seeking treatment for periodontitis.

BACKGROUND: Hardly any data are available concerning the chief complaints, or CCs, of patients with periodontitis. The authors conducted a study to determine the most common CCs among a group of subjects with periodontitis. METHODS: The authors examined the dental records of 191 patients with periodontitis to determine what CCs they orally reported having at an initial examination. Patients were referred mainly by other members of the dental health team. Eighty percent of the patients were diagnosed with moderate or moderate-to-severe periodontitis. The authors recorded the frequency of different CCs to determine the most common complaints. RESULTS: The authors recorded 336 CCs from the records of 191 subjects with periodontitis. There were 21 different CCs. The most common CC reported was, "I was told I have gum disease." The second most common CC reported was, "I would like to save my teeth." Neither of these CCs are true periodontitis symptoms. Bleeding gums--a true periodontitis symptom--was the third most common CC. Only 6.2 percent of the subjects reported having painful gingiva, and only 29.3 percent of the subjects reported having dental-emergency-related CCs. CONCLUSIONS: The authors found that the motivation to seek periodontal treatment was most commonly based on information given to the subjects by a member of the dental health team, rather than a periodontitis symptom. CLINICAL IMPLICATIONS: Renewed efforts and increased responsibility of the dental health team members to inform patients about the presence of periodontitis are needed, as well as emphasizing to the public the risk of losing teeth as a result of periodontitis.

Adolescent↗
PubMed2006

Periodontal infections and cardiovascular disease: the heart of the matter.

BACKGROUND: Oral infection models have emerged as useful tools to study the hypothesis that infection is a cardiovascular disease (CVD) risk factor. Periodontal infections are a leading culprit, with studies reporting associations between periodontal disease and CVD. The results, however, have varied, and it often is unclear what conclusions can be drawn from these data. SUMMARY: An association exists between periodontal disease and CVD. It is unknown, however, whether this relationship is causal or coincidental. Early studies predominantly used nonspecific clinical and radiographic definitions of periodontal disease as surrogates for infectious exposure. While most studies demonstrated positive associations between periodontal disease and CVD, not all studies were positive, and substantial variations in results were evident. More recent studies have enhanced the specificity of infectious exposure definitions by measuring systemic antibodies to selected periodontal pathogens or by directly measuring and quantifying oral microbiota from subgingival dental plaque. Results from these studies have shown positive associations between periodontal disease and CVD. CONCLUSIONS: Evidence continues to support an association among periodontal infections, atherosclerosis and vascular disease. Ongoing observational and focused pilot intervention studies may inform the design of large-scale clinical intervention studies. Recommending periodontal treatment for the prevention of atherosclerotic CVD is not warranted based on scientific evidence. Periodontal treatment must be recommended on the basis of the value of its benefits for the oral health of patients, recognizing that patients are not healthy without good oral health. However, the emergence of periodontal infections as a potential risk factor for CVD is leading to a convergence in oral and medical care that can only benefit the patients and public health.

Aggregatibacter actinomycetemcomitans↗
PubMed2005

Neurotrophin-4/5-depletion induces a delay in maturation of the periodontal Ruffini endings in mice.

Neurotrophin-4/5 (NT-4/5) - a member of the neurotrophic factors - is a ligand for TrkB, which has been reported to be expressed in the mechanoreceptive Ruffini endings of the periodontal ligament. The present study examined developmental changes in the terminal morphology and neural density in homozygous mice with a targeted disruption of the nt-4/5 gene and wild-type mice by immunohistochemistry for protein gene product 9.5 (PGP 9.5), a general neuronal marker, and by quantitative analysis using an image analyzer. Postnatal development of terminal Schwann cells was also investigated by enzymatic histochemistry for non-specific cholinesterase activity (ChE). Furthermore, the immuno-expression of TrkB and low affinity nerve growth factor receptor (p75-NGFR) was surveyed in the periodontal Ruffini endings as well as trigeminal ganglion. At postnatal 1 week, the lingual periodontal ligament of both types of mice contained PGP 9.5-positive nerve fibers showing a tree-like ramification with axonal swellings in their course. In both types of mice at 2 weeks of age, comparatively thick nerve fibers with a smooth outline increased in number, and frequently ramified to form nerve terminals with dendritic profiles. However, no typical Ruffini endings with irregular outlines observed in the adult wild-type mice were found in the periodontal ligament at this stage. At postnatal 3 weeks, typical Ruffini endings with irregular outlines were discernable in the periodontal ligament of the wild-type mice while the dendritic endings showing smooth outlines were restricted to the homozygous mice. After postnatal 8 weeks, both types of mice showed an increase in the number of Ruffini endings, but the morphology differed between the wild-type and NT-4/5 homozygous mice. In the wild-type mice, a major population of the Ruffini endings expanded their axonal branches and developed many microprojections, resulting in a reduction of endings with smooth outlines. In contrast, we failed to find such typical Ruffini endings in the periodontal ligament of the homozygous mice: A majority of the periodontal Ruffini endings continued to show smooth outlines at postnatal 12 weeks. Quantitative analysis on neural density demonstrated a reduction in the homozygous mice with a significant difference by postnatal 8 weeks. Enzymatic histochemistry for non-specific ChE did not exhibit a distinct difference in the distribution and density of terminal Schwann cells between wild-type and homozygous mice. Furthermore, TrkB and p75-NGFR mRNA and proteins did not differ in the trigeminal ganglion between the two types. The periodontal Ruffini endings also displayed immunoreactivities for TrkB and p75- NGFR in both phenotypes. These findings suggest that the nt-4/5 gene depletion caused a delay in the formation and maturation of the periodontal Ruffini endings in the mice by inhibiting the growth of the periodontal nerves at an early stage, and indicate that multiple neurotrophins such as NT- 4/5 and BDNF might play roles in the development and/or maturation of the periodontal Ruffini endings.

Animals↗
PubMed2002

Periodontitis in humans and non-human primates: oral-systemic linkage inducing acute phase proteins.

BACKGROUND: The acute phase response (APR) represents a systemic counterpart to the localized inflammatory response. This report describes patient-oriented and non-human primate model studies to determine the effect of periodontal disease on systemic acute phase proteins (APP). METHODS: Patient-oriented studies included comparison of the levels of APP, using enzyme-linked immunosorbent assay (ELISA), with the presence and severity of periodontitis in localized chronic periodontitis (LCP), generalized aggressive periodontitis (GAP), and Sjogren's syndrome (SS) patients. The non-human primate experiments evaluated the serum level of APPs under natural conditions, following mechanical hygiene, experimental gingivitis, and during ligature-induced periodontitis. RESULTS: Analysis of the LCP population showed what appeared to be a threshold of periodontal disease severity required for elevating the C-reactive protein (CRP) and haptoglobin (HG). The results demonstrated a significant elevation in CRP in the GAP versus the control groups, as well as lower levels of all mediators in healthy non-smokers (HNS) versus smokers (HS), suggesting that these systemic inflammatory markers were altered in response to challenge by noxious materials from smoking. Significantly different levels of CRP, HG, and alpha1-antiproteinase were noted in the SS patients suggesting that the autoimmune aspects of Sjögren's syndrome may impact upon oral health and systemic responses. Parallel evidence was also obtained from the primate studies. Providing mechanical oral hygiene, which significantly lowered clinical inflammation and bleeding of the gingiva, decreased the serum APP levels. Both CRP and fibrinogen were significantly elevated during progressing periodontitis, which also appeared to have an impact on serum lipids and lipoproteins. CONCLUSIONS: These findings supported results relating chronic oral infections and the inflammation of periodontitis as contributors to and/or triggers for systemic inflammatory responses. Finally, similarities in the clinical and microbiological parameters of gingival inflammation and periodontitis between humans and non-human primates was extended to identification of changes in serum APP in the non-human primates that appeared to be in direct response to the induction of progressing periodontitis. These systemic changes provide additional evidence for the biological plausibility of periodontal infections contributing to various systemic diseases.

Acute-Phase Proteins↗
PubMed1988

Microbiological and immunological studies of adult periodontitis in patients with noninsulin-dependent diabetes mellitus.

The subgingival microflora and serum antibody response was examined in periodontitis patients with noninsulin-dependent diabetes mellitus (NIDDM), impaired glucose tolerance (IGT), and normal glucose tolerance (NGT). The predominant cultivable microflora was determined for subgingival plaque sampled from two deep periodontal pockets in each of eight adult periodontitis patients with NIDDM. Indirect immunofluorescence for Bacteroides intermedius, Bacteroides gingivalis, and Haemophilus actinomycetemcomitans was used to examine these same samples as well as 186 additional subgingival plaque samples from 47 patients with moderate to severe generalized periodontitis including 25 subjects with NIDDM, six subjects with IGT, and 16 subjects with NGT. Serum antibody levels to 13 microorganisms including seven oral bacterial species and one nonoral control species were measured by enzyme-linked immunosorbent assays (ELISA) in 377 subjects including 84 normal subjects without periodontal disease, 112 normal subjects with periodontitis, 19 periodontally normal subjects with IGT, 65 periodontitis patients with IGT, 15 periodontally normal subjects with NIDDM, and 82 periodontitis patients with NIDDM. Three hundred eighty-two bacterial isolates were recovered from the eight patients. B. intermedius was the most frequently isolated microorganism constituting 16% of the total isolates followed by Wolinella recta and B. gingivalis, which each accounted for 13% of the total. Streptococcus sanguis was the most prevalent microorganism, which was found in 75% of the sites. Subgingival plaque samples examined by immunofluorescence demonstrate a high prevalence of black-pigmented Bacteroides and suggest that the proportion of B. gingivalis but not B. intermedius is higher in NIDDM with periodontitis than in other groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1993

Current status of systemic antibiotic usage in destructive periodontal disease.

The recognition that periodontal diseases are primarily caused by specific microorganisms has led researchers to explore the possibility that antibiotics may enhance the effect of mechanical debridement procedures such as scaling and surgery. For some selected periodontal diseases, this has proven to be true. This paper will review systemically-administered antibiotics and the clinical studies and case reports supporting their use. In periodontal therapy, the tetracyclines are the most commonly-used antibiotics in the United States. Tetracycline hydrochloride, minocycline, and doxycycline have been shown to inhibit in vitro most putative periodontal pathogens. Several studies support the use of tetracyclines in the treatment of localized juvenile periodontitis. Penicillins such as amoxicillin are effective in vitro against most periodontal pathogens but have limited efficacy due to the presence of beta-lactamases in gingival fluid. Amoxicillin/clavulanate potassium (Au) has proven effective in treating adult refractory periodontitis characterized by a Gram-positive flora. Metronidazole is an effective adjunct in adult periodontitis associated with high numbers of "black-pigmented Bacteroides" ad spirochetes. A combination of metronidazole and amoxicillin produces a synergistic effect against A. actinomycetemcomitans and has been shown to be effective at eliminating this organism. Clindamycin is an effective adjunct in the treatment of adult refractory periodontitis associated with a predominantly Gram-negative flora. The use of macrolides, quinolones, and combinations of antibiotics is discussed. Clinical studies do not support the use of systemically-administered antibiotics in routine adult periodontitis. Clinical studies do, however, support the use of antibiotics in the treatment of specific periodontal diseases.

Anti-Bacterial Agents↗
PubMed1994

Bacteria as risk markers for periodontitis.

Specific microbial species have been closely associated with periodontitis. Through longitudinal studies, some of these microbial species have been implicated in the etiology of progressive periodontal disease. Although putative periodontal pathogens are often isolated from individuals with severe periodontitis, they also frequently inhibit the subgingival environment and are not always associated with advanced disease. In this respect, it is becoming increasingly apparent that there is no single etiology of the various periodontal diseases. Destructive periodontal diseases are the result of environmental, host, and bacterial factors. Microorganisms, however, are essential components of any model for progressive periodontitis. This paper selectively reviews bacteria as risk markers for periodontitis. Attention focuses on bacteria in conjunction with behavioral patterns (oral hygiene habits and smoking) and host response (gingival crevicular fluid substances) as risk markers for periodontitis. Prospective studies implicating specific bacteria in progressive periodontitis are addressed and a bacterial risk assessment model for progressive periodontitis is discussed with respect to the interplay between bacterial, environmental, and host markers.

Bacteria↗
PubMed1998

Diabetes prevents periodontitis-induced increases in gingival platelet derived growth factor-B and interleukin 1-beta in a rat model.

Periodontitis is a chronic inflammatory disease characterized by a progression that is very much dependent on host response. The gingiva can be considered to be in a constant state of wounding (pathologic wounding by bacterial plaque) and a constant state of maintenance/repair. In this context, any metabolic disturbance in the host which compromises tissue repair/wound healing will exacerbate the progression of periodontitis. Diabetes presents an interesting example because two major complications of diabetes are delayed wound healing and periodontitis. Our previous studies indicate that delayed wound healing and periodontitis may be manifestations of a general systemic deficit in diabetes involving alteration of macrophage cytokine gene expression. The present study was designed to determine whether: 1) diabetes-induced metabolic alterations affect gingival cytokine levels; and 2) diabetes-induced metabolic alterations modify the gingival cytokine profile in periodontitis. Sprague-Dawley rats (N=12/group) were injected with streptozotocin (65 mg/kg) into the tail vein to induce diabetes (defined by blood glucose levels > 250 mg/dl) or received the injection vehicle or no treatment as controls. Periodontitis was induced in additional groups of diabetic and control rats by gavage with Porphyromonas gingivalis A7436. After 90 days, serum glucose was analyzed to document diabetes; alveolar bone level was measured to document severity of periodontitis; gingiva was harvested circumferentially from the first and second molars; and cytokines in gingival homogenates were assayed by ELISA using commercial kits. Cytokine levels were expressed as mean+/-SEM pg/microg protein. Diabetes alone did not alter the gingival cytokine profile for platelet-derived growth factor B (PDGF-B), interleukin 1-beta (IL-1beta), transforming growth factor-beta (TGF-beta), and tumor necrosis factor-alpha (TNF-alpha). Periodontitis alone demonstrated a significant increase (P < 0.05) in levels of PDGF-B and IL-1beta. Diabetes superimposed on periodontitis prevented these increases. Thus, diabetes-induced metabolic alterations do not affect gingival cytokine levels per se; however, they do alter the normal host response to periodontitis through blockage of periodontitis-induced increases in PDGF-B and IL-1beta.

Alveolar Bone Loss↗
PubMed1999

Effect of periodontitis and smoking on blood leukocytes and acute-phase proteins.

BACKGROUND: We have previously found hyperreactive neutrophils, intrinsic or induced, in periodontitis patients by in vitro quantitation of free oxygen radicals. The effects of periodontitis and cigarette smoking on blood parameters have generally been described separately. Our aim was to compare these systemic effects of periodontitis and cigarette smoking, separately and in combination, in order to study the hyperreactivity in peripheral neutrophils. METHODS: Blood cells and acute-phase proteins were studied in 40 periodontitis patients and 43 healthy controls. The generation of free oxygen radicals from neutrophils was measured as luminol-enhanced chemiluminescence (CL) after activation of their Fcgamma receptors with opsonized Staphylococcus aureus. RESULTS: An increase in CL in peripheral neutrophils from periodontitis patients was confirmed. Smoking had no significant effect on CL. The periodontitis patients had higher concentrations of C-reactive protein (CRP) than the controls. ANOVA analysis showed that the increase in neutrophil count, haptoglobin, and alpha-1 antitrypsin levels was significantly influenced by cigarette smoking. IgG2 was lower in patients than in controls (P <0.017, ANOVA), and there was an interaction between periodontitis and smoking (P<0.047, ANOVA). The lower concentration of IgG2 in patients who smoke may impair neutrophil function and be a mechanism by which smoking aggravates periodontitis. CONCLUSIONS: In general, the combination of periodontitis and cigarette smoking alters the parameters studied. The effects of periodontitis on CRP and IgG2 means that periodontal lesions may also leak agents, priming the peripheral neutrophils to increased CL.

Adult↗