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PubMed1988

A comparison of the reactivity of Eubacterium species with localized and serum immunoglobulins from rapidly progressive and adult periodontitis patients.

Immunoglobulins in sera and in supernatant fluids of explant cultures of diseased gingival tissues from 20 rapidly progressive and 20 adult periodontitis sites were tested by an ELISA assay for reactivity with typed strains of Eubacterium alactolyticum, E. brachy, E. limosum and E. nodatum. Immunoglobulins present in tissue culture fluids from both rapidly progressive and adult periodontitis samples reactive with E. brachy and E. nodatum were significantly greater (P less than 0.05) than those reactive with E. alactolyticum or E. limosum. The titers to E. brachy in tissue culture fluids from adult periodontitis were significantly greater (P less than 0.05) than those from rapidly progressive periodontitis; there was no difference in titers to the other three species. The only significant difference in serum titers was that sera from patients with rapidly progressive periodontitis had significantly greater reactivity to E. alactolyticum than did sera from adult periodontitis patients. These data indicate that immunoglobulins in the sera of rapidly progressive and adult periodontitis patients do not necessarily reflect the reactivity of localized immunoglobulins present in the diseased gingival tissue explant culture fluids from these patients.

Adolescent↗
PubMed2005

Differential induction of human beta-defensin expression by periodontal commensals and pathogens in periodontal pocket epithelial cells.

BACKGROUND: To investigate the possible role of beta-defensins in gingival health and periodontal disease, we examined the effect of several stimuli on the expression of interleukin-8 (IL-8), human beta-defensin-1, -2, -3, and -4 (hBD) in primary human diseased gingival epithelial (HGE) cell cultures from periodontitis patients by quantitative TaqMan reverse transcription polymerase chain reaction (RT-PCR). METHODS: Several strains of the periodontopathogens Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis were added to the cells, as well as the oral commensal bacteria Fusobacterium nucleatum and Escherichia coli. The induction by the proinflammatory stimuli phorbol 12-myristate 13-acetate (PMA) and tumor necrosis factor-alpha (TNF-alpha) was also tested. RESULTS: In addition to the published observations (PMA induces hBD-2 and -4; TNF-alpha induces hBD-2 and -3), it was found that PMA can upregulate hBD-1 and hBD-3, whereas TNF-alpha can induce hBD-4. The commensal bacteria were significant inducers of hBD-2, hBD-3, and IL-8. The pathogen P. gingivalis induced hBD-1 and hBD-3 at different time points than the commensals, but no induction of IL-8 and hBD-2 could be observed. These data fit with the chemokine paralysis theory. A correlation was found between the pathogenicity of different serotypes of A. actinomycetemcomitans and the induction profiles of defensins and IL-8. CONCLUSION: The results suggest that a correlation can be found in diseased oral epithelium between the defensin profiles that are induced and the pathogenicity of the oral bacterial strains.

Aggregatibacter actinomycetemcomitans↗
PubMed1987

Recurrent periodontal disease and bacterial presence in the gingiva.

Previous investigations have shown that, in biopsies taken from untreated sites of periodontitis, bacteria were present between the epithelial cells and within the connective tissue. In the present study we have examined Gram-stained sections of diseased gingival sites where the disease had recurred after surgical periodontal treatment. The six subjects chosen for the study were patients who had undergone surgical therapy for the treatment of periodontitis and who, upon subsequent recall visits, showed evidence of at least one site recurrent after treatment as detected by bleeding on probing and increased pocket depth of 5 mm or more. A normal control site from the same patient was chosen, preferably contralaterally, showing positive response to treatment with no signs of disease. Sections were stained with either hematoxylin and eosin for tissue survey or Gram for assessment of bacteria and examined by light microscopy. In many specimens, the bacterial nature of Gram-stained material was substantiated. Preliminary results showed a significantly increased number of bacteria in the refractory sites when compared with control sites which responded positively to treatment. The results of this investigation provided further evidence that bacterial presence inside the periodontal tissue may be an important pathogenic factor in periodontal disease.

Bacteria↗
PubMedDate not supplied

Risk factors for odontoclastic resorptive lesions in cats.

A cross-sectional study evaluating potential risk factors for odontoclastic resorptive lesions (ORL) in feline teeth was conducted. Owners of 32 cats with ORL and 27 cats without ORL were interviewed regarding their respective cat's demographic characteristics, diet, and medical and dental histories. Four factors were identified as significantly associated with ORL using unconditional logistic regression. A history of dental disease (gingivitis, calculus, or periodontal disease; odds ratio [OR], 4.5); city residence (OR, 4.4); and being an exclusively indoor cat (OR, 4.5) were associated with an increased risk for ORL. Consumption of commercial treats (OR, 0.3) appeared protective for ORL.

Animals↗
PubMedDate not supplied

[Health status and causes of mortality in feral cats in a delimited area of the inner city of Berlin].

Results of the veterinary examination of feral cats living in a delimited area of Berlin city are presented. Between 1996 and 1999 thirty nine cats were investigated, among them eleven individuals twice. All animals were positive for one or several pathologies, but only seven cats were in bad condition. Most common were periodontal and gingival diseases, followed by conjunctivitis. Five cats were positive for FIV, seven for FeLV, one tomcat for both. Twenty six cats vanished during the study period of 42 months, only one third of cats survived and remained in the study area throughout. Four cats were given to pet lovers, nine cats disappeared without trace, seven animals died in traffic accidents and six cats died of illnesses. Cats less than three years of age vanished more often than expected from their representation in the population. Dirty or large feeding places for cats constitute a source of infections. Feeding sites should be accessible to only few individuals and left-overs that may attract stray cats, rats or birds should not remain at feeding places.

Animals↗
PubMed2004

Dental and facial characteristics of patients with juvenile idiopathic arthritis.

OBJECTIVE: It has been shown that the temporomandibular joint is frequently affected by juvenile idiopathic arthritis, and this degenerative disease, which may occur during facial growth, results in severe mandibular dysfunction. However, there are no studies that correlate oral health (tooth decay and gingival diseases) and temporomandibular joint dysfunction in patients with juvenile idiopathic arthritis. The aim of this study is to evaluate the oral and facial characteristics of the patients with juvenile idiopathic arthritis treated in a large teaching hospital. METHOD: Thirty-six patients with juvenile idiopathic arthritis (26 female and 10 male) underwent a systematic clinical evaluation of their dental, oral, and facial structures (DMFT index, plaque and gingival bleeding index, dental relationship, facial profile, and Helkimo's index). The control group was composed of 13 healthy children. RESULTS: The mean age of the patients with juvenile idiopathic arthritis was 10.8 years; convex facial profile was present in 12 juvenile idiopathic arthritis patients, and class II molar relation was present in 12 (P =.032). The indexes of plaque and gingival bleeding were significant in juvenile idiopathic arthritis patients with a higher number of superior limbs joints involved (P =.055). Anterior open bite (5) and temporomandibular joint noise (8) were present in the juvenile idiopathic arthritis group. Of the group in this sample, 94% (P =.017) had temporomandibular joint dysfunction, 80% had decreased mandibular opening (P = 0.0002), and mandibular mobility was severely impaired in 33% (P =.015). CONCLUSION: This study confirms that patients with juvenile idiopathic arthritis a) have a high incidence of mandibular dysfunction that can be attributed to the direct effect of the disease in the temporomandibular joint and b) have a higher incidence of gingival disease that can be considered a secondary effect of juvenile idiopathic arthritis on oral health.

Adolescent↗
PubMed1989

[Clinical and clinico-histological markers in chronic destructive adult periodontitis].

This study was designed to evaluate the significance and interrelationship of clinical parameters and their association with histologic changes in advanced destructive periodontitis. 158 patients with PDI greater than 4 (Ramfjord) were selected, evaluating the size, contouring, bleeding, consistency, colour and gingival pain. Epithelial ulceration of soft periodontal pockets were also evaluated. The results showed a statistically significant association between purplish colour and gingival fibrosis and advanced stage of the disease. Gingival bleeding on probing was the most important clinical parameter in advanced phases of the disease, either alone or in association with other parameters such as the presence of epithelial ulcerations. The Periodontal Disease Index (Ramfjord) has proven effective in the evaluation of generalized patterns of disease.

Adult↗
PubMed2005

Gingival overgrowth in children: epidemiology, pathogenesis, and complications. A literature review.

Gingival overgrowth is the enlargement of the attached gingiva due to an increased number of cells. The most prevalent types of gingival overgrowth in children are drug-induced gingival overgrowth, hereditary gingival fibromatosis (HGF), and neurofibromatosis I (von Recklinghausen disease). Gingival overgrowth induced by drugs such as phenytoin, nifedipine, and cyclosporin develops due to an increase in the connective tissue extracellular matrix. According to epidemiologic studies, it is more prevalent in male children and adolescents. There is an additive effect of those drugs on the degree of gingival overgrowth. Genetic heterogeneity seems to play an important role in the development of the disease. Functional difficulties, disfigurement, increased caries, and delayed eruption of permanent teeth are the main complications of drug-induced gingival overgrowth. HGF is the most common syndromic gingival enlargement in children. This autosomal dominant disease usually appears at the time of eruption of permanent dentition. Histologically, it is characterized by highly collagenized connective tissue. The most important complications are drifting of teeth, prolonged retention of primary dentition, diastemata, and poor plaque control. Neurofibromatosis I is an autosomal dominant disease more common in mentally handicapped individuals. Gingival overgrowth is caused by the formation of plexiform neurofibromas in the connective tissue of the gingiva. Plexiform neurofibromas are pathognomonic of the disease and consist of hypertrophic nerves arranged as lobules in the connective tissue. Complications of the disease are multiple and severe due to neurofibromas and their occasional malignant transformation.

Age Factors↗
PubMed1997

Is the chemical prevention of gingivitis necessary to prevent severe periodontitis?

Gingival inflammation seldom causes discomfort, social embarrassment or loss of function. As most sites with gingival inflammation do not progress to severe periodontal disease, gingivitis should not be considered a public health problem. Periodontitis is always preceded by gingivitis. But most gingivitis remains stable for years without progressing to periodontitis. The number of gingivitis sites that do convert is small. The levels of oral cleanliness achieved by the majority of populations in industrialized countries are below the threshold for severe destructive periodontal disease of personal and public health concern. Because methods of measuring the progression of periodontal disease are unreliable, definitive answers regarding conversion of gingivitis to severe periodontitis are lacking. Gingival inflammation frequently remains contained; most gingivitis remains stable for years without progressing to periodontitis. Decreasing gingivitis does reduce shallow pocketing, but the effect on severe periodontitis is not clear. Although the underlying justification for the reduction of plaque is to reduce gingival inflammation to prevent or reduce severe periodontitis and tooth loss, the basis for the approach is equivocal. A reasonably high level of plaque appears to be compatible with acceptably low levels of periodontal disease. Reducing nonspecific plaque levels to such levels is therefore a rational goal. The conventional methods of controlling periodontal disease involve mechanical removal of plaque and calculus. A complimentary ecological approach, using chemicals, would be to alter the environment of the pocket to prevent growth of putative pathogens. Any ecological approach should be sensitive to the dangers of disrupting the natural ecology of dental plaque. Some antimicrobial and antimetabolic agents such as fluoride, chlorhexidine and triclosan and zinc citrate can selectively suppress certain organisms or inhibit bacterial proteases implicated in tissue damage. The uncertainties about factors that convert gingival inflammation into periodontitis and periodontitis into severe periodontitis coupled with insufficient data from controlled clinical trials on the effectiveness of chemical reduction of gingivitis to prevent severe periodontitis leads one to conclude that more research is required before the need for the chemical prevention of gingivitis to prevent severe periodontitis can be justified.

Dental Plaque↗
PubMed1996

[Evaluation of the biosynthesis of mono-HETES and leukotrienes in diseased periodontal tissues].

Many arachidonic metabolites have been shown to have marked potent biological effects in animals. The cyclooxygenase and lipoxygenase products of arachidonate metabolism are known to play a key role in the development of inflammatory symptoms and signs. Reports published during past decades indicate that cyclooxygenase products of arachidonic acid metabolism are present in much higher concentrations in inflamed than in healthy periodontal tissues. Since information about the role of lipoxygenase products of arachidonic acid metabolism in human periodontal disease is lacking, the objective of this study was to determine the ability of diseased and non-diseased gingival tissue to synthesize lipoxygenase products from the precursor arachidonic acid. Twenty-six samples of diseased tissue and nine samples of non-diseased tissue were included in our data analysis. After incubation of the tissue with 100,000 cpm [3H]-arachidonic acid, lipoxygenase products were separated by high performance liquid chromatography (HPLC) and identified by comparison with cochromatographed standards. Our results showed that inflamed gingival tissue synthesized significantly larger amounts, of LTB4(p < 0.01), LTC4(p < 0.01), LTD4(p < 0.01), LTE4(p < 0.01), 5-HETE(p < 0.05), 12-HETE(p < 0.01), and 15-HETE(p < 0.01), compared to non-diseased tissue. The lipoxygenases are more active in inflamed gingival tissue than in non-diseased gingival tissue. 12-HETE and 15-HETE were the the major metabolites formed by lipoxygenases in diseased and non-diseased human gingiva. Since we did not functionally determine the fractions separated by HPLC, our present data may only provided indirect evidence for the existence of lipoxygenase products in periodontal tissue. However, our study did establish a research model for the investigation of arachidonic acid metabolism in the pathogenesis of periodontal disease.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1984

In vivo crevicular leucocyte response in humans to a chemotactic challenge. Effects of periodontal diseases.

An in vivo assay was recently developed to monitor the crevicular leucocyte response to chemotactic agents, e.g., casein and N-formyl peptides. This method was used to monitor humans with little or no gingival disease (C group), gingivitis (G group), chronic periodontitis (CP group) and localized juvenile periodontitis (LJP group). Casein (0.2 microliters, 2 mg/ml) was placed into an isolated gingival crevice of each subject with a calibrated wire loop and the time recorded (t = 0). Leucocytes were counted in crevicular washes (10 microliters) 15 minutes later and every 5 minutes thereafter up to t = 50 minutes. This protocol was repeated for the crevice of an adjacent tooth except that the crevicular fluid flow response to the chemotactic challenge was monitored. The C, G and CP subjects showed a similar pattern of response to the chemoattractant with a single "peak" of leucocytes at approximately t = 25 minutes. However, the peak cell count was much greater in the G and CP groups than in the C group. LJPs showed an abnormal pattern with two leucocyte peaks, one at approximately 25 minutes and the other at 45 minutes. Both peaks tended to be higher than the single peak seen in Cs but were significantly lower than that in Gs or CPs, even at similar levels of inflammation. In addition, the peak leucocyte response (to casein) in LJPs did not increase with increasing leucocyte counts in the unchallenged (resting) crevice, whereas a positive relationship was seen in the other groups of subjects. These data suggest that this new assay may provide important diagnostic information on in vivo neutrophil migration in the gingival crevice and on susceptibility to periodontal disease.

Adolescent↗