Síndrome de boca ardiente secundario a pregabalina en un paciente con atrofia frontal leve / Burning mouth syndrome secondary to pregabaline in a patient with mild frontal lobes atrophy

No disponible

MMP-9 -1562 C>T (rs3918242) promoter polymorphism as a susceptibility factor for multiple gingival recessions.

The objective of this pilot study was to investigate the potential role of -1562 C>T single nucleotide polymorphism (SNP) in the promoter region of the matrix metalloproteinase-9 (MMP-9) gene as a risk modulator in the development of multiple gingival recessions (MGRs) in young adults in the Serbian population. The study sample comprised 161 systemically healthy people: 60 with MGRs and 101 controls with healthy periodontal tissues. Genotyping was done using polymerase chain reaction/restriction fragment length polymorphism approach on DNA obtained from buccal swabs. Clinical measurements included vertical recession depth (VRD), clinical attachment level (CAL), keratinized gingival width (KGW), visible plaque index (PI), and bleeding on probing (BOP). Heterozygotes (CT) were significantly more frequent in the MGRs group than in the control group (P = .005) and carriers of the T allele had an approximately threefold increase of MGRs risk. Patients with the CT genotype exhibited significantly higher values of VRD and CAL and significantly lower values of KGW than patients with the wildtype genotype. Associations among different genotypes and periodontal biotypes in the MGRs group remained insignificant because all participants exhibited thin biotype. The -1562 C>T SNP in the promoter region of MMP-9 appears to be a risk factor for MGR development and a potential predictor of more severe clinical phenotype.

Inter-generational continuity in periodontal health: findings from the Dunedin family history study.

OBJECTIVE: To determine whether parental periodontal disease history is a risk factor for periodontal disease in adult offspring. METHODS: Proband periodontal examination [combined attachment loss (CAL) at age 32, and incidence of CAL from ages 26 to 32] and interview data were collected during the age-32 assessments in the Dunedin Study. Parental data were also collected. The sample was divided into two familial-risk groups for periodontal disease (high- and low-risk) based on parents' self-reported periodontal disease. RESULTS: Periodontal risk analysis involved 625 proband-parent(s) groups. After controlling for confounding factors, the high-familial-risk periodontal group was more likely to have 1+ sites with 4+mm CAL [relative risk (RR) 1.45; 95% confidence interval (CI) 1.11-1.88], 2+ sites with 4+mm CAL (RR 1.45; 95% CI 1.03-2.05), 1+ sites with 5+mm CAL (RR 1.60; 95% CI 1.02-2.50), and 1+ sites with 3+mm incident CAL (RR 1.64; 95% CI 1.01-2.66) than the low-familial-risk group. Predictive validity was enhanced when information was available from both parents. CONCLUSIONS: Parents with poor periodontal health tend to have offspring with poor periodontal health. Family/parental history of oral health is a valid representation of the shared genetic and environmental factors that contribute to an individual's periodontal status, and may help to predict patient prognosis and preventive treatment need.

Interleukin-1 gene cluster polymorphisms and gingival recessions after orthodontic treatment.

INTRODUCTION: Genetic polymorphisms in the interleukin-1 gene cluster have been associated with the severity of periodontal diseases featured by a variable degree of destruction of connective tissue and bone, such as periodontitis and periimplantitis. This study was aimed to investigate if a link exists between such interleukin-1 gene polymorphisms and the development of gingival recessions during orthodontic treatment in Italian children. METHODS: We evaluated, in 74 young Italian patients of both sexes, the -889 C/T polymorphism of the interleukin-1alpha gene and the -511 C/T and +3954 C/T polymorphisms of interleukin-1alpha gene by polymerase chain reactions-restriction fragment length polymorphism method using NcoI, AvaI and TaqI as restriction enzymes. RESULTS: No association of interleukin-1 genotypes investigated and gingival recession occurring during orthodontic treatment were identified. CONCLUSION: In the population studied specific interleukin-1 genotypes (linked to a higher susceptibility to bone resorption in periodontal disease) there does not appear to be any association with the development of gingival recessions during orthodontic treatment.

Periodontal status among relatives of aggressive periodontitis patients and reliability of family history report.

OBJECTIVES: To assess the periodontal status of relatives of Aggressive Periodontitis (AgP) patients, and to evaluate the reliability of the family history report as provided by the proband. MATERIAL AND METHODS: Data from 54 AgP patients were gathered along with a family history report for each of their relatives. Only 27 patients (probands) had relatives willing to be examined. This yielded a total of 61 relatives from whom the periodontal status was obtained. The family history report for each examined relative was compared with the periodontal diagnosis made at examination to assess reliability. RESULTS: Eight percentage of the examined relatives, aged between 12-76, were diagnosed with AgP, while chronic periodontitis was present in 39%, gingivitis in 38% and 15% were healthy. If the report provided by the proband was positive, the likelihood of finding any type of periodontitis in that relative was 85.7%, whereas if the report was negative the likelihood of the absence of periodontitis was 70.6%. CONCLUSION: The percentage of examined relatives who were affected with AgP (8%), although lower than percentages reported in other AgP family studies, was still higher than the prevalence of the condition in random populations. Reliability of periodontal family history was considered good and more reliable when it was positive.

Interleukin-1 gene polymorphism and periodontal status. A case-control study.

OBJECTIVES: This case-control study examined polymorphisms at the interleukin-1 gene in relation to periodontal status, subgingival bacteria and systemic antibodies to periodontal microbiota. METHODS: 132 periodontitis patients were age- and gender-matched with 73 periodontally intact controls. Full-mouth clinical assessments of the periodontal tissues were performed. Subgingival plaque samples (2440 in total) were analyzed by genomic DNA probes, and serum IgG antibodies to periodontal microbiota were assessed by an immunoassay. Polymorphisms in the IL-1A gene at position +4845 and the IL-1B gene at position +3953 were studied by PCR. A composite positive genotype was defined as at least one rare (#2) allele present at each locus. RESULTS: No skewed distribution of the composite genotype was observed between cases and controls (45.2% vs 41.7%). In cases, both the composite genotype and the number of #2 alleles were positively correlated with the severity of attachment loss. No relationship between genotype and subgingival microbial profiles was observed. Genotype positive patients revealed both overall lower serum antibody levels and specific titers against selected bacteria. CONCLUSIONS: The composite genotype failed to distinguish between periodontitis patients and controls but correlated in patients with the severity of the disease and the antibody responses to periodontal microbiota.