白细胞介素8基因-251位点多态性与侵袭性牙周炎的相关性研究

目的研究白细胞介素8（interleukin-8,IL-8）-251位点基因多态性与侵袭性牙周炎易感性的相关性。方法采用病例对照试验设计,从广东汉族人群中选择77例侵袭性牙周炎（aggressive periodontitis,AgP）患者（AgP组）及50例牙周健康者（健康对照组）,采用聚合酶链反应—限制性内切酶片段长度多态性方法对IL-8-251位点基因进行检测,分析组间等位基因和基因型频率的分布差异。结果 IL-8-251A/T位点的基因型和A、T等位基因频率在AgP组和健康对照组的分布差异无统计学意义（P〉0.05）。结论未发现IL-8-251A/T位点基因多态性与中国广东汉族人群侵袭性牙周炎的患病易感性之间存在相关性。     

TLR2/TLR4基因多态性与慢性牙周炎的相关性研究

目的:研究TLR2/TLR4基因单核苷酸多态性(single nucleotide polymorphisms,SNP)与慢性牙周炎的相关性.方法:从2009年1月至2011年4月,收集慢性牙周炎患者638例和对照组143例,其中中度牙周炎组196例,重度牙周炎组442例.抽取静脉血提取基因组DNA,采用TaqMan MGB探针法对TLR2rs13150331, rs1898830, rs3804100;TLR4 rs10759930, rs10983755, rs11536879, rs1927907, rs11536889,rs7873784共9个多态性位点进行基因型检测.分析基因型和等位基因频率、分布规律和单倍体型,探讨TLRs单核苷酸多态性与牙周炎基因遗传易感性的关系.结果:TLR4 rs11536889 (GG)基因型频率在重度牙周炎组患者中显著高于中度牙周炎组(P＜0.05).单倍型G-C-G (rs1927907- rs11536889- rs7873784)是牙周炎的危险因素之一,OR=1.449;95％ CI [1.052-1.995].结论:TLR4基因多态性与牙周炎的易感性有密切相关性,rs11536889(C/G)的变异与之相关联.单倍型G-C-G(rs1927907-rs11536889-rs7873784)可能是牙周炎进展的危险因素.     

中文文摘

1．线粒体基因7．4 kbp大片段缺失突变与侵袭性牙周炎的关系研究／郭园…／／实用口腔医学杂志．-2014,30（1）．-99-102 选取20例AgP患者（AgP组）和20例牙周健康者（对照组）,收集外周血及牙周翻瓣术及牙冠延长术中切取的牙龈组织,同时收集10例慢性牙周炎者（CP组）牙周翻瓣术中切取的组织。采用长距离 PCR方法检测血样本和牙龈组织样本中 mtDNA 7．4 kbp 大片段缺失,比较3组间的差异。结果：AgP组20例牙龈组织中1例存在 mtDNA 7．4 kbp 大片段缺失,AgP组2例组织和 CP 组1例组织中检测到目前尚未报告过的 mtDNA 5537 bp 大片段缺失突变。所有血样和对照者牙龈组织中均未检测到大片段缺失突变。结论：AgP患者牙龈组织中存在 mtDNA 7．4 kbp大片段缺失,发现一种新的 mtDNA 5537 bp大片段缺失突变。     

白细胞介素-1基因多态性与侵袭性牙周炎的关系

目的：研究中国人群中白细胞介素-1（IL-1）基因多态性与侵袭性牙周炎（AgP）之间的关系。方法：提取122例AgP患者和95例健康对照者外周静脉血基因组DNA,采用聚合酶链反应（PCR）分析IL-1A＋4845、IL-1B＋3954位点的单核苷酸多态性（SNP）及IL-1RN第二内含子中的可变数目重复序列（VNTR）多态性,采用多因素Logistic回归模型,进行两组之间基因型、等位基因分布差异的比较。结果：在IL-1A＋4845位点,AgP组男性患者A2^＋基因型的频率较男性健康组显著升高（P〈0．05=0．039）,等位基因A2的携带率也显著升高（P〈0．05=0．049）;未发现IL-1B＋3954位点和IL-1RN VNTR的多态性与AgP关联;未发现IL-1各复合基因型与AgP存在明显关联性。结论：IL-1A＋4845位点的SNP可能与中国人群中男性个体的AgP易感性有关。     

侵袭性牙周炎与FMLP受体单核苷酸多态性

目的：研究FMLP受体作为遗传标志与局限型侵袭性牙周炎之间的关系。方法：提取目标人群（局限型侵袭性牙周炎L－AgP患者、慢性牙周炎CP患者及正常人群）的DNA，PCR扩增后，进行DNA基因测序。结果：在259－332位点中存在单核苷酸多态（SNPs),L-AgP组与其它两组之间有显著差异。结论：在汉族人群中，L－AgP患者FMLP受体分子细胞外第一环及其邻近的跨膜区氨基酸残基的改变可能是引起患者趋化功能缺陷的分子基础，由此导致的受体不能识别细菌趋化物亦可能是引起L－AgP患者外周血PMN趋化功能低下的主要原因。     

实时荧光定量PCR检测牙周炎患者龈下菌斑的分布

目的 应用实时荧光定量PCR技术探索侵袭性牙周炎（aggressive periodontitis,AgP）、慢性牙周炎（chronic periodontitis,CP）患者龈下菌斑中伴放线聚集杆菌(A. actinomycetemcomitans,Aa)、牙龈卟啉单胞菌（P. gingivalis,Pg）的分布规律。方法 采集32例AgP、33例CP、32例牙周健康者的龈下菌斑,构建含有2种待测细菌基因片段的重组质粒,建立定量标准,采用TaqManMGB探针实时荧光定量PCR方法检测样本中细菌数量。结果 本实验构建的引物及TaqManMGB探针特异性及敏感性较好。AgP组龈下菌斑Aa的检出率高于CP组（P＜0.01）,但2种细菌数量在组间无显著差异,两组内Pg的检出率及数量都明显高于Aa（P＜0.001）,另外AgP组Aa的数量、CP组Pg数量与牙周探诊深度密切相关（P＜0.01及P＜0.001）。结论 龈下菌斑Aa的检出率可能与牙周炎类型存在一定关联,Aa可能并不是中国人群样本AgP患者龈下菌斑的优势菌,实时荧光定量PCR对牙周病学研究有广泛应用前景。     

IL-6-572基因多态性与侵袭性牙周炎易感性的相关性研究

目的 研究白细胞介素-6(interleukin-6,IL-6)-572位点基因多态性与侵袭性牙周炎易感性的关系.方法 采用病例对照试验设计,从广东汉族人群中选择83例侵袭性牙周炎(aggressive periodontitis,AgP)患者(AgP组)及79例牙周健康者(对照组),采用聚合酶链反应—限制性内切酶片段长度多态性分析方法对IL-6-572位点基因多态性进行检测,分析组间基因型频率及等位基因分布的差异.结果 IL-6基因启动子区-572位点G/C基因型在AgP组、对照组中的分布频率差异有统计学意义(x2=13.710,P=0.001).AgP组与对照组相比,G、C等位基因频率分布差异有统计学意义(x2=13.213,P<0.001),G等位基因相对于C等位基因:OR值为2.988,95%CI:1.634~5.465.结论 IL-6-572 G/C位点的基因多态性同中国广东汉族人群侵袭性牙周炎患病易感性可能存在相关关系,IL-6-572 G等位基因可能是广东汉族人群AgP遗传易感性的高风险因素.     

TNFA-308基因多态性与中国人群慢性牙周炎的相关性研究

目的：探讨TNFA～308基因多态性与慢性牙周炎易感性的关系。方法：收集63例重度慢性牙周炎（CP）患者、103例轻、中度慢性牙周炎患者及80例健康对照者的颊黏膜拭子,提取DNA,采用多聚酶链反应-限制性内切酶片段长度多态性（PCR—RFLP）法测定TNFA-308位点的基因多态性,实验结果输入SPSS10．0统计软件包处理,进行各组间基因型分布和等位基因频率的X^2检验,比较各组间基因型分布的差异。计算等位基因2的OR和95％可信区间,以确定等位基因2与牙周炎易感性的关系。结果：重度CP组、轻、中度CP组及健康对照组均以TNF1／1纯合子占优势,TNF1／2杂合子基因型次之,仅在轻、中度CP组检出1例TNF2／2纯合子基因型。TNFA-308／NcoI基因型分布及等位基因频率在3组间无显著性差异。结论：对此位点基因型是否对慢性牙周炎的易感性及进程预后产生影响。尚不能肯定,需要进一步的研究。     

雌激素受体XbaI和PvuⅡ基因多态性与侵袭性牙周炎的相关研究

目的:探讨侵袭性牙周炎(aggressive periodontitis,AgP)易感性与雌激素受体XbaI和PvuⅡ基因多态性的关系.方法:收集48 例侵袭性牙周炎(AgP)患者和60 例牙周健康对照组的颊黏膜拭子,采用Chelex-100法提取DNA,应用聚合酶链式反应-限制性片段长度多态性技术检测雌激素受体XbaI和PvuⅡ的等位基因及基因型频率在各组之间分布的差异.结果:XbaI基因型分布在AgP组与对照组、AgP组女性与对照组女性、AgP组男性与对照组男性之间均有显著性差异(P<0.05).其等位基因频率在女性组间有统计学意义(P<0.05). PvuⅡ基因型分布在AgP组与对照组之间均无明显差异,其等位基因频率分布有明显差异(P<0.05). 多因素logistic回归分析显示男性患病的可能性小(OR=0.352);随年龄增大患病的可能性变小(OR=0.950);当其他条件一定时,xx、Xx基因型的人患病的可能性小(OR 值分别为0.678,0.224).结论:侵袭性牙周炎易感性与雌激素受体XbaI基因型分布有关,XX基因型最易患病,其次为xx,Xx基因型.     

肿瘤坏死因子A-308位点基因多态性与侵袭性牙周炎的关系

目的探讨肿瘤坏死因子（tumor necrosis factor，TNF）A-308位点基因多态性与侵袭性牙周炎的关系。方法选择64例侵袭性牙周炎（aggressive periodontitis，AgP）患者及78名健康对照者，提取其外周静脉血基因组DNA，采用多聚酶链反应-限制性内切酶片段长度多态性的方法检测TNF A-308位点的基因多态性。结果TNFA-308位点的GA基因型频率在两组间差异无统计学意义；但是在按性别和吸烟分层的条件下，携带基因型GA和等位基因A使男性不吸烟者患病的风险明显增加（OR值分别为22．2和16．1）。结论提示TNFA-308基因型GA和等位基因A可能与中国人群中男性个体的AgP易感性有关。     

Toll-like receptor 2 and 4 gene polymorphisms in generalized aggressive periodontitis

BACKGROUND: Toll-like receptors (TLRs) recognize exogenous ligands such as lipopolysaccharide and bacterial lipoprotein during the immune responses to pathogens. The aim of the present study was to investigate whether TLR2 and TLR4 gene polymorphisms are related to susceptibility to generalized aggressive periodontitis (GAgP). METHODS: A total of 245 subjects were included in the present study. Genomic DNA was obtained from the peripheral blood of 90 patients with GAgP and 155 periodontally healthy subjects. Probing depth, clinical attachment loss, plaque accumulation, and bleeding on probing were recorded. The TLR2 gene Arg753Gln and Arg677Trp polymorphisms and TLR4 gene Asp299Gly and Thr399Ile polymorphisms were genotyped by the polymerase chain reaction-restriction fragment length polymorphism method. The data were analyzed by chi2 and Mann-Whitney U tests and logistic regression analysis. RESULTS: There was no significant difference in the distribution of TLR2 and TLR4 genotypes and allele frequencies between GAgP patients and healthy subjects (P > 0.05). The TLR2 753Gln allele was found in 3.9% of the GAgP patients compared to 6.1% in the healthy group. The GAgP patients and healthy subjects did not show homozygosity for the TLR2 mutant alleles. The TLR2 677Trp mutant allele was not found in any of the subjects; 2.2% of the GAgP patients and 2.9% of the periodontally healthy subjects were identified as having the TLR4 299Gly polymorphic allele. With regard to the TLR4 399Ile polymorphic allele, 1.1% of the GAgP patients and 2.3% of the periodontally healthy subjects had this allele. CONCLUSIONS: The present study failed to find any significant association between the TLR polymorphisms and GAgP, potentially because of the small sample size. To the best of our knowledge, this was the first study to examine the prevalence of these polymorphisms in a Turkish population with aggressive periodontitis.     

Association between lactoferrin gene polymorphisms and aggressive periodontitis among Taiwanese patients

Background and Objective: A dramatic difference in the frequencies of the Lys/Arg single nucleotide polymorphism in the lactoferrin genotype between a small population of patients with localized juvenile periodontitis and healthy subjects has been reported. As the single nucleotide polymorphism could be associated with ethnicity, the present study aimed to investigate the association between polymorphisms of the lactoferrin gene and periodontitis. Material and Methods: Sixty‐five patients with aggressive periodontitis, 278 with chronic periodontitis and 88 healthy controls were genotyped for the Lys/Arg polymorphism of the lactoferrin gene at position 29 [reference sequence (rs) 1126478] in the N‐terminal alpha‐helical region. Results: The frequencies of the GG genotype and the G allele were highest in the aggressive periodontitis group, followed by the chronic periodontitis group and then the healthy controls. The frequency of the G allele was significantly higher in aggressive periodontitis and chronic periodontitis groups than in healthy controls (p = 0.0037 and 0.0212). Although the difference of the GG genotype distribution between subjects with chronic periodontitis and healthy controls did not reach significance, the distribution of genotypes between aggressive periodontitis and healthy controls was significantly different. The association of the gene polymorphism and aggressive periodontitis still existed, even after adjusting for age, gender and smoking status by logistic regression analysis (GG/AG+AA: odds ratio = 2.16, 95% confidence interval = 1.09–4.35, p = 0.0287). After the study, subjects were further stratified by their smoking status; the GG genotype was still significantly associated with the risk of aggressive periodontitis in the nonsmoking group (odds ratio = 2.69, p = 0.018). However, there were no statistical differences between chronic periodontitis vs. healthy controls and aggressive periodontitis vs. healthy controls in the smoking group. Conclusion: The present study revealed that the A/G polymorphism in the lactoferrin gene might be associated with aggressive periodontitis. The A allele might reduce the risk of development of aggressive periodontitis in a Taiwanese population. Our results also support the hypothesis that lactoferrin genetic polymorphisms could play a role in the risk for periodontitis separate from the smoking factor. The functionality of this gene’s polymorphisms has to be further elucidated.     

TLR2 Arg753Gly, TLR4 Asp299Gly and Thr399Ile gene polymorphisms are not associated with chronic periodontitis in a Turkish population

AIM: Toll-like receptor (TLR) gene polymorphisms could affect the host's ability to respond to microbial pathogens. In this case-control study, the association of TLR2 and TLR4 gene polymorphisms with chronic periodontitis (CP) was investigated. MATERIALS AND METHODS: Genomic DNA was obtained from the peripheral blood of 83 patients with CP and 106 periodontally healthy subjects. The TLR2 Arg753Gly, Arg677Trp and TLR4 Asp299Gly, Thr399Ile gene polymorphisms were genotyped by the polymerase chain reaction-restriction fragment length polymorphism method. The data were analysed by a chi2 test, logistic regression analysis and the Mann-Whitney U test. RESULTS: The 753Gln allele was found in 6.1% of the CP patients as compared with 6.6% in the control group (p>0.05). The frequency of the 299Gly and 399Ile allele was 2.4% and 1.8% in CP patients. For the healthy subjects, the frequency was 2.8% for the 299Gly and 2.5% for the 399Ile allele (p>0.05). None of the CP patients or healthy subjects showed homozygosity for the TLR2 and TLR4 alleles. Percentage of sites with bleeding on probing and plaque were significantly higher in 299Gly-positive patients compared with 299Gly-negative patients (p<0.05). CONCLUSION: These results showed that the TLR2 and TLR4 gene polymorphisms studied are not associated with susceptibility to CP in Turkish patients.     

Polymorphisms of TLR4 but not CD14 are associated with a decreased risk of aggressive periodontitis

OBJECTIVE: To study whether there is an association between the frequency of functional polymorphisms in the toll-like receptor 4 (TLR4) and cluster differentiation 14 (CD14) genes and periodontitis. METHODOLOGY: Genotyping for the TLR4 single-nucleotide polymorphisms (SNPs) Asp299Gly, Thr399Ile and the CD14 SNPs -159 and -1359 was completed for subjects with periodontal disease compared with control subjects. Two disease populations were investigated: 73 subjects with aggressive periodontitis (AgP; 28 males, 45 females) and 95 males with chronic periodontitis (CP). The TLR4 and CD14 polymorphisms were determined using SNaPshot primer extension with capillary electrophoresis. Comparison of allele and genotype frequencies for each polymorphism was by Fisher's exact test or chi2 analysis. RESULTS: The TLR4 Asp299Gly genotype was present in a significantly (p=0.026) lower proportion of AgP subjects (5.5%) compared with control subjects (16.3%). The unadjusted odds ratio for the Asp299Gly genotype to be associated with AgP was 0.30, 95% confidence interval 0.10-0.91. No differences were found in the prevalence of the TLR4 Asp299Gly genotype in men with CP (18.9%) compared with an age-matched control group with no evidence of periodontitis (17%). In addition, there was no difference in the distribution of the CD14 polymorphisms in either the AgP or CP populations studied compared with controls. CONCLUSION: It is concluded that in West European Caucasians, the Asp299Gly TLR4 gene polymorphism is associated with a decreased risk of AgP but not CP. Promoter polymorphisms of the CD14 gene, however, did not influence susceptibility to inflammatory periodontitis in the population cohorts studied.     

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.     

TLR4 as a risk factor for periodontal disease: a reappraisal

Aim: To determine whether genetic variants of the TLR4 gene are associated with either chronic or aggressive periodontitis.
Methods: A systematic electronic search of literature was conducted to identify all published studies without any language restriction on the association between TLR4 and periodontal diseases, including chronic periodontitis and aggressive periodontitis. All case–control studies evaluating the TLR4 Asp299Gly and Thr399Ile polymorphisms in chronic or aggressive periodontitis were identified. A meta-analysis of the studies that fulfilled the inclusion criteria was performed.
Results: Seven studies comprising 744 chronic periodontitis cases and 855 controls and four studies consisting of a total of 295 aggressive periodontitis cases and 456 controls were included in the meta-analysis. In the pooled analysis, the TLR4 299Gly allele ( TLR4 +896 A>G) appeared to be a genetic risk factor for susceptibility to chronic periodontitis with a random effects and fixed effects odds ratio (OR) of 1.43 [95% confidence interval (CI):1.04–1.97; p =0.03]. On the other hand, the TLR4 399Ile polymorphism ( TLR4 +1196 C>T) showed a protective effect against aggressive periodontitis with a random effects OR of 0.29 (95% CI: 0.13–0.61; p =0.001).
Conclusion: Our results suggest that the alleles 299Gly and 399Ile in TLR4 can be a potential genetic marker for periodontal disease.     

Polymorphism of genes encoding toll-like receptors and inflammatory cytokines in periodontal disease in the Japanese population

Periodontitis, which is a widespread and major dental disease, is a multifactorial, lifestyle-related disease and has been analyzed for gene polymorphism. We examined the frequency of the polymorphisms of the pro-inflammatory cytokine genes IL-1 A (-889) and IL-1 B (+3953) in relation to periodontitis in the Japanese population. We also examined whether polymorphism of TLR2 (Arg677Trp) and TLR4 (Asp299Gly), which are receptors recognized by periodontopathic bacteria, may also be associated with periodontitis. The subjects were 92 Japanese individuals, among whom 43 had periodontitis and 49 were healthy controls. We isolated genomic DNA from lingual mucosal cells and tested them for single nucleotide polymorphisms by polymerase chain reaction-restriction fragment length polymorphism. The incidence of polymorphisms was analyzed statistically by Fisher's exact test, and the sensitivity and specificity of the gene polymorphisms were calculated. The purpose was to determine whether such polymorphisms might be effectively used in the diagnosis of periodontitis. However, we found no evidence that the gene polymorphism of IL-1A (p = 0.082), IL-1 B (p = 0.180), TLR2 (p = 1.000) or TLR4 (p = 1.000) and overall gene polymorphism in any of the genes (p = 0.752) correlate with periodontitis. The sensitivity (14.0%) and specificity (83.7%) of the mutations found in all of the genes were low. Therefore, we advise against using the analyses of polymorphism of these genes to detect periodontitis in the Japanese population.     

Expression of transient receptor potential vanilloid receptor 1 and toll-like receptor 4 in aggressive periodontitis and in chronic periodontitis

Öztürk A, Y?ld?z L. Expression of transient receptor potential vanilloid receptor 1 and toll‐like receptor‐4 in aggressive periodontitis and in chronic periodontitis. J Periodont Res 2011; 46: 475–482. © 2011 John Wiley & Sons A/S Background and Objective: The objective of the present study was to evaluate the expression and the distribution of the transient receptor potential vanilloid receptor 1 (TRPV1) and of toll‐like receptor 4 (TLR4) in tissue samples from patients with periodontal disease (aggressive periodontitis and chronic periodontitis) and from healthy controls. Material and Methods: Ten tissue samples from each disease group (aggressive periodontitis and chronic periodontitis) and from healthy subjects were obtained during routine oral surgical procedures. Subgingival specimens were collected from sites with advanced loss of support (probing depth > 5 mm) and specimens from the corresponding healthy controls were obtained during tooth extraction for orthodontic reasons or following surgical extraction of an impacted third molar. The distribution of TRPV1 and TLR4 receptors in human gingival tissue was studied by immunohistochemistry. Results: Both TLR4 and TRPV1 were detected in gingival tissues from healthy subjects, and from patients with chronic periodontitis and aggressive periodontitis, particularly in gingival keratinocytes, fibroblasts, inflammatory cells and the endothelial lining of capillaries in connective tissues. Histologic examination of the samples from healthy controls disclosed that clinically healthy gingiva does not correspond to histologically healthy gingiva. Subsequently, these samples were redesignated as gingivitis samples. TRPV1 was down‐regulated in all cell types in samples obtained from patients with chronic periodontitis compared to samples obtained from patients with gingivitis, whereas TLR4 was down‐regulated only in the epithelium and in gingival fibroblasts. In contrast, the levels of these markers in patients with aggressive periodontitis were similar to those in healthy patients. Conclusion: Local expression of TRPV1 and TLR4 in gingival tissues may contribute to both physiological and pathological processes in the periodontium. Our data suggest that TRPV1 and TLR4 may play a role specifically in the pathophysiology of chronic periodontitis.     

Immunohistochemical localization of Toll‐like receptors 1–10 in periodontitis

Background/aim: In periodontitis, bacteria and pathogen‐associated molecular patterns are sensed by Toll‐like receptors (TLRs), which initiate intracellular signaling cascades that may lead to host inflammation. In this study, the expression and distribution of TLRs (TLR‐1 to TLR‐10) were immunohistochemically detected in gingival epithelium and connective tissue. Methods: Immunohistochemistry was used for the localization of TLRs in gingival tissue samples from 10 patients with chronic periodontitis and 10 healthy controls; these samples were obtained during routine periodontal flap operations and during extraction operations performed for retained wisdom teeth, respectively. For the evaluation, epithelial layers were stratified to basal, spinous, and superficial layers, and the percentages of TLR‐positive cells were determined. Results: Both healthy and periodontitis gingival tissues expressed all TLRs except TLR‐10. In patients with periodontitis, epithelial cells showed increased TLR expression towards the basal layer. Healthy controls showed more variable cellular TLR expression and distribution between the layers of epithelium. In the connective tissue, consistently higher TLR expression was found within the periodontitis group compared to the healthy group. Conclusions: For the first time, the cellular expression and distribution of TLR‐1 to TLR‐10 have been studied in periodontitis, indicating that TLR‐1 to TLR‐9 are differentially expressed both in connective tissue and epithelial layers. Except for TLR‐7 and TLR‐8, all the other TLRs showed statistically significant differences between patients with periodontitis and healthy controls, suggesting their involvement in the pathogenesis of periodontitis.