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PubMed1994

Distribution of keratin polypeptides in adult, juvenile and rapidly progressive periodontitis.

Inflammation of human gingival tissues including the periodontal structures occurs in response to infection in crevicular sulcus caused by microorganisms which first attach to the surface of oral squamous epithelium, penetrate into inner gingival epithelium and finally through the basement membrane of the underlying connective tissue (Murase et al., 1985). Other authors have long held the view that periodontitis is not a homogeneous disease entity but rather a group of family related diseases manifesting similar features and different etiologic factors. Immunological mechanism have long been implicated in pathogenesis of chronic periodontitis. Defect of host mechanism may have a relationship in development of rapidly progressive periodontitis (RPP) (Page et al., 1983).

Adolescent↗
PubMed1986

Papillon-Lefevre syndrome. A report of six cases in one family.

Papillon-Lefevre syndrome in six Saudi children in the same family is described. The parents were unaffected, and parental consanguinity was present. Palmoplantar keratosis started at the age of 1 1/2 years. The loss of deciduous teeth was a consequence of juvenile periodontitis. All essential features of the syndrome were present in this series.

Adolescent↗
PubMed1991

Collagenase activity in gingival crevicular fluid of patients with juvenile periodontitis.

The nature and origin of collagenases in gingival crevicular fluid of juvenile periodontitis patients was investigated. Gingival crevicular fluid collected from deep untreated periodontal pockets of juvenile periodontitis patients was found to contain only vertebrate collagenase (EC 3.4.24.7) activity that cleaved soluble type-I and -III collagens into 3/4 and 1/4 length fragments, as analyzed by SDS-polyacrylamide gel electrophoresis. Type II collagen was degraded at a markedly slower rate. This substrate specificity is indicative of collagenases produced by fibroblasts, epithelial cells and macrophages. We have previously found that collagenase in gingival crevicular fluid of adult periodontics patients appears to be mainly derived from polymorphonuclear leukocytes (PMN). The reasons for the apparent difference in collagenase source between the groups were investigated. We examined whether the pathogen characteristic for juvenile periodontitis, Actinobacillus actinomycetemcomitans, can release collagenase from normal human PMNs. All 10 A. actinomycetemcomitans strains tested, freshly isolated from the subgingival plaque of juvenile periodontitis patients, caused release of collagenase from PMNs in vitro. These results suggest that the lack of normally functioning PMNs in the periodontium of juvenile periodontitis patients may result in a colonization of bacteria that activate the resident periodontal cells to produce increased amounts of collagenase.

Aggregatibacter actinomycetemcomitans↗
PubMed1985

Microbiological and clinical effects of surgical treatment of localized juvenile periodontitis.

Since Actinobacillus actinomycetemcomitans appears to be a key etiologic agent in localized juvenile periodontitis, this study determined the effectiveness of different treatment modalities in suppressing A. actinomycetemcomitans in localized juvenile periodontitis lesions. A total of 25 deep periodontal lesions from 7 patients with localized juvenile periodontitis were included in the study. The test periodontal lesions either received scaling and root planing alone, scaling and root planing together with soft tissue curettage, or modified Widman flap surgery. Subgingival A. actinomycetemcomitans were enumerated using selective culturing. Clinical measurements included changes in probing periodontal attachment level, probing periodontal pocket depth, gingival index, plaque index, and digital subtraction of standardized serial radiographs. The microbiological and clinical effects of treatment were monitored over a period of 16 weeks. All periodontal lesions studied demonstrated high numbers of A. actinomycetemcomitans prior to treatment. Scaling and root planing alone did not markedly change the subgingival A. actinomycetemcomitans counts, nor any of the clinical parameters studied. In contrast, soft tissue curettage as well as modified Widman flap surgery suppressed A. actinomycetemcomitans to undetectable levels immediately after therapy in more than 80% of the lesions studied. A total of 5 periodontal lesions exhibited gain of probing periodontal attachment after subgingival curettage or Widman flap treatment; 3 of these sites revealed no detectable A. actinomycetemcomitans, and the remaining 2 sites harbored only low levels of A. actinomycetemcomitans. 5 periodontal lesions which lost probing attachment after treatment all demonstrated high numbers of subgingival A. actinomycetemcomitans. Changes in alveolar bone, assessed by digital subtraction of serial radiographs, correlated with changes in probing periodontal attachment level, confirming the clinical results. The present study revealed a close relationship between post-treatment A. actinomycetemcomitans levels and the clinical response to treatment, which supports the concept that A. actinomycetemcomitans is an important organism in the etiology of localized juvenile periodontitis. This study also showed that a substantial suppression of subgingival A. actinomycetemcomitans cannot be achieved by periodontal scaling and root planing alone, but can be accomplished by surgical removal of periodontal tissues.(ABSTRACT TRUNCATED AT 400 WORDS)

Actinobacillus↗
PubMed1986

Treatment of juvenile periodontitis without antibiotics. A follow-up study.

20 patients with juvenile periodontitis (JP) were treated with oral hygiene instruction, scaling and root planing, possibly with flap surgery but with no antibiotics. The patients were monitored after 6 to 12 years. Re-examination revealed that no probing depth of 7 mm or more existed any longer, and that sites with probing depth of 4 to 6 mm had decreased from 237 to 46. The bone loss scores had changed from 18% (range 2.0 to 48.1) to 14% (range 0 to 44.4) and the bleeding on probing scores from 39% (range 0 to 100) to 10% (range 0 to 40). Actinobacillus actinomycetemcomitans (A.a.) had neither been cultivated nor serologically tested at the initial examination. At the re-examination, it was found in 2 patients out of 20 at 5 sites. 7 patients, the 2 with positive cultures included, had elevated titers to A.a. strain Y4 in whole or parotid saliva or both. It is concluded that there is a marked improvement in the periodontal condition of these patients, and that good periodontal health in patients with JP can be reached without antibiotics.

Adolescent↗
PubMed1996

Periodontal diseases: epidemiology.

1. The interpretation of epidemiological data of periodontal disease is difficult, due to inconsistencies in the methodology used. It is not possible, therefore, to accurately assess if the prevalence of the periodontal diseases shows a world-wide decline. As long as the disease is assessed through accumulated clinical attachment loss, retention of the natural dentition in older ages entails increased prevalence in these cohorts. Contemporary epidemiological studies should ideally employ full-mouth examination of the periodontal tissues. Partial recording estimates are generally biased, especially when the prevalence of the disease is low. 2. Early-onset periodontitis is infrequent in all populations. Adult periodontitis is rather prevalent; however, advanced disease affects limited subfractions of the population (probably less than 10 to 15%). Although prevalence figures vary with race and geographic region, in most cases, the progression pattern of the disease seems compatible with the retention of a functional dentition throughout life. 3. Of a plethora of behavioral and environmental risk markers identified by multi-variate analysis, smoking and presence of certain subgingival microorganisms have been proven to be true risk factors. The same holds true for diabetes mellitus, a systemic condition that confers a risk for periodontal disease which is independent of the effect of other significant factors. 4. In certain cases, periodontal infections appear to have a systemic impact on the host. Most recent data indicate that periodontal disease may confer risk for coronary heart disease and pre-term low birth weight.

Adolescent↗
PubMed1984

Salivary immunoglobulins in patients with juvenile periodontitis and their healthy siblings.

The concentrations of the salivary immunoglobulins IgA, IgG and IgM were determined with a solid phase radioimmunoassay in the unstimulated whole saliva of 21 patients with juvenile periodontitis (JP), their 27 healthy siblings and 17 healthy age-matched controls. In the JP group the concentrations of IgA were increased, averaging 188 +/- 32.5 (SE) mg/L as compared with the mean of 139 +/- 21.2 mg/L in their healthy siblings and 130 +/- 24.5 mg/L in the controls. An elevation was found in the amount of IgG in the JP patients 45.6 +/- 12.5 mg/L as compared with 18.1 +/- 5.9 mg/L in the siblings and 21.0 +/- 5.6 mg/L in the controls. The mean IgM was 22.5 +/- 5.4 mg/L in the JP group, 13.3 +/- 2.9 mg/L in the siblings and 8.7 +/- 1.6 mg/L in the controls, indicating an increase of IgM in the JP group and the siblings. A significant difference was found in the mean IgM values in the juvenile periodontitis group when compared to the control group. (0.02 greater than P greater than 0.01).

Adolescent↗
PubMed1992

Destructive periodontal disease in healthy children.

This study determined the prevalence of destructive periodontal disease affecting the deciduous dentition among otherwise healthy subjects, who were diagnosed with juvenile periodontitis (JP) in their permanent dentitions. There were 4,757 subjects in this retrospective, cross-sectional study. Diagnosis of JP was based on age (< or = 15 years), negative medical history, and radiographic evidence of arc-shaped alveolar bone loss. The study population was one-third white and two-thirds black and the male/female ratio was 1:1, reflecting the general patient population. The prevalence among whites was 0.3%, with a female/male ratio 4:1; whereas among blacks the prevalence was 1.5%, with a female/male ratio approximately 1:1. Among the black JP subjects with radiographs of the mixed dentition, 85.7% presented evidence of bone loss, and of those with radiographs of the deciduous dentition, 71.4% had discernible alveolar bone loss. This study suggests that JP is much more prevalent in blacks and that it does indeed occur in the prepubertal years affecting the deciduous as well as the permanent dentitions in otherwise healthy children. These data imply the importance of including a periodontal evaluation in the examination of children, using the periodontal probe and radiographs sufficient to adequately view the alveolar bone.

Adolescent↗
PubMed1994

Elastase and alpha-1-proteinase inhibitor in gingival crevicular fluid and gingival tissue in adult and juvenile periodontitis.

The presence and localization of PMN/neutrophil elastase and its endogenous inhibitor alpha 1-proteinase inhibitor (alpha 1 PI) were studied immunohistochemically in gingival tissue specimens collected from 9 adult periodontitis (AP) patients during flap surgery after the initial phase of periodontal therapy, and from 6 healthy controls with clinically-healthy periodontium upon surgical extraction of impacted third molars. In order to evaluate how periodontal tissue destructive events are reflected in gingival crevicular fluid (GCF), GCF samples were collected from the AP patients before any periodontal treatment and prior to flap surgery, from 5 localized juvenile periodontitis (LJP) patients, and from the controls. Elastase activity in the GCF was measured with the SAAVNA-assay and the molecular forms and amount of alpha 1PI by Western- and dot-blotting. Immunohistochemical staining for PMN elastase was strongly positive in the connective tissue, but not in the epithelium, of the AP patients' gingival tissue specimens. In the healthy gingival tissue specimens only a few elastase-positive cells were present. Both in AP and in control gingival specimens, alpha 1PI was detected in the connective tissue and in the keratinized layer of the epithelium, however, its amount was markedly lower in the control specimens. Elevated levels of alpha 1PI and PMN elastase were detected in the GCF of all periodontitis patients when compared to controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1996

Immunological, genetic, and microbiological study of family members manifesting early-onset periodontitis.

From the standpoint of host-parasite interactions, family studies help us understand the host defensive factors and the molecular mechanisms involved in the periodontal immune response. In this study, we report the immunological profile of host-defensive functions, human leukocyte antigen (HLA) phenotypes, and the microflora of a mother (rapidly progressive periodontitis), an older son (periodontally healthy), a younger son (localized juvenile periodontitis), and a daughter (localized juvenile periodontitis). We examined the peripheral neutrophil functions, phenotypic and functional analysis of peripheral lymphocytes, serum immunoglobulin G (IgG) antibody titers against periodontopathic bacteria, serological type of HLA class II antigens, and bacterial flora in all periodontal pockets. The results showed that Actinobacillus actinomycetemcomitans was dominant in the pockets of all subjects. The mother and two sons showed a depressed neutrophil chemotaxis to N-formyl-methionyl-leucyl-phenylalanine. All subjects except the older son exhibited low T4/T8 ratios. The mother and daughter had raised levels of IgG titers to Porphyromonas gingivalis. All subjects had HLA phenotypes of DRw52 and DQ1 in common. We found that the family members had similar disorders in certain defensive functions. This family has been a model for our understanding of the host defensive factors in the development of early-onset periodontitis.

Adolescent↗
PubMed2000

Human herpesviruses and Porphyromonas gingivalis are associated with juvenile periodontitis.

BACKGROUND: Although herpesviruses have been associated with adult periodontitis, their relationship with juvenile periodontitis (JP) has not been established. This case-control study examined possible associations between JP and pathogenic bacteria, the human cytomegalovirus (HCMV), and the Epstein-Barr type 1 virus (EBV-1). METHODS: Subjects were participants in a larger survey of schoolchildren in North-Central Jamaica. Subgingival plaque samples from 15 subjects with JP, 20 with incipient periodontitis (IP), and 65 randomly-selected healthy controls were assayed for Porphyromonas gingivalis and Actinobacillus actinomycetemcomitans using a 16S rRNA polymerase chain reaction (PCR) identification method, and for HCMV and EBV-1 using nested PCR identification. RESULTS: Strong bivariate associations were found between JP and P. gingivalis (odds ratio [OR] = 12.7; 95% CI = 2.6, 61.4), HCMV (OR = 10.0; 95% CI = 2.7, 36.3), and A. actinomycetemcomitans (OR = 8.0; 95% CI = 2.3, 27.5), but not EBV-1. In multivariate analyses, P. gingivalis remained a significant explanatory variable (OR = 7.8; 95% CI = 1.5, 40.9); however, the associations were marginal for HCMV (OR = 4.6; 95% CI = 0.9, 22.7), and non-significant for A. actinomycetemcomitans (OR = 2.0; 95% CI = 0.4, 9.7). The associations with JP and the extent of attachment loss were even stronger when both P. gingivalis and HCMV were detected together. P. gingivalis (OR = 3.9; 95% CI = 1.3, 12.0) and EBV-1 (OR = 3.3; 95% CI = 1.0, 10.3) were the only significant explanatory variables in the multivariate analysis of IP. CONCLUSIONS: P. gingivalis is the strongest and most stable indicator of periodontitis in Jamaican adolescents. Co-infection with P. gingivalis and HCMV appears to be particularly deleterious to periodontal health.

Actinobacillus Infections↗
PubMed1992

Clinical studies on juvenile, rapidly progressive and adult periodontitis before and after periodontal therapy (I).

The sample in the present study comprised 36 patients who were referred for treatment of periodontal disease. Twenty-four of them were early onset periodontitis (EOP) patients and 12 were adult periodontitis (AP) patients. Based upon the age, number of involved teeth and the location of diseased sites, the EOP patients were divided into two groups as juvenile periodontitis (JP) and rapidly progressive periodontitis (RPP). All the patients were individually examined both clinically and radiographically. At a baseline examination and 3 months after active therapy, the patients were evaluated for plaque, gingivitis, probing depths and probing attachment levels. Following instruction in proper oral hygiene measures, all of the patients were subjected to periodontal treatment. Treatment comprised scaling and root-planing, occlusal adjustment, tetracycline administration and periodontal surgery with osteoplasty. Results showed that age limits between JP and RPP cannot be drawn with certainty. The mean age for the JP group was 21.83 years and was 30.58 years for the RPP group. The number of involved teeth was found to increase with age. The first molars were the most frequently affected teeth followed by the incisors. Three months after active treatment, the response of periodontal tissues to therapy both in EOP and AP groups was almost identical.

Adolescent↗
PubMed1998

Guided tissue regeneration in a combined periodontal and orthodontic treatment: a case report.

Periodontal defects in adolescents or young adults are often an incidental finding within an orthodontic treatment. Most of these patients suffer from a special form of periodontal disease: juvenile periodontitis. Guided tissue regeneration offers a technique for long-term therapy in such cases. In the case presented in this report, periodontal problems were aggravated by malpositioning of the affected teeth. Orthodontic and periodontal treatment enabled the correction of malpositioning and regeneration of osseous defects.

Adult↗
PubMed1999

Calprotectin in gingival crevicular fluid correlates with clinical and biochemical markers of periodontal disease.

Clinical and biochemical markers of periodontal disease have been used for precise objective diagnosis of periodontal inflammation. Interleukin 1beta (IL-1beta) and prostaglandin E2 (PGE2), inflammatory factors, levels in gingival crevicular fluid (GCF) of patients with periodontal disease are elevated and have been studied as biochemical markers. The levels of calprotectin, a leukocyte protein, in body fluids of patients with some inflammatory diseases are raised. Recently, we detected calprotectin in GCF and its concentrations in periodontal pockets were higher than those in healthy gingival crevices. In this study, we investigated the correlations between GCF calprotectin levels and clinical indicators (probing depth and bleeding on probing, BOP), and the IL-1beta or PGE2 levels in GCE Probing depth and BOP at 130 sites of 110 subjects with periodontal or other oral diseases were examined, then GCF samples were collected and their calprotectin, IL-1beta and PGE2 were determined by ELISA. The calprotectin level correlated positively with the probing depth and was significantly higher at BOP-positive than BOP-negative sites. There were significant, positive correlations between the calprotectin and IL-1beta or PGE2 concentrations. These results indicate that the calprotectin level in GCF correlates well with clinical and biochemical markers of periodontal disease and suggest that calprotectin may be useful for evaluating the extent of periodontal inflammation.

Adult↗
PubMed1992

Tetracycline inhibition identifies the cellular origin of interstitial collagenases in human periodontal diseases in vivo.

Mammalian interstitial collagenases (E.C.3.4.24.7) are considered as key initiators of collagen degradation in periodontal diseases. However, the cellular sources of collagenases present in gingival crevicular fluid have not been completely clarified. Resident fibroblasts and epithelial cells as well as infiltrating neutrophils and monocyte/macrophages are potential sources of the enzymes. We have recently found significant differences in tetracycline inhibition between human neutrophil and fibroblast interstitial collagenases. To address the cellular source of collagenase present in gingival crevicular fluid in 2 distinct periodontal diseases, we studied the tetracycline inhibition of collagenase in gingival crevicular fluid of patients with localized juvenile periodontitis and adult periodontitis. Gingival crevicular fluid samples were collected from deep (greater than 5 mm) periodontal pockets and assayed for collagenase in the presence of 0-1000 microM doxycycline as well as a chemically modified tetracycline devoid of antimicrobial activity (4-de-dimethylaminotetracycline). The drug concentration required to inhibit 50% of collagenase activity (IC50) in localized juvenile periodontitis gingival crevicular fluid was 280 microM for doxycycline and 470 microM for 4-de-dimethylaminotetracycline. Significantly lower values, 10-20 microM, were obtained for collagenase in gingival crevicular fluid of patients with adult periodontitis. We propose that systemic tetracycline levels are efficient inhibitors of collagenase in gingival crevicular fluid in affected sites of patients with adult periodontitis but not of patients with localized juvenile periodontitis and that the fibroblast type interstitial collagenase is the predominant collagenase type in gingival crevicular fluid in affected sites of patients with localized juvenile periodontitis and the neutrophil collagenase in adult periodontitis gingival crevicular fluid.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1991

Prevalence of juvenile periodontitis in Chile.

The aim of this survey was to study the prevalence of juvenile periodontitis in schoolchildren aged 15-19 years in Santiago, Chile. A random sample of 2500 schoolchildren (1318 male, 1182 female) that represented the full range of different socio-economic strata and ethnic groups seen in the population of Santiago, was used. Initially, the children were screened clinically at school by assessment of probing depths around the incisors and first molars with a WHO 621 pattern probe. Children with 2 or more teeth with 5.5 mm or deeper pockets were invited for a radiographic examination comprising bitewing radiographs of molars, and periapical radiographs of incisors. Any subject with 2 mm or more alveolar bone loss was invited for a full clinical and radiographic examination. After screening, 27 subjects had a tentative diagnosis of juvenile periodontitis. 4 of these refused radiographic examination and only accepted a thorough clinical examination. 23 subjects presented themselves for the radiographic and complete clinical examination. Of the 27 subjects selected for detailed examination, 8 subjects (7 female, and 1 male) were diagnosed as having juvenile periodontitis. There was an overall prevalence of juvenile periodontitis of 0.32% with 95% confidence, which gives a range of +/- 0.10%. When prevalence was assessed by socio-economic status, juvenile periodontitis was found more commonly in low socio-economic group. The results of the current study suggest that in Chile, there might be a relationship between socio-economic status and prevalence of juvenile periodontitis, and that this disease is more frequent in women.

Adolescent↗