Search

Periodontal disease (PD) and peri-implantitis (PI) are characterized by an immune response leading to destructive inflammation. The prominent impact of genetic factors on periodontitis has been previously evaluated and IL-17 has found to play a critical role in this process. This cytokine has a controversial behavior. This study aimed at finding out whether the polymorphism of this cytokine plays a significant role in chronic periodontitis (CP) and PI or it is just a pro-inflammatory regulatory cytokine. Fresh human blood samples were obtained and three main genotypes were traced carefully. The samples were transferred into 96-well plates and sent to KBioscience Institute in the United Kingdom for genotyping the polymorphism using Competitive Allele Specific PCR (KASP) technique. SPSS version19 software and chi-square and Kruskal-Wallis tests were used for statistical differences considering p-value less than 0.05. A significant difference was detected between the three groups in terms of specific SNP studied in this experiment (P = 0.00). The CC genotype of IL17 polymorphism (rs10484879) may contribute to the pathogenesis of peri-implantitis and periodontitis. The association of IL-17 polymorphism with PI and CP is a promising finding that may help in future similar studies on other ethnicities and larger study populations.

Objectives: The aim of this systematic review was to evaluate the relationship between genetic polymorphisms and dental implant biological complications., Material and Methods: All prospective, cross-sectional and retrospective studies reporting on dental implant loss/peri-implantitis/peri-implant marginal bone loss after loading in association with genetic polymorphism were considered for inclusion. A thorough search of electronic databases, supplemented by checking bibliographies of review articles was performed by two independent reviewers. Quality assessment of the included studies was conducted independently and in duplicate by two reviewers as part of the data extraction process., Results: The search provided 344 related articles. Twenty-two publications were identified for possible inclusion and finally, seven articles met the defined inclusion criteria. Four studies which investigated the potential relationship between early implant loss and IL-1, IL-2, IL-6, TNF-α or TGF-β1 genotype revealed no evidence to support this association. In two of the three studies which evaluated peri-implantitis in relation to IL-1 genotype, the findings indicate that IL-1RN (intron 2), IL-1A (-899), IL-1B (+3954) gene polymorphisms were correlated to increased peri-implant tissue infection and destruction., Conclusions: Methodological and study design issues restricted the possibility to draw robust conclusions. Within the limits of this review, it might be concluded that there is no obvious association between specific genetic polymorphism and dental implant failure in terms of biological complications, although a tendency should be underlined showing the potential link between IL-1 genotype and peri-implantitis. Well designed and adequately powered prospective cohort studies are needed to provide further information., (© 2011 John Wiley & Sons A/S.)

Purpose: The presence of pathogenic microorganisms associated with both chronic periodontitis and implant failure can induce a host immune response. The type of response is determined by an individual's genetic makeup. The aim of this study was to investigate the genetic relationship between interleukin-10 (IL-10) and tumor necrosis factor alpha (TNF-α) polymorphisms and patient susceptibility to chronic periodontitis or implant failure and to compare their immunogenetic functions., Materials and Methods: This study recruited subjects according to clinical diagnostic criteria for failing implants, chronic periodontitis, healthy implants, and healthy controls. Human DNA from buccal swabs was analyzed by amplification refractory mutation system-polymerase chain reaction and agarose gel electrophoresis performed for gene polymorphisms of IL-10 (IL-10, IL-1082, IL-819, and IL-592) and TNF-α (TNF-α-308). Differences in the polymorphisms between test groups and healthy controls were assessed by Pearson chi-square test., Results: A total of 95 patients (16 failing implants, 22 chronic periodontitis, 23 healthy implants, and 34 healthy controls) were enrolled in this study. No significant association of IL-10 and TNF-α alleles, genotypes, or haplotypes were observed in chronic periodontitis or failing implant patients (P > .005). However, both patient groups showed highly similar frequencies of alleles, genotypes, and haplotypes (P > .99)., Conclusion: This study found no significant association of either IL-10 or TNF-α genes in the susceptibility to the development of chronic periodontitis or implant failure.

Background and Objective: Periodontitis is a chronic inflammatory disease, and genetic factors may have an important role in its severity. Polymorphisms in the promoter regions of the interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-alpha) genes have been reported to cause changes in the production of these cytokines. The aim of this study was to evaluate the possible role of IL-6 (G-174C) and tumour necrosis factor (G-308A) polymorphisms, in the severity of chronic periodontitis in an elderly population., Materials and Methods: In this study, a group of 65 elderly women, comprising 17 patients with moderate chronic periodontitis, 21 with severe chronic periodontitis and 27 healthy patients were selected. DNA was isolated from all subjects, and polymerase chain reaction was used to study the IL-6 and TNF-alpha gene polymorphisms., Results: The results of this study showed a significant difference in the allele and genotype frequencies of IL-6 gene polymorphism between patients with periodontal disease and controls. Subjects carrying the G/G genotype of IL-6 were most severely affected by periodontitis. The TNF-alpha gene polymorphism showed no association with chronic periodontitis between patients and controls., Conclusion: The results suggest that the IL-6 gene polymorphism may be associated with chronic periodontitis, and that TNF-alpha gene polymorphism may not be involved in the progression of chronic periodontitis in the population of elderly Brazilian women.

Purpose: Early marginal bone loss around dental implants has been found during the bone healing period before stage II surgery despite a lack of apparent cause, and the etiology of this bone loss is unclear. This study was designed to investigate whether interleukin-1 gene polymorphism is associated with the marginal bone loss around the implants before stage II., Materials and Methods: One hundred forty-three implants were placed in 59 patients. The patients were divided into 2 groups: 1) test group: with 1 or more marginal bone loss greater than 0.5 mm; and 2) control group: with marginal bone resorption less than 0.5 mm. Polymorphisms of the IL-1alpha and IL-1beta genes (IL-1A-889, IL-1B-511, and IL-1B+3954) were detected by restriction fragment length polymorphism using Ncol, AvaI, and TaqI digestion after polymerase chain reactions., Results: The frequency of IL-1B-511 II/II was significantly higher among patients in early marginal bone loss (+) group than those in early marginal bone loss (-) group (P < .05). Multiple logistic regressions showed the OR of the II/II versus the I/I+I/II of the IL-1B-511 genotype was 3.933 between the 2 groups. The difference was statistically significant (P < .05). There was no significant difference between the other risk factors., Conclusion: These results suggest that the IL-1B-511 II/II genotype in individuals is associated with early marginal bone loss around implants.

Background and Objective: The plasminogen activating system is a protease/inhibitor system central to extracellular matrix remodeling with a suggested role in periodontal disease pathology. A few studies have reported polymorphisms in the genes of plasminogen activator inhibitors to be associated with periodontal disease severity. Two gene polymorphisms - a BamHI restriction fragment length polymorphism in the urokinase plasminogen activator gene (uPA) and a HindIII restriction fragment length polymorphism in the plasminogen activator inhibitor type 1 gene (PAI-1) - have been associated with conditions having a vascular component, and our objective was to assess the association of these gene polymorphisms with alveolar bone loss in chronic periodontal disease of adults., Material and Methods: Genotype was determined by polymerase chain reaction amplification of whole blood, pertinent histories were obtained by interview, and alveolar bone loss was assessed from current radiographs., Results: In 77 elderly patients with a normal distribution of alveolar bone loss, we demonstrated a significant association between levels of alveolar bone loss and these polymorphisms in the uPA and PAI-1 genes. Controlling for the contributions of smoking or diabetes to periodontal bone loss, estimated odds ratios for predicting lower levels of alveolar bone loss, associated with a greater degree of periodontal health, were strongest when defined by the concurrent presence of a homozygous urokinase plasminogen activator genotype and the nuclease-sensitive plasminogen activator inhibitor type 1 (HindIII) allele (odds ratio = 2.6; 95% confidence interval: 5.8-1.3)., Conclusion: The urokinase plasminogen activator (BamHI) and plasminogen activator inhibitor type 1 (HindIII) genotypes may serve as useful markers for heritability of bone loss associated with periodontal disease.

Dental implant surgery commonly proceeds in two stages. It is generally accepted that bone loss around implants does not occur at stage-II surgery because implants do not receive mechanical loading. However, early marginal bone loss around implants occasionally does occur during the healing period. Genetic polymorphisms in the interleukin-1 (IL-1) gene have been reported to be important for bone homeostasis and susceptibility to bone disease. We therefore investigated whether the idiopathic early marginal bone loss around implants is related to polymorphisms in the IL-1 gene. We performed a case-control study. Patients demonstrating marginal bone loss around implants at stage-II surgery were designated as the 'marginal bone loss (+)' group and those without bone loss as the 'marginal bone loss (-)' group. Polymorphisms of the IL-1alpha and IL-1beta genes (IL-1A-889, IL-1B-511 and IL-1B+3954) were detected by restriction fragment length polymorphism using NcoI, AvaI and TaqI after polymerase chain reactions. A total of 251 implants were placed in 39 patients. Marginal bone loss was observed in 36 implants. The patients with IL-1B-511 2/2 genotype exhibited a significantly higher occurrence of marginal bone loss than those with IL-1B-511 1/1 or 1/2 genotypes (OR=5.63; 95% CI=1.20-26.42; P=0.033). Multiple logistic regression analyses showed a markedly increased odds ratio (OR=10.86; 95% CI=1.64-71.90) in IL-1B-511 2/2 genotype carriers, while ORs of the other risk factors for bone loss, such as age, smoking status, post-menopausal women and bone quality, remained between 0.44 and 6.20. There was no significant difference in the distributions of the IL-1B+3954 and IL-1 A-889 genotypes between cases and controls. These data suggest that the IL-1B-511 2/2 genotype has a significant association with the incidence of early marginal bone loss around endosseous implants.

Purpose: At stage II surgery during dental implant treatment, early marginal bone loss around the implant occasionally occurs despite a lack of apparent causal events, and the etiology of this bone loss is unclear. This study was designed to investigate whether the bone morphogenetic protein-4 (BMP-4) genetic polymorphism is associated with early marginal bone loss around implants., Materials and Methods: The BMP-4 polymorphism was detected by restriction fragment length analysis using HphI digestion after polymerase chain reaction. A total of 262 implants were placed in 41 patients, and early marginal bone loss was observed in 25 of the 109 maxillary implants and 14 of the 153 mandibular implants., Results: In the mandible, the patients with the BMP-4 AV genotype had a significantly higher rate of occurrence of marginal bone loss than those with the BMP-4 W genotype (P = .012). According to multiple logistic regression analyses, the odds ratio of the AV versus the W BMP-4 genotype was 8.106 between patients with and those without bone loss in the mandible (95% CI = 1.30 to 50.51; P = .025)., Discussion: These results suggest that the BMP-4 genetic polymorphism influences early marginal bone loss around implants., Conclusion: While perhaps premature in recommendation, genetic screening before implant surgery may prove to be a very useful aid to consider the risk of implant treatment.

Background: Severe forms of periodontitis are suggested to have a genetic basis., Objective: The aim of the present investigation was to study association of an IL10 gene polymorphism (G to A transition at the -1087 position) with severe chronic periodontitis., Materials and Methods: Two groups of Swedish Caucasian subjects were included. One group consisted of 60 patients (aged 36-74 years; mean 54.5+/-8.5) with severe and generalized chronic periodontitis. The patients exhibited bone loss >50% at all teeth. Thirty-nine periodontally healthy subjects between 35-78 years of age (mean 51.0+/-10.9) were also recruited. DNA was isolated from peripheral blood cells and genotyping was performed by combination of PCR with restriction endonuclease mapping., Results: The proportion of subjects that exhibited the GG genotype was significantly larger in the group with severe periodontitis than in the periodontally healthy group. The difference regarding the occurrence of the GG genotype between the two groups was more conspicuous in non-smokers and yielded an odds ratio of 6.1. The G allele carriage in non-smokers was >90 % in the periodontitis group and was significantly higher than in the healthy controls., Conclusion: It is suggested that the -1087 IL10 polymorphism in Caucasian subjects of a north European origin is associated with severe chronic periodontitis.

The aim of this controlled retrospective study was to evaluate the influence of an IL-1 gene polymorphism on the clinical and radiographic healing outcomes of GTR therapy. The study included 47 adult periodontitis patients with 94 deep intrabony defects treated by GTR using different membrane materials. The following clinical parameters were recorded at baseline and 12 months after surgery: papillary bleeding index (PBI), gingival recession (REC), probing pocket depth (PPD), clinical attachment level (CAL), and the vertical relative attachment gain (V-rAG). Bone changes in the defect regions due to GTR therapy were quantitatively evaluated using digital subtraction radiography (DSR). Polymorphisms of the IL-1A gene at position - 889 and of the IL-1B gene at position + 3953 were analyzed by PCR. Statistical analysis was performed using the Mann-Whitney-U and the Wilcoxon-Signed-Rank tests (alpha = 0.05). The study comprised 19 IL-1 genotype positive (IL-1 +) patients and 28 IL-1 genotype negative (IL-1 -) patients. Twelve months after GTR therapy, both patient groups revealed statistically significant PPD reductions and CAL gain [median (25/75% percentiles)]: Delta PPD [IL-1 + : 4.0 (2.5/5.0) mm; IL-1-: 3.8 (3.0/4.9) mm], Delta CAL [IL-1 + : 3.5 (3.0/4.8) mm; IL-1 -: 3.0 (1, 2/4, 5) mm]. V-rAG amounted to 60.0 (47.7/78.6)% in IL-1 + patients and 53.1 (43.4/81.9)% in IL-1 - patients. Both patient groups showed significant bone density gain in 40% (IL-1 +) and 43.6% (IL-1 -) of the initial defect area due to GTR. Neither the clinical nor the radiographic healing parameters revealed any statistically significant differences in the GTR healing outcome between IL-1 + and IL-1 - patients. In conclusion, these 12-month findings indicate that the IL-1 gene polymorphism has no influence on the clinical and radiographic regeneration results following GTR therapy.

Unlabelled: Recent studies have shown that vitamin D receptor (VDR) gene polymorphism had regulatory effects on bone mineral density (BMD) and bone turnover. The VDR gene has also been indicated as a candidate gene for the susceptibility of osteoporosis. However, it is unclear whether VDR genotypes could be associated with alveolar bone loss of patients with periodontitis, or whether vitamin D receptor gene could be a candidate gene for susceptibility to periodontitis. The purpose of this study was to answer these two questions., Methods: Twenty-four cases of adult periodontitis (AP), 37 cases of early onset periodontitis (EOP) and 39 healthy controls were recruited for the study. Individual samples of venous blood and DNA were obtained from each subject. Genotypes of the TaqI VDR gene were determined by PCR and TaqI restriction endonuclease digestion., Results: One out of 24 AP patients, nine out of 37 EOP patients and two out of 39 healthy controls were detected with Tt genotype, while the rest had the TT genotype. The detected frequency of Tt genotype was significantly higher in EOP patients (24.3%) than in AP patients (4.2%) and healthy controls (5.1%). The frequency of t allele was also significantly higher in EOP patients. There was no statistical difference in the distribution of TaqI VDR genotypes between AP patients and healthy controls. The study suggests that Tt genotype might be a risk indicator for the susceptibility to EOP. Carriage of the allele (t) of the TaqI VDR gene may increase the risk of developing EOP.

Background: Polymorphisms within the interleukin-1 cluster are known to be associated with adult periodontal disease. However, interactions of genetic with other risk factors, especially smoking, remain questionable. The aim of this cross-sectional study was to evaluate the genetic influence on periodontal variables in relation to environmental factors., Methods: One-hundred fifty-four (154) Caucasian subjects were clinically and radiographically assessed for their periodontal status, their smoking history recorded, and their allelic pattern of IL-1alpha, IL-1beta, and IL-1RN polymorphisms determined by genotyping., Results: In assessing periodontitis with mean probing depth, mean attachment loss, or mean bone loss, no differences were found in allele frequencies or combined allotypes between subjects with mild or moderate versus those with severe signs of periodontitis. However, the extent of attachment loss defined as percentage of sites >4 mm was significantly associated with the composite genotype of IL-1alpha/1beta in smokers (odds ratio [OR] = 4.00; 95% confidence interval [CI] 1.03 to 16.70; P= 0.02). No differences were found in genotype negative subjects irrespective of their smoking status. They had nearly identical attachment loss as genotype positive non-smokers. Similar non-significant results were found with respect to extent of bone loss. An increased risk of more extended attachment loss was observed also in individuals carrying mutations of the combined genotype IL-1alpha/IL-1RN, again showing enhanced risk only in genotype-positive and smoking subjects., Conclusions: The results provide evidence that the composite genotypes studied show interaction with smoking, the main exposition-related risk factor of periodontal disease. Non-smoking subjects are not at increased risk, even if they are genotype-positive.

Background: Early-onset periodontal diseases (EOP) are caused by interactions between host factors, specific microbial pathogens, and environmental factors. It is, therefore, of interest to investigate the nature of host factors as they may provide useful risk markers and reveal important information regarding the disease pathogenesis. Genetic polymorphisms in the vitamin D receptor (VDR) gene are associated with parameters of bone homeostasis and with diseases in which bone loss is a cardinal sign, in particular osteoporosis. Rapidly progressive bone loss is one feature of EOP. We, therefore, sought to determine whether EOP is associated with a polymorphism in the VDR gene., Methods: A restriction fragment length polymorphism (RFLP) for Taq I in exon nine of the VDR gene was analyzed by PCR, followed by restriction digestion with Taq I and gel electrophoresis. We analyzed the genotypes of 69 EOP patients, including 20 patients with unequivocal evidence of localized disease (L-EOP), and 72 controls with no history of EOP., Results: The genotype distribution in the L-EOP patient group was 7 (35%), 5 (25%) and 8 (40%) and in the control group 31 (43.1%), 36 (50.0%) and 5 (6.9%) for TT, Tt and tt respectively (where t and T represent the alleles with and without the Taq I RFLP respectively). Chi2 analysis indicated that the distribution of the genotypes between these two groups was highly significantly different (P = 0.001). Allele frequencies were 47.5% and 52.5% for T and t in the L-EOP group; 68.1% and 31.9% in the control group, showing a significant association between the prevalence of the less frequent allele (t) and L-EOP (P = 0.017). There was no significant difference in the genotype distribution or the allele frequencies between the control samples and the larger EOP patient group (n = 69) which included patients with generalized and localized disease., Conclusions: These data indicate that carriage of the less frequent allele of the Taq I RFLP (t) in the VDR gene significantly increases the risk of developing L-EOP. However, VDR genotype may not affect the incidence of all cases of EOP. These findings contribute to our understanding of the genetic basis for periodontal disease and may help define sub-groups of this disease which share common pathogenic factors.