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PubMed2005

The prevalence and pathogenic differences of Porphyromonas gingivalis fimA genotypes in patients with aggressive periodontitis.

BACKGROUND: The fimA gene, which encodes fimbrillin (FimA), is found in Porphyromonas gingivalis and has been classified into six genotypes based on nucleotide sequence. P. gingivalis that possesses the type II fimA gene is prevalent in adult periodontitis. OBJECTIVES: The aim of this study was to investigate the prevalence of P. gingivalis fimA genotypes in Japanese aggressive periodontitis patients, and to examine their virulence. METHODS: Subgingival plaque samples were obtained from 223 sites in 18 aggressive periodontitis patients and 95 sites in 22 periodontally healthy young adults. Actinobacillus actinomycetemcomitans, P. gingivalis and Tannerella forsythensis detection, determination of the fimA genotype in P. gingivalis, and the quantification of P. gingivalis were analyzed by polymerase chain reaction (PCR) methods. The proteolytic activities of the P. gingivalis fimA type I and fimA type II were also examined. RESULTS: In aggressive periodontitis patients, the most prevalent fimA genotype was the type II (46.7%), followed by the type Ib and type I, whereas in healthy subjects, the type I fimA was the only genotype detected. The number of P. gingivalis pathogens was the greatest in the type I fimA positive sites, and the frequency of coexisting A. actinomycetemcomitans and T. forsythensis was highest in the type II fimA positive sites in the aggressive periodontitis patients. Both the arginine-specific cysteine proteinase (Arg-gingipain) and lysine-specific cysteine proteinase (Lys-gingipain) activity of the P. gingivalis fimA type I strain were significantly higher than those of the fimA type II strains. CONCLUSIONS: These results suggest that differences in virulence exist among different fimA genotypes. Coadherence with other pathogens in P. gingivalis fimA type II-associated aggressive periodontitis and quantitative increases in P. gingivalis in fimA type I-associated aggressive periodontitis are related to this virulence.

Adult↗
PubMed2005

Gingival crevicular fluid levels of monocyte chemoattractant protein-1 and tumor necrosis factor-alpha in patients with chronic and aggressive periodontitis.

BACKGROUND: Monocyte chemoattractant protein-1 (MCP-1) is a well-known chemotactic cytokine that regulates mononuclear inflammatory cell recruitment. This recruitment has particular importance in the oral cavity because inflammatory cells will be challenged with periodontopathogenic bacteria during infections. Tumor necrosis factor-alpha (TNF-alpha) is a cytokine that induces bone resorption by stimulating proliferation and differentiation of osteoclasts' progenitors and also stimulates MCP-1 expression. The aims of this study were to investigate the presence of MCP-1 in gingival crevicular fluid (GCF) samples from patients with chronic periodontitis (CP) and aggressive periodontitis (AgP) and to examine the possible correlations between the GCF levels of MCP-1 and TNF-alpha. METHODS: Twenty-five CP, 20 AgP, and 20 healthy control (C) patients were selected for the study. Plaque index (PI), gingival index (GI), probing depth (PD), and clinical attachment level (CAL) measurements were recorded from each sampling area. Assays for GCF MCP-1 and TNF-alpha were carried out by an enzyme-linked immunosorbent assay (ELISA) method. RESULTS: The concentration (nanograms per microliters) and total MCP-1 and TNF-alpha (nanograms per site) were not statistically significant between CP and AgP groups, but total MCP-1 and TNF-alpha was statistically different between CP and C and between AgP and C groups (P <0.001). All clinical parameters were statistically different between CP and C and between AgP and C groups (P <0.001). A positive statistical correlation was detected between the levels of MCP-1 and TNF-alpha, and there was also a positive correlation between all clinical parameters and total MCP-1 and TNF-alpha levels. CONCLUSIONS: These results suggest that MCP-1 could have an important role in the activation and recruitment of inflammatory and immune cells in periodontal diseases, and both AgP and CP patients may have the same pattern of MCP-1 expression. A strong positive correlation between the GCF levels of MCP-1 and TNF-alpha may account for the mechanism of amplification of inflammatory events in gingival inflammation.

Adult↗
PubMed2005

[The relationship between the calcaneus density and the degree of inflammation in patients with generalized aggressive periodontitis].

PURPOSE: To evaluate the relationship between the calcaneus density and the degree of inflammation in patients with generalized aggressive periodontitis. METHODS: Thirty one volunteers with healthy periodontium (as control group) and 38 patients with generalized aggressive periodontitis (as experimental group) were involved in this study. The average ages of the two groups were 27 and 23 years respectively. The clinical periodontal indexes and panoramic films were measured first. And the broadband ultrasonic attenuation(BUA) and T-score of the calcaneus were then determined using ultrasonic bone densitometer. SAS6.12 software package was used to analyse the data obtained. RESULTS: The BUA values of the two groups were 62.76+/-4.61 and 70.47+/-4.41 respectively, the BUA value of the experimental group was significantly lower than that of the control group (P<0.001). Moreover, T-score was different between the two groups and the score in the experimental group was significantly lower than that in the control (P<0.001). CONCLUSIONS: The BUA and T-score in patients with generalized aggressive periodontitis were significantly lower than that in the controls with healthy periodontium, which indicated that patients with generalized aggressive periodontitis had overall bone density decrease.

Absorptiometry, Photon↗
PubMed2005

Cytokine profiles in peripheral blood and whole blood cell cultures associated with aggressive periodontitis, juvenile idiopathic arthritis, and rheumatoid arthritis.

BACKGROUND: Cytokines play a key role in the pathogenesis of inflammatory diseases. An obvious question is whether patients with aggressive periodontitis, juvenile idiopathic arthritis, or rheumatoid arthritis share blood cytokine profiles distinguishing them from individuals free of disease. METHODS: The study population consisted of Danish white adults, <35 years of age, diagnosed with localized aggressive periodontitis (LAgP; N = 18), generalized aggressive periodontitis (GAgP; N = 27), juvenile idiopathic arthritis (JIA; N = 10), or rheumatoid arthritis (RA; N = 23) and healthy individuals with no systemic or oral diseases (control [CTRL]; N = 25). Enzyme-linked immunosorbent assays were used to determine the levels of interleukin (IL)-1alpha, IL-1beta, IL-1 receptor antagonist (IL-1Ra), IL-6, IL-10, tumor necrosis factor (TNF)-alpha, and lymphotoxin (LT)-alpha in peripheral blood (plasma) and unstimulated and stimulated whole blood cell cultures from the same blood collection. Autoantibodies (aAb) to IL-1alpha and IL-6 were quantitated by radioimmunoassay. RESULTS: Similar patterns of slightly higher IL-10 levels in plasma were found for GAgP and RA patients and in unstimulated cultures for GAgP, RA, and JIA patients. Interestingly, unstimulated cultures also demonstrated similar patterns of higher TNF-alpha levels for these three groups of patients. Similar group patterns of periodontitis patients (LAgP and GAgP) included increased IL-1Ra levels in stimulated cultures, which also showed similar group patterns of arthritis patients (JIA and RA) with respect to higher IL-1alpha and lower LT-alpha levels. Low titers of aAb to IL-1alpha and IL-6 were found in almost all individuals. CONCLUSION: Patients with aggressive periodontitis and types of arthritis presented with similar components of blood cytokine profiles distinguishing them from individuals free of disease.

Adolescent↗
PubMed2006

Evidence for a specific crevicular lymphocyte profile in aggressive periodontitis.

BACKGROUND AND OBJECTIVE: It is undisputed that the periodontal pocket is a particular region of the host defense that is dominated by polymorphonuclear leukocytes. However, little is known about the lymphocytes in the crevice. It was the aim of this study to analyse the proportions of T cells (CD3+), T-helper cells (CD4+), T-suppressor cells (CD8+), and B cells (CD20+) in the crevice of patients with localized aggressive periodontitis (LAP), generalized aggressive periodontitis (GAP), and generalized chronic periodontitis (CP). The results were compared with those obtained from periodontally healthy controls. MATERIAL AND METHODS: Crevicular cells were collected according to a previously described method. The lymphocyte subpopulations were analysed by using an indirect immunofluorescence method. RESULTS: Significant differences were established between the test groups and the controls regarding the mean number of CD8+ lymphocytes (LAP > CP and controls; p < 0.05) and CD20+ lymphocytes (LAP/GAP > CP, p < 0.05 and LAP/GAP > controls; p < 0.001). Significant variations in the CD4+/CD8+ ratio were observed (LAP < controls and GAP < controls; p < 0.01), as well as a correlation between the number of T cells and the degree of inflammation. CONCLUSION: In the present study, patients with LAP and patients with GAP were found to have increased numbers of crevicular T-suppressor/cytotoxic and B cells. This supports the hypothesis of a changed immune pathology in patients with aggressive periodontitis.

Acute Disease↗
PubMed2004

Real-time PCR quantification of cytomegalovirus in aggressive periodontitis lesions using TaqMan technology.

BACKGROUND: Herpesviruses are implicated in the pathogenesis of human periodontitis. However, the quantity of herpesviruses in periodontal sites remains unknown. OBJECTIVE: The aim of this study was to compare levels of subgingival human cytomegalovirus (HCMV) in aggressive periodontitis patients and in periodontally healthy subjects. METHODS: A total of 16 consecutive subjects with aggressive periodontitis and 15 healthy control subjects were included in the study. Subgingival specimens were collected by a periodontal curette. TaqMan real-time polymerase chain reaction (PCR) assay was used to quantify HCMV. RESULTS: HCMV was detected in 68.8% of aggressive periodontitis lesions but not in any of the periodontally healthy study sites. HCMV viral load in positive subgingival specimens ranged from 5 x 10(2) to 7.4 x 10(3) copies/ml. CONCLUSIONS: The TaqMan real-time PCR technology seems to provide a rapid and sensitive method for quantifying HCMV in periodontal pockets. The present findings confirm the frequent presence of HCMV in aggressive periodontitis lesions. Determining HCMV levels in different types of periodontitis may help elucidate the periodontopathic role of the virus and advance our understanding of the disease pathogenesis.

Adolescent↗
PubMed2004

Novel mutations in the cathepsin C gene in patients with pre-pubertal aggressive periodontitis and Papillon-Lefèvre syndrome.

Aggressive periodontitis (AP) in pre-pubertal children is often associated with genetic disorders like Papillon-Lefèvre syndrome (PLS). PLS is caused by mutations in the cathepsin C (CTSC) gene. We report a novel CTSC mutation (c.566-572del) in an otherwise healthy AP child and two novel compound heterozygous mutations (c.947T>G, c.1268G>C) in a PLS patient. We conclude that at least a subset of pre-pubertal AP is due to CTSC mutations and therefore may be an allelic variant of PLS.

Adolescent↗
PubMed2004

Detection of a highly toxic clone of Actinobacillus actinomycetemcomitans (JP2) in a Moroccan immigrant family with multiple cases of localized aggressive periodontitis.

The JP2 clone of Actinobacillus actinomycetemcomitans, a high-leukotoxin-producing strain, characterized by a 530-basepair (bp) deletion in the promoter region of the leukotoxin gene operon and mainly found among individuals with African origin, is associated with localized aggressive periodontitis. The objective of the study was to examine the occurrence of periodontal disease in a Moroccan immigrant family living in Denmark in which the oldest son (14 year) was referred and treated for localized aggressive periodontitis. Further, the potential occurrence of the JP2 clone of A. actinomycetemcomitans in the family was examined. Here we present the clinical, radiographic, and microbiological findings from the family. Clinical and radiographic examination of the other family members revealed that 3 of 5 younger siblings had localized aggressive periodontitis, one had gingivitis and the mother had chronic periodontitis. Despite scaling followed by intensive maintenance therapy several family members, including the sibling with gingivitis, had further attachment loss at the 1-year examination. The JP2 clone of A. actinomycetemcomitans was isolated from subgingival plaque samples from 4 children with periodontitis. In contrast, it was not detected in plaque from the oldest boy, who had been treated for localized aggressive periodontitis by surgery combined with antibiotic therapy. The 4 children with periodontitis and colonized with the JP2 clone were treated by scaling and antibiotic administration. One month later the JP2 clone could still be detected in plaque samples. In conclusion, it is confirmed that members of immigrant families with African origin are potential carriers of the JP2 clone and that those families often have multiple family members with localized aggressive periodontitis. It is proposed that those families are given periodontal examination frequently to benefit from early diagnosis and treatment of the disease.

Actinobacillus Infections↗
PubMed2005

Association of matrix metalloproteinase-1 promoter polymorphism with generalized aggressive periodontitis in a Chinese population.

BACKGROUND: A single nucleotide polymorphism in the promoter region of -1607 bp of the human matrix metalloproteinase-1 (MMP-1) gene has been found to be associated with an increased risk of various inflammatory diseases and cancer metastasis. OBJECTIVES: The present study aimed to examine the distribution of MMP-1 genotypes in a group of Chinese subjects with generalized aggressive periodontitis and a group of periodontally healthy subjects, and to evaluate the possible association of the MMP-1 promoter polymorphism with aggressive periodontitis. METHODS: Genomic DNA was obtained from whole blood samples in 40 Chinese subjects with generalized aggressive periodontitis and 52 periodontally healthy subjects as controls. MMP-1 promoter fragment was amplified by polymerase chain reaction, and the polymorphisms were analyzed by restriction endonuclease cleavage. The alleles were detected by polyacrylamide gel electrophoresis and visualized with ethidium bromide. RESULTS: The detection frequency of 2G allele was significantly higher in the subjects with generalized aggressive periodontitis (68.7%) than in the control subjects (49%) (p < 0.01). The genotype of 2G/2G was found in 52.5% of the patients, which was significantly greater than that of control subjects (23.1%) (p < 0.05). CONCLUSION: The present study suggests that a single nucleotide polymorphism in the MMP-1 promoter region of -1607 bp may be associated with generalized aggressive periodontitis in Chinese population.

Adult↗
PubMed2004

Aggressive periodontitis with supernumerary teeth: a retrospective study.

BACKGROUND: There are four key studies in the periodontology literature reporting the correlation between supernumerary teeth and aggressive periodontitis. The aim of this study is to detect such a relationship. METHODS: Patients with supernumerary teeth were identified retrospectively from their orthopantomographs and were invited to the periodontology department for intraoral examination. They were then evaluated for aggressive periodontitis. The number of existing teeth, age, family histories, attachment loss, probing depths, and bleeding on probing scores were recorded. RESULTS: Of the 5,850 subjects randomly observed among 48,000 patients, only 174 exhibited supernumerary teeth. Of these 174 subjects, only three patients were diagnosed with aggressive periodontitis. One of the patients was also suffering from Fanconi's anemia. CONCLUSIONS: Despite the similarities (aggressive periodontitis accompanied by supernumerary teeth) in the previous reports, we do not agree with the earlier results. We rather suggest that this association might be a random occurrence, rather than a biological one, although this observation should be further investigated using genetic testing.

Adult↗
PubMed2004

Relationship of Actinobacillus actinomycetemcomitans serotype b to aggressive periodontitis: frequency in pure cultured isolates.

BACKGROUND: To our knowledge, the association of the five serotypes of Actinobacillus actinomycetemcomitans (A. actinomycetemcomitans) to the new diagnostic classification scheme defined by the American Academy of Periodontology in 1999 has not yet been described. The goal of this study was to characterize the frequencies of the five serotypes of A. actinomycetemcomitans in A. actinomycetemcomitans isolates from various forms of periodontitis using both old and new diagnostic classifications and to determine the relationships between serotype and age and clinical diagnosis. METHODS: A total of 345 A. actinomycetemcomitans isolates from 115 A. actinomycetemcomitans culture-positive subjects (mean age 38.0 +/- 18.3 years, 59% female) were collected. Based on the new classifications, 33 subjects had aggressive periodontitis and 82 chronic periodontitis. According to old classifications, there were six prepubertal periodontitis (PPP), 12 localized juvenile periodontitis (LJP), 15 post-localized juvenile periodontitis (PLJP), 28 refractory periodontitis (Ref-P), and 54 adult periodontitis (AP) cases. Serotypes of A. actinomycetemcomitans were determined by an indirect immunofluorescence assay using serotype-specific polyclonal antisera to A. actinomycetemcomitans strains ATCC 29523, ATCC 43728, ATCC 33384, IDH 781 and IDH 1705 (serotype a, b, c, d, and e, respectively). Proportions of serotype b were examined between different diagnostic and age groups with a Z-test for proportions. RESULTS: Most subjects (n = 100, 86.96%) were infected with a single serotype (22 serotype a, 44 serotype b, 30 serotype c, 1 serotype d, and 3 serotype e). There were 11 subjects (9.57%) with two serotypes and two subjects (1.74%) with 3 serotypes. Two individuals had isolates lacking any detectable serotype antigen. Serotype b was the predominant serotype in children under 18 years of age and young adults between 19 to 35 years, although serotype b status was not significantly associated with age. Serotypes d and e were not found in patients under 35 years old. In 62 adult patients, one subject had serotype d and three had serotype e. Serotype b was the most common serotype in aggressive periodontitis (60.61%). The proportion of cases with serotype b was significantly higher in aggressive periodontitis compared to chronic periodontitis (P = 0.031). Other serotypes were not significantly associated with new diagnostic categories. Serotypes d and e were not detected in aggressive periodontitis. CONCLUSION: The results of this study show that proportions of serotype b of A. actinomycetemcomitans are significantly greater in culture-positive patients with aggressive periodontitis than those with chronic periodontitis.

Acute Disease↗
PubMed2006

CSF1 gene associated with aggressive periodontitis in the Japanese population.

Aggressive periodontitis (AgP) is characterized by the early onset of the rapid and progressive destruction of the alveolar bone. We investigated the correlation of single nucleotide polymorphisms (SNPs) in candidate genes with AgP in the Japanese population in order to determine the genetic risk factors for this complex disease. Among 11 genes related to bone formation and resorption, 43 known SNPs were tested in 98 case and 88 control samples for association with AgP by using SNP genotyping techniques. Among these, three polymorphisms located in the colony stimulating factor 1 (CSF1) gene showed a positive association with AgP. This is the first case of an association between a CSF1 polymorphism and a human disease.

Adolescent↗
PubMed2004

Single nucleotide polymorphisms associated with aggressive periodontitis and severe chronic periodontitis in Japanese.

Periodontitis is a common inflammatory disease causing destruction of periodontal tissues. It is a multifactor disease involving genetic factors and oral environmental factors. To determine genetic risk factors associated with aggressive periodontitis or severe chronic periodontitis, single nucleotide polymorphisms (SNPs) in multiple candidate genes were investigated in Japanese. We studied 134 patients with aggressive periodontitis, 117 patients with severe chronic periodontitis, and 125 healthy volunteers without periodontitis, under case-control setting, and 310 SNPs in 125 candidate genes were genotyped. Association evaluation by Fisher's exact test (p < 0.01) revealed statistically significant SNPs in multiple genes, not only in inflammatory mediators (IL6ST and PTGDS, associated with aggressive periodontitis; and CTSD, associated with severe chronic periodontitis), but also in structural factors of periodontal tissues (COL4A1, COL1A1, and KRT23, associated with aggressive periodontitis; and HSPG2, COL17A1, and EGF, associated with severe chronic periodontitis). These appear to be good candidates as genetic factors for future study.

Adult↗
PubMed2002

Aggressive periodontitis: 5-year follow-up of treatment.

BACKGROUND: The hypothesis that in subjects with aggressive periodontitis, a long-term stability of periodontal health can be achieved following comprehensive mechanical/surgical and systemic antimicrobial therapy was tested in this prospective study. METHODS: Thirteen patients (36.9+/-7.4 years) with aggressive periodontitis were monitored before and up to 5 years following periodontal therapy. Clinical attachment levels (CAL) were assessed pretherapy, and at 3 months following completion of active periodontal therapy supplemented by amoxicillin plus metronidazole. All subjects were subsequently enrolled in a maintenance program and provided with supportive periodontal therapy with 3 to 4 appointments annually. Reexaminations were performed after 6 months and 1, 2, 3, 4, and 5 years. The data were analyzed using the method of generalized estimating equations (GEE) for CAL changes from baseline to the 3-month visit, and from completion of periodontal therapy to each annual visit up to the 5-year follow-up reappointment. RESULTS: During the 5-year study, all subjects strongly benefited from periodontal treatment. Between baseline and the 3-month reexamination, the CAL levels revealed a significant decrease of 2.23 mm (95% confidence interval [CI]: 1.77 to 2.69 mm; P < or =0.001). At the 5-year maintenance visit, the CAL changes ranged from -0.04 to +0.29 mm with no further statistically significant periodontal breakdown (P >0.05). Five years after surgery, 3.2% of the treated sites demonstrated a further CAL gain > or =3 mm. A stabilization (CAL -2 to +2 mm) occurred in 94.6% of the cases. The number of periodontal sites experiencing a breakdown varied from 5.3% at 6 months to 2.2% at 5 years. CONCLUSIONS: In aggressive periodontitis, comprehensive mechanical/surgical and antimicrobial therapy is an appropriate treatment regimen for long-term stabilization of periodontal health. In this study, periodontal disease progression was successfully arrested in 95% of the initially compromised lesions, while 2% to 5% experienced discrete or recurrent episodes of loss of periodontal support.

Adult↗
PubMed2004

Gene expression signatures in chronic and aggressive periodontitis: a pilot study.

This pilot study examined gene expression signatures in pathological gingival tissues of subjects with chronic or aggressive periodontitis, and explored whether new subclasses of periodontitis can be identified based on gene expression profiles. A total of 14 patients, seven with chronic and seven with aggressive periodontitis, were examined with respect to clinical periodontal status, composition of subgingival bacterial plaque assessed by checkerboard hybridizations, and levels of serum IgG antibodies to periodontal bacteria assayed by checkerboard immunoblotting. In addition, at least two pathological pockets/patient were biopsied, processed for RNA extraction, amplification and labeling, and used to study gene expression using Affymetrix U-133 A arrays. Based on a total of 35 microarrays, no significantly different gene expression profiles appeared to emerge between chronic and aggressive periodontitis. However, a de novo grouping of the 14 subjects into two fairly robust clusters was possible based on similarities in gene expression. These two groups had similar clinical periodontal status and subgingival bacterial profiles, but differed significantly with respect to serum IgG levels against the important periodontal pathogens Porphyromonas gingivalis, Tannerella forsythensis and Campylobacter rectus. These early data point to the usefulness of gene expression profiling techniques in the identification of subclasses of periodontitis with common pathobiology.

Acute Disease↗
PubMed2006

CARD15 gene variants in aggressive periodontitis.

OBJECTIVE: The CARD15 gene encodes a protein that acts as an intracellular receptor of bacterial products, thus playing an important role in the innate immune response. Recently, CARD15 gene variants have been identified as a cause of increased susceptibility to Crohn's disease. The present study aimed to examine a potential association of CARD15 gene variants with aggressive periodontitis susceptibility. MATERIAL AND METHODS: The three main known CARD15 gene variants (p.R702W, p.G908R, and p.L1007fsX1008) were analysed by direct sequencing of exon 4, 8, and 11 of the gene in a total of 86 generalized aggressive periodontitis patients in comparison with 67 healthy controls. RESULTS: The mutant allele frequencies of the CARD15 variants were low in the generalized aggressive periodontitis group as well as in the control group and not significantly different (R702W: 3.5% versus 5.2%; G908R: 1.7% versus 1.5%; L1007fsX1008: 5.2% versus 4.5%). Two rare variants (A755V and R791Q), previously described only in patients with other inflammatory diseases, were observed in three patients having aggressive periodontitis but not in controls. CONCLUSIONS: Unlike in Crohn's disease, our results did not show an association between the three main CARD15 mutations and aggressive periodontitis. The role of rare variants remains unclear.

Adult↗
PubMed2005

A non-conservative, coding single-nucleotide polymorphism in the N-terminal region of lactoferrin is associated with aggressive periodontitis in an African-American, but not a Caucasian population.

Lactoferrin is an antimicrobial protein which plays an important role in regulating bacteria that are associated with aggressive periodontitis. Lactoferrin kills directly (via its strongly cationic N-terminal region) and indirectly, through sequestering the iron that bacteria require for growth. As aggressive periodontitis has a strong heritable component, we hypothesized that genetic variation within the lactoferrin gene may play a role in susceptibility to this condition. We have identified and examined a novel, functional, single-point A/G nucleotide mutation causing a threonine/alanine substitution at position 11 (T11A) of the secreted lactoferrin protein. In a pilot case-controlled study of aggressive periodontitis, analysis of 46 African-American patients and 78 controls showed that patients were twice as likely to express the G nucleotide (alanine) allele over controls (60.3 vs 30.4%; P=0.0007, odds ratio=2.564, 95% CI=1.475-4.459). A Caucasian population of 77 patients and 131 controls showed no such association (P=0.5201, odds ratio=0.862, 95% CI=0.548-1.356). The data presented provide a new insight into the genetic susceptibility to aggressive periodontitis.

Black or African American↗
PubMed2001

Generalized aggressive periodontitis in a prepubertal patient: a case report.

A 10-year-old boy presented with generalized gingival inflammation, extensive alveolar bone loss, and tooth mobility. Clinical and radiographic examination supplemented by microbiologic investigation led to a diagnosis of classically termed prepubertal periodontitis (now known as generalized aggressive periodontitis). Other than severe periodontitis, the child was systemically healthy. Neither unusual infections nor abnormalities in neutrophil functions were detected. Microbiologic examinations by culture revealed the presence of the periodontal pathogen Actinobacillus actinomycetemcomitans. Treatment consisted of extraction of mobile teeth, supragingival and subgingival debridement, subgingival curettage, and root planing combined with a 1-week prescription of a combination of metronidazole and amoxicillin. Scanning electron microscopy of extracted teeth revealed hypoplastic and aplastic cementum at the periodontally exposed and intact surfaces. Clinical and microbiologic follow-up was continued over a 1-year period. No periodontal lesions have been detected, and A actinomycetemcomitans could not be isolated from the subgingival areas of the remaining teeth at the end of the first year. Since A actinomycetemcomitans was the main pathogen present in the subgingival microflora of the patient, it might play a key role in the etiology of prepubertal periodontitis.

Actinobacillus Infections↗