Association between the IL-10 rs1800872 polymorphisms and periodontitis susceptibility: A meta-analysis.

BACKGROUND: Periodontitis is a common disease with an unclear pathological mechanism. No precise consensus has been reached to evaluate the association between the IL-10 rs1800872 (- 592, -590, -597 C>A) polymorphism and periodontal disease. Thus, we performed this meta-analysis to collect more evidence-based information. METHODS: Four online databases, PubMed, Embase, Web of Science, and China Biology Medicine disc (CBM), were searched in August 2018. An odds ratio (OR) with a 95% confidence interval (CI) was applied to evaluate the association of the rs1800872 with periodontitis susceptibility. RESULTS: Twenty three case-control studies with 2714 patients and 2373 healthy controls were evaluated. The overall analyses verified that the IL-10 rs1800872 polymorphism was significantly associated with an increased risk of periodontitis in the allelic model, homozygote model, dominant model, and recessive model (A vs C: OR = 1.28, 95%CI = 1.11-1.49, P = .00, I = 56.87%; AA vs CC: OR = 2.06, 95%CI = 1.32-3.23, P = .00, I = 73.3%; AA + AC vs CC: OR = 1.42, 95%CI = 1.03-1.96, P = .03, I = 76.2%; AA vs AC + CC: OR = 1.78, 95%CI = 1.26-2.56, P = .00, I = 76.7%). Moreover, the subgroup analysis based on ethnicity, periodontitis type, and smoking status showed significant differences. CONCLUSIONS: The results of our meta-analysis demonstrate that rs1800872 is associated with periodontitis susceptibility in Caucasians and Asians. Moreover, A allele, AA genotype, CC genotype may be closely associated with chronic periodontitis (CP), while A allele, AA genotype may be closely associated with aggressive periodontitis (AgP).

The role of three interleukin 10 gene polymorphisms (- 1082 A > G, - 819 C > T, - 592 A > C) in the risk of chronic and aggressive periodontitis: a meta-analysis and trial sequential analysis.

BACKGROUND: Periodontitis is a major oral health problem and it is considered as one of the reasons for tooth loss in developing and developed nations. The objective of the current review was to investigate the association between IL10 polymorphisms - 1082 A > G (rs1800896), -819C > T (rs1800871), - 592 A > C (rs1800872) and the risk of either chronic periodontitis or aggressive periodontitis. METHODS: This is a meta- analysis study, following the preferred reporting items for systematic reviews and meta- analyses (PRISMA). Relevant studies were searched in the health related electronic databases. Methodological quality of the included studies were assessed using the Newcastle-Ottawa Scale. For individual studies, odds ratio (OR) and its 95%confidence interval (CI) were calculated to assess the strength of association between IL10 polymorphisms (- 1082 A > G, -819C > T, - 592 A > C) and the risk of periodontitis. For pooling of the estimates across studies included, the summary OR and its 95% CIs were calculated with random-effects model. The pooled estimates were done under four genetic models such as the allelic contrast model, the recessive model, the dominant model and the additive model. Trial sequential analysis (TSA) was done for estimation of the required information size for this meta-analysis study. RESULTS: Sixteen studies were identified for this review. The included studies were assessed to be of moderate to good methodological quality. A significant association between polymorphism of IL10-1082 A > G polymorphism and the risk of chronic periodontitis in the non-Asian populations was observed only in the recessive model (OR,1.42; 95% CI:1.11, 1.8,I2: 43%). The significant associations between - 592 A > C polymorphism and the risk of aggressive periodontitis in the non-Asian populations were observed in particular genetic models such as allele contrast (OR, 4.34; 95%CI:1.87,10.07,I2: 65%) and recessive models (OR, 2.1; 95% CI:1.16, 3.82,I2: 0%). The TSA plot revealed that the required information size for evidence of effect was sufficient to draw a conclusion. CONCLUSIONS: This meta-analysis suggested that the IL10-1082 A > G polymorphism was associated with chronic periodontitis CP risk in non-Asians. Thus, in order to further establish the associations between IL10 (- 819 C > T, - 592 A > C) in Asian populations, future studies should include larger sample sizes with multi-ethnic groups.

Interleukin-10 polymorphisms affect the key periodontal pathogens in Chinese periodontitis patients.

Interleukin-10 (IL-10) polymorphisms have been shown to affect IL-10 production. This study investigated the influences of IL-10 polymorphisms on the susceptibility to chronic periodontitis (CP) and aggressive periodontitis (AP), and their possible role in the quantity of subgingival bacteria Aggregatibacter Actinomycetemcomitans and Porphyromonas gingivalis. 92 CP patients, 83 AP patients and 91 periodontal healthy controls were recruited. Serum IL-10 concentration was analyzed by enzyme-linked immunosorbent assay (ELISA). Gene polymorphisms were determined by multiplex SNaPshot technique. Bacteria were quantified by real-time polymerase chain reaction with TaqMan MGB probes. Taking into account age, gender and periodontal status, IL-10-592 AA, -819 TT and ATA/ATA genotype occurred more frequently in patients with CP than in healthy controls. In CP cases, higher quantity of subgingival A. actinomycetemcomitans and lower serum IL-10 levels could be detected in homozygous ATA/ATA carriers. These findings indicate that variants in IL-10 promoter gene were not only associated with predisposition to chronic periodontitis but also affected the subgingival number of A. Actinomycetemcomitans in a Chinese Han population.

Genetic polymorphisms and periodontal disease in populations of African descent: A review.

Aggressive periodontitis is a rare but rapidly progressing form of periodontal disease that usually affects otherwise systemically healthy individuals, at a young age. It usually affects first molars and incisors, which are usually lost if treatment is not properly and early rendered. Although of low prevalence, it affects individuals of African descent at a higher prevalence, and usually multiple members within the same family. Several studies have been performed in the attempt to evaluate specific single nucleotide polymorphisms (SNPs) that could be associated with this disease. To the best of our knowledge, the present article provides the first review of the literature focusing on studies that evaluated SNPs in patients of African descent with aggressive periodontitis. Several SNPs have been evaluated in different genes according to their role in the pathogenesis of the disease, with positive and negative associations (such as IL1, FCGR3B, FPR1, LTF, CYBA, GLT6D1, TLR4) with both the localized and generalized forms of aggressive periodontitis. Given the complexity of periodontitis, the difficulty in gathering large cohorts diagnosed with this rare form of disease, and the fact that candidate gene studies may only determine part of the genetic risk of a disease, the search for specific SNPs associated with aggressive periodontitis seems to be a long one, most likely to result in the combination of multiple SNPs, in multiple genes.

Analysis of polymorphisms in Interleukin 10, NOS2A, and ESR2 genes in chronic and aggressive periodontitis.

The objective of this study was to investigate the association between single nucleotide polymorphisms (SNPs) in the IL10, NOS2A, and ESR2 genes and chronic periodontitis (CP) and aggressive periodontitis (AgP). Three groups of patients underwent periodontal and radiographic evaluations: CP (n = 61), AgP (n = 50), and periodontally healthy (control group=61). Genomic DNA was extracted from oral epithelial cells and used for genotyping by real-time polymerase chain reaction using TaqMan® probes. The investigated SNPs were: -1087G > A, -819C > T and -592C > A in the IL10; +2087G > A in the NOS2A, and +1730G > A in the ESR2 gene. Differences in genotype and allele frequencies of each polymorphism and some individual characteristics were analyzed using the chi-square test and multivariate logistic regression analysis. Analysis of SNPs and haplotypes in the IL10 and SNP in the ESR2 gene did not present any significant association with AgP or CP. The +2087G allele of the NOS2A gene tended to be significantly associated with periodontal disease. Patients carrying the genotype +2087GG in the NOS2A gene were genetically protected against the development of CP (p = 0.05; OR = 0.44; 95%CI = 0.20-0.95). This result showed greater significance when patients with AgP and CP were combined (total PD) (p = 0.03; OR = 0.46; 95%CI = 0.23-0.92). In conclusion, the studied Brazilian population had a significantly higher frequency of the GG genotype for the +2087 SNP in the NOS2A gene in individuals without periodontitis, although statistical significance was not maintained after multiple logistic regression.

Complementary clinical effects of red complex bacteria on generalized periodontitis in a caucasian population.

OBJECTIVES: To relate five periodontopathogenic bacteria, including the red complex, to the severity, extent, and inflammation of the periodontal lesion in Caucasian patients with generalized aggressive and chronic periodontitis and to explore whether tobacco use is associated with a specific bacterial profile. MATERIALS AND METHODS: A cross-sectional and analytic study was conducted in patients with aggressive and chronic periodontitis. Data were gathered on socio-demographic and periodontal variables, and RH-PCR was used to determine subgingival bacterial profile. Linear and logistic regression analyses were performed. RESULTS: The study included 60 patients with aggressive and 123 with chronic periodontitis. Total red complex bacteria count was higher in aggressive periodontitis, mainly due to T. denticola (P = 0.015). In both periodontitis types, models showed an association between T. forsythia count and probing depth (B = 0.157, P = 0.030) and between T. denticola count and higher bleeding scores (B = 2.371, P = 0.027). Smoking did not affect the red complex bacteria count in either disease. CONCLUSIONS: The prevalence of red complex bacteria was similar between aggressive and chronic periodontitis, but their count was higher in the former. In both diseases, T. forsythia was associated with greater severity and T. denticola with more severe bleeding. Tobacco smoking was not associated with the presence of red complex bacteria in either disease.

Analysis of polymorphisms in Interleukin 10, NOS2A, and ESR2 genes in chronic and aggressive periodontitis

Abstract The objective of this study was to investigate the association between single nucleotide polymorphisms (SNPs) in the IL10, NOS2A, and ESR2 genes and chronic periodontitis (CP) and aggressive periodontitis (AgP). Three groups of patients underwent periodontal and radiographic evaluations: CP (n = 61), AgP (n = 50), and periodontally healthy (control group=61). Genomic DNA was extracted from oral epithelial cells and used for genotyping by real-time polymerase chain reaction using TaqMan® probes. The investigated SNPs were: -1087G > A, -819C > T and -592C > A in the IL10; +2087G > A in the NOS2A, and +1730G > A in the ESR2 gene. Differences in genotype and allele frequencies of each polymorphism and some individual characteristics were analyzed using the chi-square test and multivariate logistic regression analysis. Analysis of SNPs and haplotypes in the IL10 and SNP in the ESR2 gene did not present any significant association with AgP or CP. The +2087G allele of the NOS2A gene tended to be significantly associated with periodontal disease. Patients carrying the genotype +2087GG in the NOS2A gene were genetically protected against the development of CP (p = 0.05; OR = 0.44; 95%CI = 0.20-0.95). This result showed greater significance when patients with AgP and CP were combined (total PD) (p = 0.03; OR = 0.46; 95%CI = 0.23-0.92). In conclusion, the studied Brazilian population had a significantly higher frequency of the GG genotype for the +2087 SNP in the NOS2A gene in individuals without periodontitis, although statistical significance was not maintained after multiple logistic regression.

Epidemiology and demographics of aggressive periodontitis.

Epidemiologic studies of aggressive periodontitis have used different study designs and a range of examination methods and case definitions, and this greatly complicates the study of disease prevalence in populations. The wide range of disease case definitions, in particular, profoundly impacts the reported rate of disease, and the use of a standard disease definition is strongly recommended. Surveys of aggressive periodontitis that use only clinical examinations, without radiographic examination to confirm the presence of a distinctive pattern of tissue loss, may overestimate the prevalence of this disease, particularly when a low threshold of attachment loss is used. The prevalence of aggressive periodontitis varies significantly between populations, and differences in race/ethnicities seem to be a key factor. Studies consistently show that aggressive periodontitis is most prevalent in Africa and in populations of African descent and is least prevalent in Caucasians in Europe and North America. Among children and young adults the prevalence of this disease is higher in older than in younger age groups. Most studies show comparable disease prevalence in male and female subjects. These findings show that aggressive periodontitis is a significant health problem in certain populations. This review also highlights a lack of information on the epidemiology and demographics of this disease in many parts of the world, particularly in Asia and Africa. Epidemiologic studies of aggressive periodontitis in high-risk populations are important and could provide vital data on the determinants of this disease, and this information is needed for the establishment of effective health-promotion measures.

Presence of JP2 and Non-JP2 Genotypes of Aggregatibacter actinomycetemcomitans and attachment loss in adolescents in Ghana.

BACKGROUND: Limited data are reported concerning the presence of A. actinomycetemcomitans and attachment loss (AL) in sub-Saharan countries. The authors investigate the carrier frequency of JP2 and non-JP2 genotypes of A. actinomycetemcomitans and the presence of AL in Ghanaian adolescents and evaluate socioeconomic conditions and oral hygiene practices. METHODS: Five hundred individuals (mean ± SD age: 13.2 ± 1.5 years) in public and private schools were interviewed about demographic characteristics and oral hygiene practices and were given a full-mouth periodontal examination. Subgingival plaque samples were obtained from periodontal sites around permanent first molars and incisors. The carrier status of A. actinomycetemcomitans at the individual level was determined based on results obtained by cultivation and polymerase chain reaction. RESULTS: The findings of this study show a relatively high carrier rate of JP2 and non-JP2 genotypes of Aggregatibacter actinomycetemcomitans in the Ghanaian adolescent population and the presence of this bacterium is associated with the occurrence of AL. The overall carrier rate of A. actinomycetemcomitans was 54.4%, and the highly leukotoxic JP2 genotype was detected in 8.8% of the study population. A total of 107 (21.4%) individuals had ≥ 1 tooth with AL ≥ 3 mm. The majority of the individuals carrying A. actinomycetemcomitans (80.1%) (P <0.001) and of the periodontally diseased individuals (91.6%) (P <0.001) were found in public schools. CONCLUSIONS: A. actinomycetemcomitans and AL were frequently found in Ghanaian adolescents. The school type was the strongest predictor of both presence of A. actinomycetemcomitans and AL.

Genetic polymorphism of Fcγ-receptors IIa, IIIa and IIIb in South Indian patients with generalized aggressive periodontitis.

Recent evidence suggests that polymorphisms in Fcγ receptors are associated with different forms of periodontitis. However, the FcγR genotypes and their allele frequency differ among subjects from different ethnic backgrounds. The aim of the present study was to determine whether specific FcγRIIa, FcγRIIIa, and FcγRIIIb alleles and/or genotypes are associated with susceptibility to generalized aggressive periodontitits (GAgP) in a South Indian population. Buccal scrapings were obtained from 60 subjects with GAgP and 60 periodontally healthy individuals, and DNA was extracted from each of the samples. FcγRIIa and FcγRIIIa genotyping was performed by polymerase chain reaction (PCR) amplification of DNA with allele-specific primers followed by allele-specific restriction digestion of the products, whereas FcγRIIIb genotyping was done by allele-specific PCR. There was no significant difference in the distribution of the FcγRIIa H/R genotype between GAgP patients and healthy subjects, although significant over-representation of the R allele was noted in GAgP patients. With regard to FcγRIIIa F/V genetic polymorphism, the homozygous V/V genotype and V allele were significantly over-represented in the GAgP group, whereas the F/F genotype and F allele were over-represented in the controls. Furthermore, there was significant over-representation of the FcγRIIIb-NA2 allele and NA2/NA2 genotype in GAgP patients, and of the NA1/NA1 genotype and NA1 allele in the controls. These data suggest that the FcγRIIIa V/V genotype and/or V allele, as well as the FcγRIIIb NA2/NA2 and/or NA2 allele, along with the FcγRIIa- R allele, may be risk factors for GAgP in the population of South India.

MMP-8 -799 C>T genetic polymorphism is associated with the susceptibility to chronic and aggressive periodontitis in Taiwanese.

AIM: Matrix metalloproteinase (MMP)-8 is a protease that degrades numerous extracellular molecules and has been implicated in the pathogenesis of periodontitis. Polymorphism in the MMP-8 could affect the susceptibility to disease. Our aim was to evaluate the association between periodontitis and MMP-8 -799 C>T polymorphism. MATERIAL AND METHODS: Genomic DNA was obtained from 361 chronic periodontitis patients (CP), 96 aggressive periodontitis patients (AgP), and 106 periodontally healthy controls (HC). MMP-8 -799 C>T polymorphism was determined using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). RESULTS: The frequencies of genotypes in diseased groups were similar but were significantly different from those in the HC. Multivariate logistic regression analysis with adjustment for age, gender and smoking indicated that increased risks of AgP and CP were associated with the -799 T allele (in AgP, adjusted OR = 1.99, p = 0.04; in CP, adjusted OR = 1.87, p = 0.007). To avoid the confounded effect of smoking on MMP-8 polymorphism to periodontitis, the analysis was conducted on non-smokers and the associations were significant. CONCLUSIONS: These results suggested that non-smoking Taiwanese with the MMP-8 -799 T allele were associated with the risks of both CP and AgP. Further studies in other ethnic populations are necessary.

Occurrence of Aggregatibacter actinomycetemcomitans serotypes in subgingival plaque from United States subjects.

This study examined the distribution pattern of Aggregatibacter actinomycetemcomitans serotypes in the subgingival plaque of subjects residing in the United States. A. actinomycetemcomitans was identified in 256 subgingival plaque samples from 161 subjects. For 190 of the 256 samples, the total cultivable bacteria and selected periodontal pathogenic species were determined. A. actinomycetemcomitans isolates were confirmed by a16S rDNA-based PCR analysis, genotyped by arbitrarily-primed PCR, and serotyped by PCR analysis of serotype-specific gene clusters. A total of 82 distinct A. actinomycetemcomitans strains were identified. The serotype distribution pattern of the strains was 21 (25.6%) serotype a, 12 (14.6%) b, 41 (50%) c, 6 (7.3%) e, 1 (1.2%) f, and 1 (1.2%) non-typeable. For 14 subjects where multiple colonies of A. actinomycetemcomitans were identified, 11 subjects (78.6%) were each infected by a single serotype, while the remaining three subjects (21.3%) were each infected by two serotypes of A. actinomycetemcomitans. There was an inverse relationship between the level of cultivable A. actinomycetemcomitans and Porphyromonas gingivalis. Within subgingival plaque of study cohort A. actinomycetemcomitans serotype c was the dominant serotype and comprised 50% of all strains, followed by (in order of detection frequency) serotypes a and b. Serotypes d, e, and f strains were either not detected or less frequently found. Serotype distribution patterns of subgingival A. actinomycetemcomitans may vary among subjects of different race orethnicity.

Ethnic disparities in the prevalence of periodontitis among high school students in Sudan.

BACKGROUND: There are limited data on the epidemiology and risk factors of periodontitis in young populations in developing nations. This study assesses the prevalence of periodontal attachment loss and aggressive periodontitis and the association with ethnicity among high school students in Sudan. METHODS: The study sample consisted of 1,200 students, 13 to 19 years old, selected from 38 public and private high schools using a multistage, stratified sampling design. The subjects were interviewed and examined clinically. Periodontal parameters were assessed at six sites per tooth. Subjects with aggressive periodontitis were identified. RESULTS: A total of 3.4% of the subjects had aggressive periodontitis, and 16.3% and 8.2% of the subjects had at least one tooth with > or = 4 and > or = 5 mm attachment loss, respectively. A significantly higher percentage of subjects of African tribal ethnicity had attachment loss > or = 4 and > or = 5 mm compared to Afro-Arab tribes (19.8% versus 14.7%, P = 0.02; and 12% versus 6.4%, P = 0.004, respectively), and had a higher prevalence of aggressive periodontitis (6% versus 2.3%; P = 0.01) and higher risk of being diagnosed with this disease (odds ratio = 2.7; P <0.0001). African ethnicity was also associated with a significantly higher number of teeth with attachment loss than in Afro-Arabs (P <0.01). Comparison by gender showed a significantly higher percentage of males with aggressive periodontitis (4.9% versus 2%; P <0.01) and a higher risk for this disease (odds ratio = 2.5; P = 0.01) than in females. However, the prevalence of subjects with attachment loss > or = 4 and > or = 5 mm was comparable in the two gender groups. CONCLUSIONS: Our results show that aggressive periodontitis is highly prevalent in this population. African ethnicity (versus Afro-Arab) and male gender were risk factors for aggressive periodontitis.

Association of single nucleotide gene polymorphism at interleukin-1beta +3954, -511, and -31 in chronic periodontitis and aggressive periodontitis in Dravidian ethnicity.

BACKGROUND: Interleukin (IL)-1beta gene polymorphisms are considered a potential risk factor for periodontal disease. The aim of this study is to identify the association of IL-1beta gene polymorphisms with chronic periodontitis and aggressive periodontitis in a Malayalam-speaking Dravidian population from South India. METHODS: The case-control study consisted of 43 patients with chronic periodontitis and 54 patients with aggressive periodontitis as cases, and the control group consisted of 101 healthy subjects. All subjects were genotyped for IL-1beta +3954, -511, and -31 loci by polymerase chain reaction amplification followed by restriction enzyme digestion and gel electrophoresis. Genotype, allele, and haplotype analyses were done. RESULTS: Analyses for allele and genotypes showed a high frequency of the C allele and CC genotype for single nucleotide polymorphism IL-1beta +3954 in the group with chronic periodontitis and no difference for patients with aggressive periodontitis compared to controls (P <0.05). Haplotype analysis showed that IL-1beta -31 and -511 were in strong linkage disequilibrium in all groups. The IL-1beta -31 allele T was in linkage with allele T of IL-1beta +3954 in the control group. CONCLUSIONS: In the Malayalam-speaking Dravidian population, allele C of IL-1beta +3954 appeared to be an important risk factor for chronic periodontitis. The IL-1beta -31 allele T was in linkage with allele T of IL-1beta +3954 in the control group. No gene polymorphisms were found in patients with aggressive periodontitis. More studies with a larger sample size involving the entire cluster of the IL-1beta gene are necessary to determine the exact role of IL-1beta gene polymorphisms in periodontal disease.

Serotypes of Aggregatibacter actinomycetemcomitans in patients with different ethnic backgrounds.

BACKGROUND: The identification of Aggregatibacter actinomycetemcomitans (previously Actinobacillus actinomycetemcomitans) serotypes may add some important information to the understanding of the pathogenetic background of severe periodontal infections. This study compared serotypes of A. actinomycetemcomitans in two groups of periodontal patients with different ethnic backgrounds. METHODS: A total of 194 patients (96 Germans and 98 Koreans) with aggressive or severe chronic periodontitis participated in the study. Microbiologic analysis of pooled samples from subgingival plaque was performed by using a real-time polymerase chain reaction (PCR) test for A. actinomycetemcomitans. In patients who tested positive for A. actinomycetemcomitans, serotypes (a through f) were determined by nucleic acid-based methods. RESULTS: The prevalence of patients who tested positive for A. actinomycetemcomitans with the real-time PCR was comparable in both groups (Germans: 27.0%; Koreans: 22.2%). In German patients, the serotypes detected most frequently were b (33.3%), c (25.0%), and a (20.8%), whereas in Korean patients, the serotype distribution was different, with serotypes c (61.9%) and d (19.0%) accounting for >80% of the complete serotype spectrum. CONCLUSION: Even if the percentage of patients who tested positive for A. actinomycetemcomitans was identical in patients with generalized aggressive and severe chronic periodontitis and different ethnic backgrounds, the distribution of A. actinomycetemcomitans serotypes may exhibit marked differences.

[Genetic background of periodontitis. Part I. Basic principles and inherited syndromes. Literature review]. / A fogágybetegség genetikai háttere I. Alapfogalmak és örökletes szindrómák. Irodalmi összefoglaló.

Periodontitis is an infectious disease. It had previously been considered as a diseases caused merely by dental plaque. During the 1990-ies a substantial number of publications indicated the role of other risk factors in its pathogenesis, such as behavioral, systemic and genetic causes. Based on recent research data, genetic and ethnic factors have become the leading susceptibility or severity factors for destructive periodontitis. The family background of early onset aggressive periodontitis has long been known. Hereditary syndromes can very frequently be associated with severe periodontitis. Both facts can support the alleged connection between certain genes' mutation and periodontal manifestation. Periodontal disease associated with systemic hereditary syndromes mainly shows a Mendelian inheritance. The locus and the characteristics of the gene mutations have in many cases been identified. Nevertheless several polygenic gene single nucleotide mutations can also be a predisposing or severity factor for periodontitis. Part I of the literature review is focusing on those syndromes in which major PMN leukocyte deficiency or dysfunction or certain structural protein deficiency occur.

Polymorphisms in the interleukin-1 (IL1) gene cluster are not associated with aggressive periodontitis in a large Caucasian population.

Polymorphisms in the interleukin-1 (IL1) gene have been suggested to influence transcription of IL1A (interleukin-1alpha) and IL1B (interleukin-1beta) and thereby the pathophysiology of periodontitis. This case-control association study on 415 northern European Caucasian patients with aggressive periodontitis (AgP) and 874 healthy controls was conducted to examine 10 single-nucleotide polymorphisms (SNPs) in the genes of the IL1 cluster for association with IL1A, IL1B, CKAP2L (cytoskeleton-associated protein 2-like), and IL1RN (IL-1 receptor antagonist). The results do not support an association between variants in the IL1 gene cluster and AgP. This case-control study had at least 95% power to detect genuine associations with variants carrying relative risks of at least 1.5 for heterozygous carriers and 2.25 for homozygous carriers. Previous reports of an association between IL1 promoter SNPs and periodontitis might reflect subpopulation effects and have to be interpreted with care.

Aggressive periodontitis among young Israeli army personnel.

BACKGROUND: The aim of this study was to assess the prevalence of aggressive periodontitis among young Israeli army recruits and to evaluate its association with smoking habits and ethnic origin. METHODS: The study population consisted of 642 young army recruits (562 men [87.5%] and 80 women [12.5%]), aged 18 to 30 years (average: 19.6 +/- 1.6 years), who arrived at a military dental clinic for dental examinations between January and December 2004. Subjects filled out a questionnaire regarding their ethnic origin and family periodontal history, followed by radiographs and a clinical periodontal examination of four first molars and eight incisors. RESULTS: Aggressive periodontitis was found in 5.9% of the subjects (4.3% localized and 1.6% generalized). At least one site with a probing depth > or =5 mm was found in 20.1% of the subjects. A radiographic distance between crestal bone height and the cemento-enamel junction >3 mm was found in 43 (6.7%) subjects. Current smokers (39.9%) (P = 0.03) and subjects of North African origin (P <0.0001) correlated with a high prevalence of aggressive periodontitis. CONCLUSION: A relatively high prevalence of aggressive periodontitis was found in young Israeli army recruits, which was particularly associated with smoking and ethnic origin.

The Fcgamma receptor genotype as a risk factor for generalized early-onset periodontitis in Japanese patients.

BACKGROUND: Genetic polymorphisms of immunoglobulin G (IgG) Fc receptors (FcgammaR) were recently shown to be associated with recurrence rates of adult periodontitis (AP). The purpose of this study was to evaluate whether FcgammaR polymorphisms are also associated with generalized early-onset periodontitis (G-EOP) in Japanese patients. METHODS: Thirty-eight Japanese patients with G-EOP and 83 Japanese patients with AP were identified according to established clinical criteria, including measurements of probing depth, clinical attachment level, and alveolar bone level. FcgammaR genotypes for 3 bi-allelic polymorphisms were determined in these G-EOP and AP patients and 104 race-matched healthy controls by means of allele-specific polymerase chain reactions. RESULTS: There was a significant difference in the distribution of FcgammaRIIIb genotypes between G-EOP patients and healthy controls (P = 0.02). Additionally, a significant over-representation of FcgammaRIIIb-NA2 allele was observed in G-EOP patients as compared to AP patients and controls (P= 0.02, P= 0.009, respectively). Moreover, we found a strong association between G-EOP and the composite genotype comprising FcgammaRIIIb-NA2 and FcgammaRIIIa-158F (G-EOP versus controls: odds ratio 2.4, 95% CI 1.0-6.0, chi2 = 4.13, P= 0.04). CONCLUSIONS: This study indicates that the FcgammaRIIIb-NA2 allele and possibly FcgammaRIIIa-158F could be associated with susceptibility to G-EOP in Japanese patients.

Clinical and genetic analysis of a large North European Caucasian family affected by early-onset periodontitis.

Genetic studies of early-onset periodontitis (EOP) are hampered by several factors. These include delayed onset of the trait, an upper age limit of expression of the disease, and lack of phenotypic information for edentulous family members. Segregation analyses of families with EOP support a major locus hypothesis but fail to define clearly the criteria used for diagnosis of the relatives. Confirmation of a proposed mode of inheritance and the identification of risk genes is awaited by means of family linkage studies. It is suggested that a system can be developed for the current and retrospective diagnosis of relatives of EOP probands. In addition, it is hypothesized that the large family presented here is suitable for a linkage study. Relatives of the proband who were unavailable for a full periodontal examination, were edentulous, or were deceased, were diagnosed by means of documented clinical evidence of periodontal disease or from reported case histories. Segregation analysis was performed. Analysis of the power of the pedigree to detect linkage was carried out by means of the SIMLINK program. Three different categories were defined according to the reliability of diagnosis of EOP. Segregation analysis indicated either autosomal-dominant or X-linked-dominant inheritance in this family. The simulations showed lod scores above 3.0 for all locations of the disease gene, and for each category of diagnosis. In conclusion, a method has been developed which can be used for the diagnosis of relatives of EOP probands when ideal clinical data are unavailable. The simulations suggest that this family is suitable for a genetic linkage study with the aim of identifying the location of one or more susceptibility genes.