牙周炎对2型糖尿病患者血清C反应蛋白水平的影响

目的 探讨牙周感染对2型糖尿病患者血清C反应蛋白（CRP）水平的影响。方法 选择伴重度慢性牙周炎的2型糖尿病患者32例为试验组,以年龄（±3岁）、性别、体重 指数（±1 kg/m2）配比单纯2型糖尿病患者32例为对照组。采用超敏CRP酶联免疫法测定所有患者的血清CRP水平。结果 试验组患者血清CRP水平平均为3.07 mg/L,对照组为1.78 mg/L,试验组高于对照组（P<0.05）;试验组血清CRP≥3.0 mg/L的患者占53.13％,对照组为28.13％,试验组高于对照组（P<0.05）。结论 牙周感染可升高2型糖尿病患者血清CRP水平,这种炎性因子的升高可能会加重胰岛素抵抗,增加2型糖尿病患者大血管并发症的危险性。     

A trend of increase in periodontal interleukin-6 expression across patients with neither diabetes nor periodontal disease, patients with periodontal disease alone, and patients with both diseases

Background and Objective: Epidemiological studies have established that patients with diabetes have increased prevalence and severity of periodontal disease. However, the periodontal expression of inflammatory cytokines and matrix metalloproteinases (MMPs) in diabetic patients has not been well characterized. The objective of this study was to determine the difference in the periodontal expression of MMP‐1, MMP‐8, interleukin‐6, tumor necrosis factor‐α and interleukin‐1β between diabetic and nondiabetic patients. Material and Methods: Periodontal tissue specimens were collected from nine nondiabetic patients without periodontal disease (group 1), from 11 nondiabetic patients with periodontal disease (group 2) and from seven diabetic patients with periodontal disease (group 3). The expression of MMP‐1, MMP‐8, interleukin‐6, tumor necrosis factor‐α and interleukin‐1β was quantified using real‐time polymerase chain reaction. Results: The nonparametric Kruskal–Wallis test showed that the difference in interleukin‐6 expression among the groups was statistically significant (p = 0.04). Furthermore, the generalized Kruskal–Wallis nonparametric linear‐by‐linear association test showed a statistically significant trend of increase in the expression of interleukin‐6 from group 1 to group 2 to group 3 (p = 0.02) and a suggestion of such a trend for MMP‐1 (p = 0.05). No increase in MMP‐8 expression was observed in patients in group 3 compared to patients in groups 1 and 2. Although the average expression levels of MMP‐1, interleukin‐1β and tumor necrosis factor‐α were increased from group 1 to group 3, the differences were not statistically significant. Conclusion: A trend of increased interleukin‐6 expression in periodontal tissues was observed across patients with neither diabetes nor periodontal disease, patients with periodontal disease alone, and patients with both diseases.     

Knowledge About the Association Between Periodontal Diseases and Diabetes Mellitus: Contrasting Dentists and Physicians

Background: There is a strong body of evidence that supports the relationship between periodontal diseases and diabetes mellitus (DM). Many patients are unaware of the effects of diabetes on oral health. Whether health care providers are applying the information about the link between DM and periodontal diseases in their practices depends on the levels of their knowledge of such valuable information. Therefore, the aims of this study are to evaluate the knowledge of dental and medical practitioners concerning the effects of diabetes on periodontal health and to find out if the practitioners are aware of the bidirectional relationship between periodontal diseases and DM. Methods: This was a cross‐sectional survey of randomly selected general practitioners practicing in Kuwait. Participants were asked about specific periodontal complications that they believed patients diagnosed with diabetes were more susceptible to, and their awareness of the bidirectional relationship between diabetes and periodontal diseases was evaluated. Results: A total of 510 general practitioners (232 physicians and 278 dentists) participated in the study. There were no significant differences between the two groups regarding mean ages, sex distributions, and years in practice. Only 50% of all study participants believed that patients with diabetes were more susceptible to tooth loss because of periodontal diseases than were individuals without diabetes. Dentists were significantly more aware of gingival bleeding, tooth mobility, and alveolar bone resorption than were physicians. Factors significantly associated with having knowledge about the effects of diabetes on periodontal health in logistic regression analyses were older age, female sex, and the dental profession. Conclusion: The knowledge about the association between periodontal diseases and DM should be increased among dental and medical practitioners to effectively prevent, manage, and control diabetes and periodontal diseases.     

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目的探讨牙周基础治疗对2型糖尿病（T2DM）伴慢性牙周炎患者血清炎性细胞因子及糖化血红蛋白（HbAlc）含量的影响。方法选择2012年3月至2013年9月就诊于沈阳市口腔医院牙周科患者135例,其中T2DM伴慢性牙周炎患者63例（T2DM组）,单纯慢性牙周炎患者72例（CP组）;另从沈阳市口腔医院体检中心选择牙周健康正常人50名,作为正常对照组。于牙周基础治疗前及治疗后3个月,检查各组的牙周状况以及检测血清炎性细胞因子和HbAlc含量,并对检测结果进行比较分析。结果牙周基础治疗能改善慢性牙周炎患者的牙周健康状况,降低炎性细胞因子水平。牙周基础治疗前T2DM组和CP组的C反应蛋白（CRP）、肿瘤坏死因子-α（TNF-α）及白细胞介素-6（IL-6）含量均高于正常对照组,差异有统计学意义（均P〈0.05）。与牙周基础治疗前比较,T2DM组和CP组的CRP、TNF-α及IL-6含量在牙周基础治疗后3个月均明显下降,差异有统计学意义（均P〈0.05）。牙周基础治疗前,T2DM组的HbAlc含量明显高于CP组和正常对照组;牙周基础治疗后3个月,T2DM组的HbAlc含量显著下降,且其治疗前后差异有统计学意义（P〈0.05）。结论 T2DM伴慢性牙周炎患者进行牙周基础治疗,可改善患者的牙周状况和全身健康状况,从而减少糖尿病及其并发症的发生和发展。     

Expression of periodontal interleukin‐6 protein is increased across patients with neither periodontal disease nor diabetes,patients with periodontal disease alone and patients with both diseases

Ross JH, Hardy DC, Schuyler CA, Slate EH, Mize TW, Huang Y. Expression of periodontal interleukin‐6 protein is increased across patients with neither periodontal disease nor diabetes, patients with periodontal disease alone and patients with both diseases. J Periodont Res 2010; 45: 688–694. © 2010 John Wiley & Sons A/S Background and Objective: Epidemiological studies have established that patients with diabetes have an increased prevalence and severity of periodontal disease. Interleukin (IL)‐6, a multifunctional cytokine, plays a role in the tissue inflammation that characterizes periodontal disease. Our recent study has shown a trend of increase in periodontal IL‐6 expression at the mRNA level across patients with neither periodontal disease nor diabetes, patients with periodontal disease alone and patients with both diseases. However, the periodontal IL‐6 expression at the protein level in these patients has not been investigated. Material and Methods: Periodontal tissue specimens were collected from eight patients without periodontal disease and diabetes (group 1), from 17 patients with periodontal disease alone (group 2) and from 10 patients with both periodontal disease and diabetes (group 3). The frozen sections were prepared from these tissue specimens and IL‐6 protein expression was detected and quantified. Results: The nonparametric Kruskal–Wallis test showed that the difference in IL‐6 protein levels among the three groups was statistically significant (p = 0.035). Nonparametric analysis using the Jonckheere–Terpstra test showed a tendency of increase in periodontal IL‐6 protein levels across group 1 to group 2 to group 3 (p = 0.006). Parametric analysis of variance (ANOVA) on IL‐6 protein levels showed that neither age nor gender significantly affected the difference of IL‐6 levels among the groups. Conclusion: Periodontal IL‐6 expression at the protein level is increased across patients with neither periodontal disease nor diabetes, patients with periodontal disease alone and patients with both diseases.     

Periodontal diseases and stress: a brief review

Periodontal diseases are common chronic inflammatory diseases caused by pathogenic microorganisms colonising the subgingival area and inducing local and systemic elevations of pro‐inflammatory cytokines resulting in tissue destruction. Apparition and evolution of periodontal diseases are influenced by many local or systemic risk factors. Psychological stress has been suggested as one of them and may negatively influence the outcome of periodontal treatment. However, mechanisms explaining the possible relationship between stress and increased susceptibility to periodontal disease remain poorly understood. Several stress markers are found in blood and saliva of patients with periodontal diseases and influence the development of periodontal diseases by several mechanisms including modifications of the inflammatory response and changes in the composition of the dental biofilm. The aim of this review is to provide an insight into the relationship between psychological stress and periodontal diseases.     

High glucose-boosted inflammatory responses to lipopolysaccharide are suppressed by statin

BACKGROUND AND OBJECTIVE: It has been established that periodontal diseases are more prevalent and of greater severity in diabetic patients than in nondiabetic patients. Recent studies have underscored the role of monocytes and macrophages in periodontal tissue inflammation and destruction in diabetic patients. Although it has been shown that monocytes isolated from diabetic patients produce more inflammatory cytokines and that gingival crevicular fluid collected from diabetic patients contains higher levels of inflammatory cytokines than that obtained from nondiabetic patients, the underlying mechanisms are not well understood. MATERIAL AND METHODS: U937 histiocytes cultured in medium containing either normal (5 mM) or high (25 mM) glucose were treated with 100 ng/ml of lipopolysaccharide for 24h. After the treatment, cytokines in the medium and cytokine mRNA in the cells were quantified using enzyme-linked immunosorbet assay and real-time polymerase chain reaction, respectively. RESULTS: In this study, we demonstrated that the pre-exposure of U937 histiocytes to high glucose concentrations markedly increased the lipopolysaccharide-induced secretion of pro-inflammatory cytokines and chemokines and the cellular inducible nitric oxide level compared with pre-exposure to normal glucose. Our data also showed that the increased secretion of cytokines was a result of increased mRNA expression. Furthermore, the effects of statin and peroxisome proliferators-activated receptor agonists on high glucose-enhanced secretion of cytokines were determined. The results showed that simvastatin, but not fenofibrate or pioglitazone, inhibited high glucose-enhanced cytokine release. CONCLUSION: This study has shown that high glucose concentrations and lipopolysaccharide act synergistically to stimulate the secretion of inflammatory mediators, and that statin is capable of suppressing the high glucose-boosted proinflammatory response. This study therefore delineates a novel mechanism by which hyperglycemia enhances the inflammatory responses of macrophages and suggests that statin may be useful in the treatment of periodontal disease in diabetic patients.     

2型糖尿病合并牙周炎患者血清白细胞介素-1水平的检测

目的探讨2型糖尿病合并牙周炎患者血清白细胞介素-1（interleukin-1,IL-1）蛋白水平的表达。方法选择健康对照、糖尿病、重度慢性牙周炎和重度慢性牙周炎伴2型糖尿病患者各32例。用酶联免疫ELISA法测定血清IL-1α、IL-1β水平。结果 2型糖尿病合并牙周炎患者的血清IL-1β含量明显高于不伴牙周炎的糖尿病患者（P〈0.05）,牙周炎组高于健康对照组。4组中IL-1α水平无显著差异。结论 2型糖尿病合并牙周炎患者血清IL-1β水平明显升高。     

Role of receptors of advanced glycation end‐products (RAGE) in type 2 diabetic and non‐diabetic individuals with chronic periodontal disease: an immunohistochemical study

Aim: The relationship between diabetes and periodontal disease is well established. It has been shown that advanced glycation end‐products might exert noxious effects on several tissues of the body through its receptor. Evidence for the role of receptors of advanced glycation end‐products in periodontal disease for diabetes is limited, and their presence in human gingival tissues has been demonstrated in few studies. In this study, we demonstrate the presence of receptors of advanced glycation end‐products in patients with chronic periodontitis, with and without type 2 diabetes. Methods: Gingival biopsies from 19 patients with both type 2 diabetes and chronic periodontitis, and 18 healthy controls with chronic periodontitis, were immunohistochemically stained for receptors of advanced glycation end‐products. Results: On immunohistochemical analysis, positive staining for receptors of advanced glycation end‐products was seen in the endothelium and the basal and spinous layers of the inflamed gingival epithelium in both type 2 diabetes and non‐diabetes tissue, with a statistically‐significant difference between both groups (P < 0.05). Conclusions: There was a significant difference in receptors of advanced glycation end‐product immune reactivity between both groups. Receptors of advanced glycation end‐product increase in type 2 diabetes gingival tissue might indicate possible involvement of this receptor in periodontal destruction in individuals with type 2 diabetes.     

Ⅱ型糖尿病合并牙周病患者龈沟液中肿瘤坏死因子α水平和意义

目的：比较Ⅱ型糖尿病合并牙周病患者、牙周病患者与健康者龈沟液中肿瘤坏死因子-α（TNF-α）含量和龈沟液量,以及Ⅱ型糖尿病合并牙周病患者龈沟液中TNF-α量与糖代谢状况的关系。方法：使用滤纸条法采集龈沟液,Ⅱ型糖尿病合并牙周病患者、牙周病患者和全身健康者各30例;放射免疫法测定龈沟液中TNF-α含量;运用高效液相层析法测定Ⅱ型糖尿病合并牙周病患者的糖化血红蛋白水平。结果：糖尿病合并牙周病组和牙周病组龈沟液量及龈沟液TNF-α量均显著高于正常对照组（P〈0.01）,糖尿病合并牙周病组龈沟液TNF-α量显著高于牙周病组（P〈0.01）。糖尿病合并牙周病组龈沟液中TNF-α含量与糖化血红蛋白（HbA1c）水平无显著直线相关性。结论：龈沟液中TNF-α含量受牙周炎症影响同时全身因素调控,导致糖尿病合并牙周病患者龈沟液TNF-α水平显著升高,造成牙周病加重。     

Local inflammatory reactions in patients with diabetes and periodontitis

The impact of diabetes mellitus on the prevalence, severity and progression of periodontal disease has been known for many years and intense efforts have been made to elucidate the underlying mechanisms. It is widely reported that hyperglycemia causes numerous systemic changes, including altered innate immune‐cell function and metabolic changes. The aim of this review was to summarize and discuss the evidence for mechanisms that probably play a role in the altered local inflammatory reactions in the periodontium of patients with diabetes, focusing on local changes in cytokine levels, matrix metalloproteinases, reactive oxygen species, advanced glycation end‐products, immune‐cell functions, the RANKL/osteoprotegerin axis and toll‐like receptors. Apart from the systemic effects of diabetes, recent evidence suggests that local changes in the periodontal tissues are characterized by enhanced interactions between leukocytes and endothelial cells and by altered leukocyte functions [resulting in increased levels of reactive oxygen species and of proinflammatory cytokines (interleukin‐1β, interleukin‐6 and tumor necrosis factor‐α)]. These local changes are amplified by the enhanced accumulation of advanced glycation end‐products and their interaction with receptors for advanced glycation end‐products. Furthermore, the increased levels of proinflammatory cytokines lead to an up‐regulation of RANKL in periodontal tissues, stimulating further periodontal tissue breakdown.     

龈沟液成分及含量变化与糖尿病及心血管疾病的关系

牙周病与多种系统性疾病相关。其中与糖尿病和心血管疾病之间的关系是近年来的研究热点。龈沟液成分的种类和含量可受到糖尿病、心血管疾病的影响而发生变化。分析龈沟液有关成分的变化可提示疾病的进展,并且可以了解这些疾病如何影响牙周病的进展。本文就牙周病患者龈沟液成分与糖尿病及心血管疾病的相关性做一综述。     

Periodontal manifestations of systemic disease

Periodontitis is a chronic bacterial infection of the supporting structures of the teeth. The host response to infection is an important factor in determining the extent and severity of periodontal disease. Systemic factors modify periodontitis principally through their effects on the normal immune and inflammatory mechanisms. Several conditions may give rise to an increased prevalence, incidence or severity of gingivitis and periodontitis. The effects of a significant number of systemic diseases upon periodontitis are unclear and often it is difficult to causally link such diseases to periodontitis. In many cases the literature is insufficient to make definite statements on links between certain systemic factors and periodontitis and for several conditions only case reports exist whereas in other areas an extensive literature is present. A reduction in number or function of polymorphonuclear leukocytes (PMNs) can result in an increased rate and severity of periodontal destruction. Medications such as phenytoin, nifedipine, and cyclosporin predispose to gingival overgrowth in response to plaque and changes in hormone levels may increase severity of plaque-induced gingival inflammation. Immuno-suppressive drug therapy and any disease resulting in suppression of the normal inflammatory and immune mechanisms (such as HIV infection) may predispose the individual to periodontal destruction. There is convincing evidence that smoking has a detrimental effect on periodontal health. The histiocytoses diseases may present as necrotizing ulcerative periodontitis and numerous genetic polymorphisms relevant to inflammatory and immune processes are being evaluated as modifying factors in periodontal disease. Periodontitis severity and prevalence are increased in diabetics and worse in poorly controlled diabetics. Periodontitis may exacerbate diabetes by decreasing glycaemic control. This indicates a degree of synergism between the two diseases. The relative risk of cardiovascular disease is doubled in subjects with periodontal disease. Periodontal and cardiovascular disease share many common risk and socio-economic factors, particularly smoking, which is a powerful risk factor for both diseases. The actual underlying aetiology of both diseases is complex as are the potential mechanisms whereby the diseases may be causally linked. It is thought that the chronic inflammatory and microbial burden in periodontal disease may predispose to cardiovascular disease in ways proposed for other infections such as with Chlamydia pneumoniae. To move from the current association status of both diseases to causality requires much additional evidence. Determining the role a systemic disease plays in the pathogenesis of periodontal disease is very difficult as several obstacles affect the design of the necessary studies. Control groups need to be carefully matched in respect of age, gender, oral hygiene and socio-economic status. Many studies, particularly before the aetiological importance of dental plaque was recognised, failed to include such controls. Longitudinal studies spanning several years are preferable in individuals both with and without systemic disease, due to the time period in which periodontitis will develop.     

Update on diabetes mellitus: prevention, treatment, and association with oral diseases

Diabetes mellitus is a prevalent disease that affects millions of people worldwide and has paralleled the growing population of overweight and obese individuals. Early detection of prediabetes and diabetes, as well as lifestyle interventions including diet and exercise, are the overarching objectives in preventing and managing diabetes. For individuals who do not achieve glycemic control with lifestyle modification, there are newer medication classes that assist with weight loss, more physiologic insulins with convenient delivery systems, and old standbys like metformin and thiazolidinediones. Glycemic control along with blood pressure and cholesterol management reduce microvascular and macrovascular disease including cardiovascular events. Mounting evidence demonstrates that diabetes is a risk factor for periodontitis and possibly oral premalignancies and oral cancer. The systemic inflammatory response generated by inflamed periodontal tissue may in turn exacerbate diabetes, worsen cardiovascular outcomes, and increase mortality. Thus, oral medical and surgical physicians are vital in treating oral pathology, recognizing new cases of diabetes, and counseling people with diabetes to promote oral health. This article presents updates in the diagnosis, risk factors, prevention, management, and peri-oral complications of diabetes to assist oral health professionals in providing optimal care to patients with diabetes.     

The relationship of inflammatory periodontal disease to diabetic status in insulin-dependent diabetes mellitus patients

This study was designed to evaluate the relationship of inflammatory periodontal disease to the diabetic status of the insulin-dependent diabetes mellitus (IDDM) patient. 52 IDDM patients, ages 11-22 years, were evaluated. These patients were closely monitored at regular intervals in the University of Kentucky pediatric diabetic clinic. A periodontal examination was carried out for each patient. The patients were then assigned to a periodontitis or non-periodontitis group. Moderate to advanced periodontitis was found in 5.8% of the subjects. The gingival index and sulcular bleeding index were significantly higher in the periodontitis group (P less than 0.05). There was no significant difference between groups for plaque index, age of diabetic onset, duration of diabetes, present age, insulin dosage/weight, or serum glucose (P greater than 0.05). There was a greater % of ketoacidosis, retinopathy and neuropathy in the periodontitis group. IDDM patients with neurological complications or a history of chronic infections had a significantly higher gingival index score than those without the complication (P less than 0.05).     

Principles of periodontology

Periodontal diseases are among the most common diseases affecting humans. Dental biofilm is a contributor to the etiology of most periodontal diseases. It is also widely accepted that immunological and inflammatory responses to biofilm components are manifested by signs and symptoms of periodontal disease. The outcome of such interaction is modulated by risk factors (modifiers), either inherent (genetic) or acquired (environmental), significantly affecting the initiation and progression of different periodontal disease phenotypes. While definitive genetic determinants responsible for either susceptibility or resistance to periodontal disease have yet to be identified, many factors affecting the pathogenesis have been described, including smoking, diabetes, obesity, medications, and nutrition. Currently, periodontal diseases are classified based upon clinical disease traits using radiographs and clinical examination. Advances in genomics, molecular biology, and personalized medicine may result in new guidelines for unambiguous disease definition and diagnosis in the future. Recent studies have implied relationships between periodontal diseases and systemic conditions. Answering critical questions regarding host‐parasite interactions in periodontal diseases may provide new insight in the pathogenesis of other biomedical disorders. Therapeutic efforts have focused on the microbial nature of the infection, as active treatment centers on biofilm disruption by non‐surgical mechanical debridement with antimicrobial and sometimes anti‐inflammatory adjuncts. The surgical treatment aims at gaining access to periodontal lesions and correcting unfavorable gingival/osseous contours to achieve a periodontal architecture that will provide for more effective oral hygiene and periodontal maintenance. In addition, advances in tissue engineering have provided innovative means to regenerate/repair periodontal defects, based upon principles of guided tissue regeneration and utilization of growth factors/biologic mediators. To maintain periodontal stability, these treatments need to be supplemented with long‐term maintenance (supportive periodontal therapy) programs.     

Evaluation of periodontal status and effectiveness of non-surgical treatment in patients with type 2 diabetes mellitus in Taiwan for a 1-year period

Background: The periodontal status and effects of non‐surgical periodontal treatment in patients with type 2 diabetes mellitus and periodontal disease are assessed. Methods: One‐hundred patients with type 2 diabetes (mean ± SD hemoglobin (Hb)A1c level: 7.3% ± 0.94%) and periodontal disease were recruited for this study. The group with moderate‐to‐severe periodontal disease included patients with >1 tooth with a probing depth (PD) ≥5 mm and >2 teeth with a clinical attachment loss (AL) ≥6mm, and the group with mild periodontal disease included patients with <1 affected tooth, and >2 affected with a clinical AL ≥6mm. Patients (28 patients in the mild group and 72 patients in the moderate‐to‐severe group) underwent non‐surgical periodontal treatments. We analyzed differences in serum concentrations of metabolic parameters (glycated hemoglobin and low‐density lipoprotein), inflammatory parameters (interleukin [IL]‐1β and C‐reactive protein [CRP]), and periodontal parameters between the two groups before treatment and at 3, 6, 9, and 12 months post‐therapy. Results: Seventy‐five patients with diabetes (21 patients in the mild group and 54 patients in the moderate‐to‐severe group) completed the study. Significant differences in the plaque index (PI), gingival index (GI), PD, and clinical AL at examination times were observed in the whole cohort (P <0.05). We observed significant differences in the PI, GI, and PD in the moderate‐to‐severe group (P <0.05), whereas there was only a significant difference in PD in the mild group (P <0.05) between baseline and 12 months post‐treatment. Both groups experienced improved glycemic control, but the difference was insignificant. CRP and IL‐1β levels were significantly different at examination times for the whole cohort (P <0.05). No significant positive association among metabolic and inflammatory parameters at 12 months post‐therapy were found. Conclusion: Non‐surgical periodontal treatment improved and maintained the periodontal health of patients with well‐controlled diabetes, but no significant reduction of metabolic parameters was observed over a 1‐year period.     

Do patients with aggressive periodontitis have evidence of diabetes? A pilot study

Davies RC, Jaedicke KM, Barksby HE, Jitprasertwong P, Al‐Shahwani RM, Taylor JJ, Preshaw PM. Do patients with aggressive periodontitis have evidence of diabetes? A pilot study. J Periodont Res 2011; 46: 663–672. © 2011 John Wiley & Sons A/S Background and Objective: Complex relationships exist between diabetes and periodontal disease. Diabetes is accepted as a risk factor for periodontal disease, and recent evidence supports the existence of a bidirectional relationship between these two diseases. It has been hypothesized that inflammation, lipids and adipokines may mediate these relationships. However, research regarding the above relationships with respect to aggressive periodontitis is very limited. This pilot study aimed to investigate whether patients with aggressive periodontitis (not previously diagnosed with diabetes) have evidence of diabetes and have altered serum levels of inflammatory mediators, lipids and adipokines. Material and Methods: Glycaemic control markers (random plasma glucose and glycated haemoglobin), inflammatory mediators (high‐sensitivity C‐reactive protein, tumour necrosis factor‐α, interleukin‐1β, interleukin‐6, interferon‐γ and interleukin‐18), lipids (triglycerides, total cholesterol and high‐density lipoprotein‐cholesterol) and adipokines (leptin, adiponectin and resistin) were measured in serum samples from 30 patients with aggressive periodontitis and 30 age‐ and sex‐matched periodontally healthy control subjects, none of whom had a previous diagnosis of diabetes. Results: Levels of glycaemic control markers, inflammatory mediators, lipids and adipokines were not significantly different (p > 0.05) between the aggressive periodontitis patients and healthy subjects for unadjusted and adjusted analyses (adjusting for body mass index, smoking, ethnicity, age and sex). The p‐value for the adjusted analysis of adiponectin in female aggressive periodontitis patients compared with the female control subjects reached 0.064, the mean adiponectin level being lower in the female aggressive periodontitis patients (4.94 vs. 5.97 μg/mL). Conclusion: This pilot study provided no evidence to suggest that patients with aggressive periodontitis (not previously diagnosed with diabetes) have evidence of diabetes or altered serum levels of inflammatory mediators, lipids and adipokines.