钙通道阻滞剂导致牙龈增生的Meta分析

目的 钙通道阻滞剂(CCB)是治疗心血管疾病的常用药物,文献报道其所致药物性牙龈增生(DIGO)的患病率为7.3％～77.6％,不同文献得出的结果差别较大,本研究旨在通过系统综述及Meta分析,以明确CCB与DIGO的关系及其影响因素.方法 两位不同的研究者分别系统地搜索了PubMed、Cochrane Library...     

钙离子拮抗剂致药物性牙龈增生的危险因素分析

目的调查高血压患者服用钙离子拮抗剂后引起药物性牙龈增生的患病率,并分析其危险因素。方法将北京医院心血管内科的681例高血压或冠心病患者纳入本研究,其中330例服用钙离子拮抗剂(CCB组),351例未服用钙离子拮抗剂(对照组)。记录患者的性别、年龄、用药种类、持续时间、剂量、是否联合用药。临床检查牙龈出血指数(BI)、菌斑指数(PLI)、牙龈增生指数(HI)。结果服用钙离子拮抗剂组牙龈增生的患病率为41.21%,显著高于对照组4.84%(P<0.05)。对调查的各种因素进行Logistic回归分析,结果显示:BI(OR=2.17,95%可信区间:1.60-2.94)PLI(OR=1.99,95%可信区间:1.38-2.87)是患者出现牙龈增生的危险因素。结论口腔卫生状况和牙龈炎症反应是药物性牙龈增生的危险因素。     

The calcium channel blocker used with cyclosporin has an effect on gingival overgrowth

BACKGROUND/AIMS: To investigate whether the choice of calcium channel blocker, used in conjunction with cyclosporin A, affected the prevalence of gingival overgrowth. METHOD: A cohort of 135 renal transplant recipients who had been medicated with cyclosporin A in combination with either nifedipine (89) or amlodipine (46) since transplant, took part in the study. The inclusion criteria were that eligible subjects had been in receipt of a kidney transplant for at least 12 months, had at least 10 teeth and had not received specialist periodontal treatment. The age, gender, current drug regimen and dosage were recorded for each participant and alginate impressions taken of both arches. The presence and severity of gingival overgrowth were scored from plaster models. RESULTS: A higher proportion (72%) of the amlodipine group were categorised as having gingival overgrowth compared with only 53% of the nifedipine group, chi square=4.5, p<0.05. Logistic regression analysis was used to explore the relationship between the presence or absence of gingival overgrowth (dependent variable) and age, gender, time since transplant, dose of cyclosporin A, centre in which the patient was treated, and the calcium channel blocker used (independent variables). Independent predictors of gingival overgrowth in this multivariate analysis were whether the individual was treated with amlodipine or nifedipine (p=0.01) and whether the individual was young or old (p=0.01). Within the multivariate analysis, the odds ratio for amlodipine to be associated with gingival overgrowth compared with nifedipine was 3.0 (confidence interval 1.3-6.9). CONCLUSIONS: The prevalence of gingival overgrowth in renal transplant recipients maintained on cyclosporin A and nifedipine is lower than those treated with cyclosporin A and amlodipine.     

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目的探讨钙拮抗剂诱导的牙龈增生与钙拮抗剂种类和牙周局部因素的关系。方法2007年3月至10月对河北省人民医院心血管内科和口腔科门诊240例服用钙拮抗剂类药物患者进行牙周检查,记录牙龈增生指数、出血指数和菌斑指数等。结果240例患者中64例(26.67%)发生了牙龈增生,服用不同类型钙拮抗剂的患者间牙龈增生的发生率差异无统计学意义(P均>0.05)。牙龈增生程度越重,菌斑指数和出血指数均值越高,与0度组相比,Ⅰ～Ⅳ度牙龈增生组的菌斑指数和出血指数差异均有统计学意义(P均<0.01)。结论钙拮抗剂诱导的牙龈增生程度与牙周局部因素密切相关,与钙拮抗剂种类无关。     

Diode激光辅助治疗对服用钙通道拮抗剂老年患者龈沟探诊出血改善的研究

目的：比较Diode激光辅助牙周基础治疗（实验组）与单纯牙周基础治疗（对照组）对服用钙通道拈抗剂老年患者龈沟出血的改善效果。方法：选择10位服用钙通道拮抗剂的老年患者共30颗牙,左右对称,随机确定一侧为实验组,对侧牙为对照组。口腔卫生宣教和龈上洁治后2周为基线,治疗2周、4周、8周后记录龈沟出血指数（SBI）,并进行统计分析。结果：实验组和对照组的SBI在2周、4周和8周后与基线比较均有明显改善（P〈0．01）;两组之间比较,SBI的改善没有明显差异（P〉0．01）;实验组中、深牙周袋位点SBI的改善较浅袋明显（P〈0．01）,对照组不同袋深位点SBI的改善没有明显差异（P〉0．01）。结论：Diode激光辅助牙周基础治疗能显著改善服用钙通道拮抗剂老年患者的SBI,尤其在中深牙周袋位点;Diode激光辅助牙周基础治疗与牙周基础治疗在SBI改善的差异上没有显著性。     

Felodipine-induced gingival hyperplasia: a clinical and histologic study

This paper reports, for the first time, gingival hyperplasia in a patient treated with felodipine, a drug which belongs to the group of calcium ion antagonists. The observed gingival overgrowth was most significant in the area of interdental papillae of the anterior region of the mouth. The described hyperplastic tissue was characterized by a firm and pale appearance, with a normally stippled pattern. Histopathologically, a conspicuous increase of fibrous connective tissue, as well as an inflammatory infiltrate and hyperplasia of the overlying epithelium were observed. Consequently, the present observation adds another drug to the list of substances capable to induce gingival hyperplasia.     

钙离子拮抗剂致药物性牙龈增生的危险因素分析

目的：探讨高血压患者服用钙离子拮抗剂后出现牙龈增生的患病率。方法：对我院查体中心和心血管内科门诊服用钙离子拮抗剂抗高血压类药物的262和未服用钙离子拮抗剂的197例患者进行横断面调查。方法包括问卷调查和口腔牙周检查,其中牙龈增生的判定以牙龈增生指数（HI ）为诊断标准。对调查结果进行统计学分析。结果：服用钙离子拮抗剂类药物患者的牙龈增生患病率为20．23％,显著高于对照组的2．54％（χ2＝32．276,P＜0．05）。随年龄增大,药物性牙龈增生的患病率降低（r＝－0．155,P＜0．05）;单一用药者较联合用药者患病率高;服药时间越长患病率降低;随服药剂量的增加,患病率明显增长;口腔卫生状况差者可加重牙龈增生程度。结论：药物性牙龈增生是多方面作用的结果,其主要影响因素为患者年龄、服药方式、剂量、时间和牙周局部因素。     

Clinical assessment of gingival hyperplasia in patients treated with nifedipine

Abstract Gingival hyperplasia caused by the use of nifedipine has been extensively reported. In this paper, the gingiva of 18 patients suffering from cardiopathy and treated with nifedipine were compared with those of 10 patients with cardiac disorders who had not been treated with calcium antagonists and with a no-treatment group of 12 patients. Nifedipine produced gingival hyperplasia although patients who had not been treated with calcium antagonists also had mild hyperplasia. Hyperplasia first appeared in the interproximal areas, an observation which may be important for early detection. There was a direct correlation between the degree of hyperplasia and the bacterial plaque score. When we studied the influence of administration time and dose of nifedipine with the degree of hyperplasia, no statistically significant differences were found.     

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目的    观察牙周基础治疗对钙拮抗剂导致牙龈增生的治疗效果。方法    选取2006年6月至2009年3月在沈阳市口腔医院牙周科就诊,因高血压病服用钙拮抗剂导致牙龈增生的患者16例,在不更换药物或未停药的情况下进行牙周基础治疗,在治疗前基线和治疗后1、3、6个月时记录牙龈增生指数（GO）、菌斑指数（PIL）、龈沟出血指数（SBI）和探诊深度（PD）。结果    在观察期间,各指数持续改善（P < 0.01）,牙龈炎症持续减轻,牙龈增生状况明显改善。结论    牙周基础治疗对钙拮抗剂导致的牙龈增生有效,这为不能换药或停药的高血压患者提供了较合理的治疗方法。     

硝苯地平引起牙龈增生20例临床观察

目的 观察服用硝苯地平引起的牙龈增生。方法 门诊随机观察与服用硝苯地平有关的牙龈增生病人20例,并了解停药前后的变化。结果 20例牙龈增生病人,通过停药和局部治疗,6月后随访,局部症状有所缓解。结论 服用硝苯地平可引起牙龈增生。     

钙离子拮抗剂诱导牙龈增生发病机理的研究进展

钙离子拮抗剂广泛应用于治疗高血压和冠心病,但该类药物可以导致部分病人牙龈增生。该文分别从组织病理、组织代谢、药物浓度、牙龈上皮凋亡以及遗传免疫学等角度对钙离子拮抗剂导致牙龈增生的发病机理的研究进展做一综述。     

Proteus syndrome: association with gingival hyperplasia

A 9-year old Black boy with gigantism of the hands and feet, and recurrent gingival hyperplasia, diagnosed as Proteus syndrome is presented. The oral manifestations of this syndrome are described. To the best of our knowledge, this is the first reported case of gingival hyperplasia associated with Proteus syndrome.     

钙离子拮抗剂致老年人牙龈增生危险因素分析

目的:数据分析西安交通大学医院内科门诊的高血压或其他心血管疾病患者服用的钙离子拮抗剂对诱导牙龈增生的影响.方法:经筛选后符合此次调研标准的2019年我院内科门诊的高血压或其他心血管疾病的临床资料共483份,其中服用钙离子拮抗剂(Calcium Channel Blockers,CCB)者252例,未服用CCB(对照组)...     

On the mechanism of drug-induced gingival hyperplasia

Proposed mechanisms of the side effect of drug-induced gingival hyperplasia are reviewed. Hypotheses with regard to inflammation from bacterial plaque, increased sulfated glycosaminoglycans, immunoglobulins, gingival fibroblast phenotype population differences, epithelial growth factor, pharmacokinetics and tissuebinding, collagenase activation, disruption of fibroblast cellular sodium/calcium flux, folic acid and a combination hypothesis are evaluated.     

Reappraising localized juvenile spongiotic gingival hyperplasia

Background

Localized juvenile spongiotic gingival hyperplasia (LJSGH) is a gingival lesion of unknown cause. The purpose of this study is to present a series of LJSGH cases and compare the findings with the literature.

Folate treatment of diphenylhydantoin-induced gingival hyperplasia

Abstract – It has recently been reported that folic acid supplementation reduced DPH-induced gingival hyperplasia in cat and in a pilot study also in man. The present study was performed to further evaluate this therapy in man. Twenty-three children with DPH-treatment for more than 1 yr, and eight children with short-time DPH-treatment were randomly assigned to groups with and without daily supplementation of folic acid (5 mg Folacin) for 1 yr. Although the DPH-levels were in many cases below the lower reference value, the seizure control of the children was good before and during the year of study. The plasma and red cell folate levels were within or above the given reference values in all but one child. There were no significant changes in the size of the gingival hyperplasias after 1 yr of folate supplementation. Nine severely mentally retarded DPH-treated adults were also given supplementation with folic acid. Their serum DPH-levels were above the higher reference values both at the start and during the study. Their plasma and red cell folic acid levels were below the reference value at the start of the study, but as a consequence of the Folacin supplementation these values rose. The size of the gingival hyperplasias was significantly reduced. Seizure control was unchanged. Folate levels should be checked and supplementation with folic acid considered in patients on long-term anticonvulsive multipharmacy therapy.     

The subgingival microflora in phenytoin-induced gingival hyperplasia

OBJECTIVES: Microbial flora and gingival conditions were compared between a group of patients with phenytoin-induced gingival hyperplasia as a test group, a control group of patients who were administered phenytoin without gingival hyperplasia and a blank group who took no phenytoin and no gingival hyperplasia in mentally retarded patients. MATERIALS AND METHODS: Subgingival plaque samples were collected from a PHT-induced overgrown gingival pocket and microbiological experiments were performed by culture and PCR methods. RESULTS: The predominant genera in total cultivable bacteria from subgingival plaque samples were streptococcus and actinomyces with recovery ranges of 37.6-42.1% and 23.4-25.5% of total bacteria, respectively, in all groups. The test group showed a significantly higher level of obligate Gram-negative rods than the control and blank groups. Black-pigmented obligate anaerobic Gram-negative rods were detected in 10.3% of total cultivable bacteria in the test group. The black-pigmented rods were predominantly Prevotella intermedia in the test group and Prevotella nigrescens in the control and blank groups. Porphyromonas gingivalis and Porphyromonas endodontalis were also detected in the test group with small values. CONCLUSIONS: These results suggested that black-pigmented rods, particularly P. intermedia, could be habitable in the environment of gingival hyperplasia.