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PubMed2004

Longitudinal stability of serum immunoglobulin G responses to periodontal bacteria.

BACKGROUND: The value of seroepidemiology in the study of periodontal infections has not been adequately explored. This study examined serum immunoglobulin (IgG) responses to periodontal bacteria in patients with periodontitis and periodontitis-free individuals over a 30-month period. METHODS: Eighty-nine patients with chronic periodontitis and 42 control subjects with no deep periodontal pockets and no or minimal attachment loss (30-72 years old, 43% men) were included. Patients were examined at baseline, after completed periodontal therapy 4 months post-baseline, and at 30 months, and controls, at baseline and 30 months. IgG antibodies to 19 periodontal species were determined by checkerboard immunoblotting. RESULTS: On average, patients displayed at baseline up to 800-fold higher titers than controls to all but three species. Over the 30-month period, titers remained stable at low levels in controls. In patients, periodontal conditions improved from a baseline mean probing depth of 3.6 mm, bleeding on probing of 62% and an average of 21.5 pockets of=6 mm/person, to 2.5 mm mean pocket depth, 30% bleeding on probing, and 1.2 deep pockets, at 30 months. Over time, antibody titers showed a modest decline in patients, but remained significantly elevated at 30 months in comparison with controls. Antibody-level changes over time were not significantly different between subjects that did and did not receive adjunctive systemic antibiotics. CONCLUSIONS: Conspicuous differences in IgG titers to periodontal bacteria exist between periodontitis patients and periodontally healthy controls. Despite successful periodontal therapy, titers remained elevated over a 30-month period, suggesting that serology may mark the history of past periodontal infection.

Adult↗
PubMed1989

Differential diagnosis of severe periodontal lesions.

In current clinical practice, a differential diagnosis of severe localized periodontal lesions is rarely made; such lesions are considered to be manifestations of periodontitis caused by specific microbes from the commensal oral flora. However, deep seated lesions of the periodontium which are in communication with the alveolar crest, are well documented periodontal consequences of pulpal pathoses and can mimic the signs and symptoms of 'periodontitis'. The very low incidence of tooth-threatening periodontal disease in ancient and modern man is revealed when differential diagnoses are used in the examination of alveolar defects in anthropological materials and when epidemiological studies use more appropriate indices. However, no periodontal index to date has incorporated a differential diagnosis between gingival and pulpal causes of alveolar bone loss. The gingival and periodontal signs of severe localized periodontal lesions are reviewed and the imprecise nature of current clinical diagnostic tests (radiography, 'pulp testing', darkfield microscopy, bleeding on probing, periodontal probing) is discussed. None of these tests is able to detect disease activity and cannot be used to predict future patterns of disease behaviour. However, the commonly held belief that the tests are accurate has resulted in most severe periodontal lesions being falsely labelled as periodontitis. Failure to carry out differential diagnosis of severe periodontal lesions has resulted in the instigation of periodontal therapy for many lesions of non-gingival origin. Whenever severe localized lesions of the periodontium are detected, the differential diagnosis between pulpal and periodontal origins should be made. The results of diagnostic tests in current use should be interpreted with extreme caution; clinicians are left to exercise their judgment based on consideration of all the available evidence.

Bone Resorption↗
PubMed1980

Actinobacillus actinomycetemcomitans in human periodontal disease: a cross-sectional microbiological investigation.

Actinobacillus actinomycetemcomitans is a facultative gram-negative bacterium which has been associated with severe oral and nonoral infections. This study examined its occurrence in the oral cavities of 10 normal juveniles, 11 normal adults, 10 juvenile periodontitis patients, and 12 adult periodontitis patients. Four deep periodontal pockets and two normal periodontal sites were sampled in the diseased patients, and six normal periodontal sites were sampled in the healthy individuals. In all subjects samples were obtained from the cheek, tongue, and saliva. Samples from a total of 172 normal periodontal sites, 83 deep periodontal pockets, 42 cheek mucosae, 42 tongue dorsa, and 42 salivas were examined. Isolation was performed by using a medium for selective isolation of A. actinomycetemcomitans (Trypticase soy agar [BBL Microbiology Systems] supplemented with 10% serum and 75 mug of bacitracin per ml). The carrier rates were 20% for normal juveniles, 36% for normal adults, 50% for adult periodontitis patients, and 90% for juvenile periodontitis patients. A. actinomycetemcomitans was on average recovered in about fivefold-higher numbers from infected deep periodontal pockets than from infected normal subgingival areas. Samples of periodontal pockets generally contained 100-fold-more cells of A. actinomycetemcomitans than did samples of the cheek, tongue, and saliva. A. actinomycetemcomitans is commonly isolated from patients with juvenile periodontitis, often isolated from patients with adult periodontitis, and occasionally isolated from normal juveniles and adults. Its primary oral ecological niche appears to be dental plaque and periodontal pockets.

Actinobacillus Infections↗
PubMed2005

Capnocytophaga spp. in periodontitis patients manifesting diabetes mellitus.

BACKGROUND: The subgingival microflora in patients presenting concurrently with periodontitis and diabetes mellitus (DM) are poorly understood. While traditional putative periodontal pathogens are implicated, research involving other oral organisms; e.g., Capnocytophaga spp., is lacking. These organisms produce a range of bacterial enzymes relevant to periodontal breakdown. It is inferred that periodontal bacteria acquire systemic access through the ulcerated periodontal pocket surface; conclusive evidence supporting this notion is limited. The aims of this investigation were to: 1) quantify and identify Capnocytophaga spp. present in healthy and diseased sites in periodontitis patients with and without DM, and 2) isolate periodontal pathogens from these patients' blood. METHODS: Twenty-one DM-periodontitis and 25 periodontitis patients were recruited. Subgingival plaque was collected from three healthy and three diseased sites per subject. Capnocytophaga spp. and total (facultative and obligate) anaerobic counts from each site were estimated. Capnocytophaga spp. were identified using 16S rRNA polymerase chain reaction (PCR) restriction fragment length polymorphism (RFLP). Statistical analyses were performed using multilevel modeling. Blood samples were subjected to HbA(1c) estimation and bacterial culture. RESULTS: A total of 848 Capnocytophaga spp. were isolated and identified. Significantly higher numbers of Capnocytophaga spp. (P <0.001) and anaerobes (P <0.001) were present in diseased sites in DM-periodontitis subjects compared to healthy sites in non-DM-periodontitis and DM-periodontitis subjects. C. ochracea (and variant) and C. granulosa were the most prevalent species. Blood samples were negative for Capnocytophaga spp. CONCLUSIONS: Total mean counts for Capnocytophaga spp. were significantly higher in DM-periodontitis subjects versus non-DM-periodontitis (P = 0.025) and at diseased sites versus healthy sites (P <0.001). Analysis of individual species revealed that the outcome varied with site status and DM status.

Adult↗
PubMed2005

Determination of smoking and obesity as periodontitis risks using the classification and regression tree method.

BACKGROUND: A model that focuses on personal risk factors associated with poor lifestyle has been proposed for the etiology of generalized periodontitis. Numerous investigations have linked individual lifestyle-related factors to periodontitis risk; however, a definite relationship among lifestyle-related factors remains unclear. The objective of this study was to determine which lifestyle-related factors demonstrated the greater impact on periodontitis risk. METHODS: The association of lifestyle-related factors, such as smoking status and obesity, with periodontitis was assessed in 372 Japanese workers via a self-administered questionnaire. Smoking status and obesity were evaluated in terms of pack-years and body mass index (BMI), respectively. Clinical periodontal examination included probing depth (PD). The effective impact on periodontitis risk was analyzed by the classification and regression tree (CART) method and multiple logistic regression analysis. RESULTS: Simple logistic regression analyses revealed that factors such as age, gender, alcohol consumption, smoking status, BMI, and frequency of toothbrushing were associated with periodontitis. CART results demonstrated a significant correlation between periodontitis and pack-years, BMI, and age; in contrast, alcohol consumption, gender, and toothbrushing frequency were not correlated with periodontitis. The strongest factor for periodontitis risk was pack-years of smoking. Additionally, both pack-years and BMI exhibited clear dose-response relationships with periodontitis. These relationships were maintained despite adjustment for known confounding factors. CONCLUSIONS: Smoking displays the greatest impact on periodontitis among lifestyle-related factors. Both smoking and obesity are independent risk indicators for periodontitis; moreover, these parameters exhibit a dose-response relationship with respect to periodontitis risk.

Adult↗
PubMed1992

Two critical confounding factors in periodontal epidemiology.

The prevalence and severity of periodontitis is considerably lower than was previously estimated. The available epidemiological methods are based on the premise that loss of periodontal attachment is a unique sign of periodontitis. However, additional factors resulting in loss of periodontal attachment confound data obtained from modern studies. The physiological process of continuous tooth eruption results in loss of periodontal attachment over a lifetime, at an approximate rate of 0.1 mm/year. Anthropological and clinical evidence for continuous tooth eruption is reviewed. The position of the alveolar crest appears to be stable; loss of periodontal attachment occurs as the teeth erupt and less of the root is embedded in bone. Retrograde periodontitis caused by pulpal disease is a known cause of severe, localised destruction of periodontal tissues. Its signs and symptoms include periodontal pocket formation, purulent inflammatory exudates, angular bone loss, swelling and bleeding of the gingival tissues and increased tooth mobility. Anthropological, experimental and clinical evidence for retrograde periodontitis is discussed. Misdiagnosis of angular (hemiseptal), furcal and other forms of localised periodontal damage as periodontitis has probably resulted because of the inability to determine the quality of pulpal health and the assumption of a gingivitis-periodontitis continuum. New epidemiological methods need to be developed in which physiological and all pathological conditions which affect the periodontal attachment are recognised and appropriately categorised.

Confounding Factors, Epidemiologic↗
PubMed1992

Considerations for physicians caring for older adults with periodontal disease.

Periodontal disease is a generic term encompassing a variety of inflammatory conditions affecting the supporting tissues of the teeth. Periodontitis is inflammation associated with net resorption of supporting alveolar bone and periodontal ligament. Gingivitis is inflammation limited to the covering gingival tissues and does not directly lead to tooth mobility or loss. Periodontal diseases are very prevalent. Because the bone and ligament resorption are essentially irreversible, accumulated tissue damage of periodontitis is reflected in a prevalence and severity that increase with age. Periodontitis is not caused by aging per se but by a complex host-parasite relationship in which specific pathogens among the subgingival microbiota not only injure tissues directly but stimulate a cascade of inflammatory mediators to damage host tissues. Analytic epidemiology has identified several risk indicators for advanced periodontitis in older adults. These are microbiologic (prevalence of certain anaerobes in the microbiota), behavioral (tobacco smoking and infrequent professional dental care), medical (older age, preexisting and generalized periodontitis, gingival bleeding), and social (financial worries). Periodontitis in older adults is treated by reducing the impact of these risk indicators. The infections are controlled by combinations of debridement, antimicrobial agents, and surgical procedures as indicated. Medically well older adults can be treated similarly to younger adults. Management of periodontal conditions can be complicated for patients who are medically compromised. Communication between physicians and dental personnel is often required to ascertain the medical history and list of medications taken by older patients. Many of the medications prescribed for medical problems associated with aging impact on treatment choices for managing periodontitis. Moreover, periodontists frequently prescribe analgesics, antibiotics, and anti-inflammatory agents that might interact with others among the numerous drugs taken by older patients. Older adults with cognitive or physical disabilities have special needs for individualized hygiene instruction and implements. Periodontal health promotion and improving access to periodontal care for the elderly are challenges, because dental services are most often in the private sector and dental insurance does not often apply after retirement. Because they grew up in an era in which tooth loss due to "gum" diseases was considered inevitable, their current motivation toward regular preventive care must be improved by removing barriers and impediments to care. In addition to life-threatening medical conditions, frail individuals institutionalized in collective living centers face compounded problems concerning the provision of adequate, not even optimal, dental care. Their periodontal health often deteriorates rapidly after institutionalization, and in some instances it can possibly predispose to aspiration pneumonia or other disseminated infections.(ABSTRACT TRUNCATED AT 400 WORDS)

Aged↗
PubMed2006

[Correlation between infection of different glycoprotein B genotypes of human cytomegalovirus and human chronic periodontitis].

OBJECTIVE: To investigate the correlation between infection of different human cytomegalovirus (HCMV) glycoprotein B (gB) genotypes and human chronic periodontitis. METHODS: A nested-polymerase chain reaction (nPCR) was employed to detect HCMV gB gene in the subgingival plaque samples from 65 chronic periodontitis patients and in the gingival crevicular fluid samples from 24 periodontally healthy control. The amplification fragments of gB gene were further genotyped by restriction fragment length polymorphism (RFLP). The correlation among infection with the different HCMV genotypes and the severity of periodontal lesion were evaluated. RESULTS: In terms of teeth examined, the prevalence of HCMV (59.23%, 154/260) in the chronic periodontitis lesions was significantly higher than that of HCMV (32.29%, 31/96) in the periodontally healthy control (P < 0.01). Of the HCMV DNA positive samples from the chronic periodontitis lesions, 11.7% (18/154) was genotyped as gB I, 80.5% (124/154) as gB II, and 7.8% (12/154) as gB I and gB II co-infection, and of the HCMV DNA positive samples from the periodontal healthy control, 45.2% (14/31) was genotyped as gB I, 38.7% (12/31) as gB II, and 16.1% (5/31) as gB I and gB II co-infection. The gB II genotype was more dominant among the chronic periodontitis lesions compared with that among the periodontally healthy control (P < 0.01). In chronic periodontitis, no statistical significance could be found between infection of different HCMV gB genotypes and the different clinical parameters of CAL, PD and GI (P > 0.05). CONCLUSIONS: Subgingival infection with HCMV is closely associated with chronic periodontitis. Infection of HCMV may not correlate directly with severity of periodontitis. However, gB II may be the dominant genotype of HCMV, which is associated with the chronic periodontitis.

Adult↗
PubMed2004

Association of T CD4 lymphocyte levels and subgingival microbiota of chronic periodontitis in HIV-infected Brazilians under HAART.

OBJECTIVE: The aim of this study was to determine the subgingival microbiota of HIV-infected patients with chronic periodontitis and different T CD4 lymphocyte levels under HAART. STUDY DESIGN: 64 HIV+ patients (mean age 34.5 +/- 7.3; 75% males) were distributed into Group I: chronic periodontitis (> or = 3 sites with probing pocket depth (PPD) and/or clinical attachment level (CAL) > or = 5 mm); and Group II: periodontal health (no sites with PPD > 3 mm and/or CAL > 4 mm). All subjects received conventional periodontal therapy. Periodontal clinical parameters were evaluated at 6 sites/tooth in all teeth at baseline and 4 months after therapy. The levels of T CD4 were obtained from the patient's medical record. Subgingival plaque samples were taken from the 6 sites with the largest pocket depth in each subject of Group I, and 6 randomly selected sites in subjects of Group II. The presence of 22 subgingival species was determined using the checkerboard DNA-DNA hybridization method. Significant microbiological differences within and among groups were sought using Wilcoxon signed-rank and Mann-Whitney tests, respectively. Relationships between T CD4 levels and microbiological parameters were determined using Kruskal-Wallis test. RESULTS: Sixty-one percent of the HIV-infected patients represented AIDS cases, although 69% of them were periodontally healthy. The T CD4 lymphocyte mean level was 333 cells/mm3 and viral load was 12,815 +/- 24,607 copies/mm3. Yet, the prevalence of chronic periodontitis was relatively low (36%). Several periodontal pathogens, in particular T. forsythensis (P < .05), were more prevalent in HIV-positive patients with periodontitis than in HIV-positive subjects with periodontal health. Most of the species decreased in frequency after therapy, particularly P. gingivalis (P < .05). E. faecalis and F. nucleatum were significantly more prevalent in the subgingival microbiota of patients with chronic periodontitis and lower levels of T CD4 (P < .05), while beneficial species tended to be more frequently detected in individuals with T CD4 counts over 500 cells/mm3. CONCLUSION: The subgingival microbiota of HIV-infected patients with chronic periodontitis include a high prevalence of classical periodontal pathogens observed in non-infected individuals. Furthermore, the severe immunosuppression seems to favor the colonization by these species, as well as by species not commonly found in the subgingival microbiota.

Adult↗
PubMed1986

Design of clinical trials of traditional therapies of periodontitis.

The present paper on the design of clinical trials of periodontal therapy first addresses the issue of the etiology of periodontal disease. It is suggested that most if not all forms of destructive periodontal disease are caused by microorganisms and that there are different forms of disease with different microbial etiologies. The progressive nature of destructive periodontal disease is subsequently discussed and it is emphasized that, in a given patient, periodontal sites which show signs of inflammation and attachment loss may not over a period of several months and years show further sign of attachment loss. The present methods of assessing periodontal disease do not allow us to discriminate between potentially active and inactive sites in untreated patients. The significance and variability of indicators of periodontal disease such as bleeding on probing, probing pocket depth and probing attachment level measurements are discussed. The errors inherent in the various measurements are analyzed and suggestions are presented describing how alterations in any of the above parameters could be identified and presented in a clinical trial. Of concern for the statistical analysis of clinical data of periodontal disease is the definition of the "experimental unit". For a number of years, the "experimental unit" in periodontal trials was the patient. It is clear, however, that different sites within the same individual show different patterns of disease progression and lesion morphology and often respond differently to periodontal therapy. Statistical analyses must consequently be designed which recognize differences in site-to-site infection and lesion morphology within a common host. Until such analyses are available, the investigator should be wary of pooling data within the same individual, since such pooling may obscure meaningful alternatives which may take place in individual periodontal sites. Some goals of periodontal therapy are subsequently identified. 4 goals are discussed more in detail, namely: to establish conditions which will allow the patient to maintain a dentition without further breakdown of the periodontium; to reduce pocket depth to establish an anatomy in the dentogingival region which with proper maintainance care will prevent the re-establishment of the subgingival infection; to gain attachment as a result of treatment; to assess the effect of a certain chemotherapeutic agent on periodontal disease.

Clinical Trials as Topic↗
PubMed2006

Distribution of genotypes of Porphyromonas gingivalis in type 2 diabetic patients with periodontitis in Mexico.

OBJECTIVE: To determine and compare the distribution of Porphyromonas gingivalis fimA genotypes in type 2 diabetes mellitus (T2DM) patients affected by periodontitis, using non-diabetic subjects with and without periodontitis as control groups. MATERIAL AND METHODS: This study involved 75 subjects divided into three groups of 25 subjects each: Group 1 (non-T2DM without periodontitis), Group 2 (non-T2DM with periodontitis) and Group 3 (T2DM with periodontitis). The outcome variable was periodontitis, and explanatory variables were age, sex, T2DM and specific P. gingivalis fimA genotypes. RESULTS: In non-T2DM subjects with healthy periodontal tissues, type I fimA was the most frequently detected individually (40%) or in combinations (40%). In non-T2DM subjects with periodontitis, the most frequently detected type was Ib individually (20%) or in combinations (36%). In T2DM patients with periodontitis, the most frequently detected types were types I (20%) and III (20%), but there was no statistical difference (p>0.05) with non-T2DM periodontitis subjects. CONCLUSIONS: Type I genotype was more frequently detected in periodontally healthy sites from non-T2DM subjects than in periodontitis sites from either subjects with or without T2DM. However, in sites affected by periodontitis from T2DM subjects the predominating types were I and III, which are less virulent strains of P. gingivalis.

Adult↗
PubMed2002

Relationships among clinical measures of periodontal disease and their associations with systemic markers.

BACKGROUND: Recent investigations of the relationship between periodontitis and systemic disease require that periodontal disease also must be thought of as a disease process that is an exposure for a systemic disease or condition (outcome), rather than as the outcome itself. When viewing periodontal disease as an exposure, investigators must consider the clinical, microbiological, and inflammatory components of periodontitis that potentially convey risk for the systemic outcome of interest, which may or may not be the same as those associated with the assessments used to define tooth-based disease. Another important consideration is the temporal relationship between the exposure and the outcome of interest. METHODS: To explore which definitions of periodontal disease or clustering of clinical signs are important with regards to systemic exposure to inflammatory stress, we examined the relationship between clinical periodontal disease measures and 2 systemic inflammatory markers of increased risk for cardiovascular disease: serum soluble intercellular adhesion molecule (sICAM), which is a measure of vascular stress and serum C-reactive protein (CRP), which is a measure of hepatic acute-phase response. The Dental Arteriosclerosis Risk in Communities (ARIC) study, a cross-sectional study of the relationship between periodontal disease and cardiovascular disease, forms the basis for the examples used in this investigation. RESULTS: Our findings demonstrated that while attachment loss, probing depth, (PD) and bleeding on probing (BOP) are individually associated with sICAM and CRP, only BOP remains significant for sICAM when all 3 are in the model and, for CRP, only PD remains significant. Both of these clinical parameters were more robust in estimating the degree of systemic inflammation than traditional classifications of mild, moderate, and severe periodontitis or other measures of disease severity such as attachment loss. CONCLUSIONS: When selecting a definition of "systemic periodontitis" (periodontal disease that represents an exposure for a systemic condition), it is helpful to think of periodontal disease as a chronic oral infection with a number of clinical signs, rather than as the dento-centrically defined entity, periodontal disease. Thus, "systemic periodontitis" should be defined predicated upon those clinical signs that best represent the underlying mechanisms and temporal sequence that may affect that systemic outcome.

Acute-Phase Reaction↗
PubMedDate not supplied

Microbiology and management of periodontal infections.

The term periodontal disease refers to all diseases that involve the supportive structures of the periodontium. Peridontal diseases commonly begin as a gingivitis and progress to periodontitis. Necrotizing ulcerative gingivitis (NUG) is the most fulminate form of gingivitis. The two main forms of periodontitis are chronic periodontitis (also known as adult periodontitis) and aggressive periodontitis (also known as early onset periodontitis, destructive periodontitis, and juvenile periodontitis). Gingivitis treatment involves removing dental plaques and maintaining good oral hygiene. Periodontitis therapy should include root debriding, draining the infected root, and surgically resecting inflamed periodontal tissues. Systemic antimicrobials often are indicated in NUG, chronic periodontitis, and aggressive periodontitis. When possible, antimicrobial selection should be based upon culture and susceptibility testing of the subgingival flora.

Adult↗
PubMed2004

[Two-year disease progression in mild, moderate and advanced chronic periodontitis patients].

OBJECTIVE: To observe two-year natural progression of chronic periodontitis in mild, moderate and advanced periodontitis patients. METHODS: The periodontal status of 169 untreated chronic periodontitis patients aged from 22 to 64, were examined for two years. Periodontal measurements were performed on all teeth except the third molars and 6 sites examined for each tooth. Probing depth (PD), attachment loss (AL), and bleeding on probing (BOP) were measured at baseline, one year, and two year by a same experienced periodontist. Forty-five patients were diagnosed as having mild periodontitis, 87 with moderate, and 37 with advanced periodontitis. The changes of attachment level in these three group patients were analyzed. The site with change of AL greater than 3 mm (DeltaAL > or = 3 mm) were defined as periodontal disease activity (PDA) sites. The occurrence of PDA in three groups was compared. RESULTS: (1) The average AL levels at 1 year and at 2 year were greater than that at baseline in mild, moderate and advanced periodontitis. (2) The percentage of sites with AL > or = 1 mm in three groups all increased from baseline to 1 year and to 2 year. (3) The occurrence of periodontal disease activity increased significantly from mild (0.14% at site level, 15.56% at subject level), moderate (0.39%, 29.89%) to advanced (0.73%, 43.24%) periodontitis patients. (4) The mean baseline AL and PD levels in active sites were greater than that in inactive sites (PD: 3.03 +/- 0.45 vs. 2.87 +/- 0.38, P < 0.05; AL: 2.25 +/- 0.93 vs. 1.77 +/- 0.90, P < 0.01). CONCLUSION: Untreated advanced periodontitis patients were the risk population for further periodontal breakdown.

Adult↗
PubMed2004

Influence of the matrix metalloproteinase inhibitor batimastat (BB-94) on periodontal bone destruction in Sprague-Dawley rats.

BACKGROUND: Matrix metalloproteinases (MMPs) are proteolytic enzymes capable of degrading most macromolecules of the extracellular matrix. It has been assumed that an association exists between MMP activity and periodontal disease progression, but the precise role of MMPs in disease progression is still not fully clarified. Batimastat, or BB-94, is a synthetic broad-spectrum MMP inhibitor not previously examined in periodontal research. If there is an association between MMP activity and periodontal disease progression, then batimastat might be expected to reduce the progression of experimental periodontal disease in rats. OBJECTIVES: The objective of the present study was to determine the effects of batimastat on periodontal status in healthy Sprague-Dawley (SPRD) rats as well as in rats with ligature-induced experimental periodontal disease. METHODS AND RESULTS: Periodontal bone destruction was used as a means of evaluating periodontal destruction by measuring periodontal bone loss on defleshed rat jaws and periodontal bone support on radiographs of the jaws. There was significantly more periodontal bone destruction in the groups treated with batimastat than in the placebo and control groups. This accounted for both ligated and non-ligated groups, irrespective of whether periodontal bone loss (p < 0.05) or periodontal bone support (p < 0.05) were measured. CONCLUSION: In conclusion, the results of this study did not support the hypothesis that the MMP inhibitor batimastat could reduce the progression of experimental periodontal disease in rats. Instead, significantly increased bone destruction was found in rats treated with batimastat.

Alveolar Bone Loss↗
PubMed1999

Associations amongst three feline Porphyromonas species from the gingival margin of cats during periodontal health and disease.

Digoxigenin labelled whole chromosomal DNA probes directed against three feline members of the genus Porphyromonas (P. gingivalis VPB 3492, P. circumdentaria NCTC 12469T and P. salivosa VPB 3313) were used to identify and quantify organisms in samples taken from the gingival margins of 40 domestic cats with different grades of periodontal disease. At the right upper canine tooth, the grade of periodontal disease ranged from 0 to 5 and the cfu of facultative/obligate anaerobes ranged from 5.5 x 10(4) to 2.0 x 10(6)). In 38 of the 40 cats, at least one of the three Porphyromonas species was isolated and regression analysis showed that the cfu of total Porphyromonas sp. was a highly significant indicator of the grade of periodontal disease (p < 0.001, R2 0.510). Feline P. gingivalis was isolated from 37 of the 40 cats and regression analysis showed that it was a highly significant predictor of the grade of periodontal disease (p < 0.001, R2 0.561). The cfu of P. salivosa was a significant predictor of the grade of periodontal disease (p < 0.001, R2 0.286) and regression analysis showed that there was a significant positive relationship between cfu of P. circumdentaria and grade of periodontal disease (p = 0.018, R2 0.116). The periodontal grades at the right upper third premolar tooth ranged from 0 to 6. The cfu of facultative/obligate anaerobes isolated ranged from 1.2 x 10(5) to 7.9 x 10(6), and regression analysis showed that cfu was a significant predictor of periodontal grade (p < 0.001, R2 0.378). The cfu of total Porphyromonas species ranged from 1.2 x 10(4) to 1.7 x 10(6) and regression analysis of the cfu against the grade of periodontal disease showed a highly significant association (p < 0.001, R2 0.633). The cfu of P. gingivalis ranged from 0 to 1.1 x 10(6) and regression analysis of the cfu of P. gingivalis against the grade of periodontal disease showed a highly significant association (p < 0.001, R2 0.439). The cfu of P. salivosa was a significant predictor of the grade of periodontal disease (p < 0.001, R2 0.479) and the same association was found between cfu of P. circumdentaria and grade of periodontal disease (p = 0.002, R2 0.204). This study has established Porphyromonas as anumerically significant and highly prevalent genus in feline periodontal disease.

Animals↗
PubMed2004

Herpesviral-bacterial interrelationships in aggressive periodontitis.

BACKGROUND: Recent findings have begun to provide a basis for a causal link between herpesviruses and aggressive periodontitis. One theory is that herpesviruses cooperate with specific bacteria in the etiopathogenesis of the disease. This study examined whether the presence of herpesviruses [human cytomegalovirus (HCMV), Epstein-Barr virus (EBV) type 1, herpes simplex virus (HSV) type 1 and 2] is associated with the presence of putative pathogenic bacteria (Porphyromonas gingivalis, Prevotella intermedia, Tannerella forsythia, Campylobacter rectus, Actinobacillus actinomycetemcomitans) in aggressive periodontitis lesions. METHODS: The study included 18 young adults with advanced periodontitis and 16 periodontally healthy subjects from Ankara, Turkey. Subgingival specimens pooled from two sites in each subject were collected by a periodontal curette. Qualitative polymerase chain reaction methodology was used to identify herpesviruses and bacteria. Chi-square tests were employed to determine statistical associations among herpesviruses, bacteria and periodontal disease. RESULTS: HCMV, EBV-1 and HSV-1 were each detected in 72-78% of the aggressive periodontitis patients. HSV-2 occurred in 17% of the periodontitis patients. EBV-1 was detected in one periodontally healthy subject. The study bacteria occurred in 78-83% (P. gingivalis, T. forsythia, C. rectus) and in 44% (P. intermedia, A. actinomycetemcomitans) of the periodontitis samples, and in 0-19% of the samples from healthy periodontal sites. HCMV, EBV-1 and HSV-1 were positively associated with P. gingivalis, P. intermedia, T. forsythia and C. rectus, but not with A. actinomycetemcomitans. HSV-2 was not associated with any test bacteria. CONCLUSIONS: These results support the notion that the clinical outcome of some types of severe periodontal infection depends on the presence of specific herpesviruses and bacterial pathogens. Our findings open the door to testing a variety of hypotheses regarding the deleterious aspects of combined herpesviral-bacterial infections in periodontal sites.

Adolescent↗
PubMed1997

Overview of clinical trials on periodontal regeneration.

Periodontal regeneration means healing after periodontal surgery that results in the restoration of the tooth-supporting tissues; namely, cementum, alveolar bone, and periodontal ligament. The response of the periodontium to conventional periodontal flap surgery is primarily repair. Regenerative flap procedures involve modifications intended to alter variables in the normal wound healing response to shift the outcome from repair to regeneration. Technical manipulations, devices, pharmacological agents, and biologicals have been used to obtain regeneration. Evaluation of periodontal therapy is done by clinical and histological assessments. Human clinical trials depend on probing, re-entry, and radiographic measurements which cannot distinguish between periodontal repair and regeneration. Histological studies are difficult in humans because they require the retrieval of tissue blocks containing the teeth and their surrounding tissues, and for this reason these studies have largely been done in animal models; however, the use of animal models creates problems of interpretation when applying the information to the human. There are other fundamental problems related to assessment of new methods of periodontal regeneration. Ideally, periodontal regeneration is attempted after resolving the periodontitis that produced the loss of periodontal support. Does the type of periodontal disease affect the outcome? If it does, then separate clinical trials would be indicated to manage defects produced by different diseases. Furthermore, certain types of periodontal defects apparently respond better than others (for example, intrabony defects versus suprabony defects). Does each type of defect require a separate trial? Do subjects respond differently and, if so, how should this be factored into selection of the study population and sample size? There appear to be more questions than answers concerning the design of clinical trials for periodontal regeneration. This is not surprising since regeneration has been possible for only a few years, is apparently unpredictable, and the origin and nature of the new tissue are poorly understood. These factors make it important that the design of clinical trials be openly and thoroughly discussed so that practical solutions are forthcoming.

Animals↗