Analysis of the association of polymorphism in the osteoprotegerin gene with susceptibility to chronic kidney disease and periodontitis

Baioni, C. S.; Souza, Cleber Machado de; Braosi, Ana Paula Ribeiro; Luczyszyn, Sônia Mara; Silva, Marco Antonio Dias da; Ignácio, Sérgio Aparecido; Machado, Maria Ângela Naval; Martins, Wilson; Riella, Miguel C.; Pecoits-Filho, R.; Trevilatto, Paula Cristina

doi:10.1111/j.1600-0765.2008.01098.x

Cited by 14 publications

(9 citation statements)

References 69 publications

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“…When the periodontal parameters such as PI, GI, PPD, CAL, percentage of sites with periodontal pockets, and CAL were compared between the groups, all of the periodontal parameters were significantly higher in the CKD+CP group. This was in accordance with results of Baioni et al who suggested that renal tissue damage is linked to the severity of periodontitis, where large amounts of periodontal bacteria such as Porphyromonas gingivalis, Tannerella forsythia, Fusobacterium nucleatum, Aggregatibacter actinomycetemcomitans, and their toxins such as gingipains, leukotoxin A, outer membrane vesicles, and cytolethal distending toxin are capable of invading the renal tissues, resulting in oxidative imbalance in the kidneys [18].…”

Section: Discussionsupporting

confidence: 92%

“…GPx levels were also assessed among the groups. Among the demographic variables, age was significantly higher in the CKD+CP group, which was in accordance with studies by Baioni et al and Mahendra et al who stated that the prevalence and adverse events associated with both CP and CKD was found to be higher and positively associated with older individuals (Table 1) [18,19]. Thus, from the above findings, it can be postulated that the patients have prolonged exposure to their etiology as age increases, and thus the predisposition to periodontal as well as CKD also increases.…”

Section: Discussionsupporting

confidence: 90%

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A Cross-Sectional Study of Serum Glutathione Peroxidase: An Antioxidative Marker in Chronic Periodontitis and Chronic Kidney Disease

Palathingal¹,

Mahendra²,

Annamalai³

et al. 2022

Cureus

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Background and aim: Oxidative stress as an individual risk for periodontitis and chronic kidney disease (CKD) has been elaborated through various mechanical pathways, yet its role in association with both diseases remains unexplored. Thus, the current study aims in evaluating serum glutathione peroxidase, an oxidative stress marker in CKD patients with periodontitis, and compare it with the healthy controls.Methodology: One hundred and twenty subjects were divided into four groups as control (C=30 subjects), periodontitis and non-CKD patients (CP=30 patients), non-periodontitis and CKD patients (CKD=30 patients), and periodontitis and CKD patients (CKD+CP=30 patients). Demographic variables, periodontal parameters, such as plaque index (PI), gingival index (GI), probing pocket depth (PPD), percentage proportion of sites with probing pocket depth more than 5 mm, clinical attachment loss (CAL), percentage proportion of sites with clinical attachment loss more than 3 mm and serum stress marker, and glutathione peroxidase were compared between the groups and the results were statistically analyzed.Results: The demographic variables did not differ significantly between the groups, except for age. The means PI, GI, PPD, percentage proportion of sites with probing pocket depth more than 5 mm, CAL, percentage proportion of sites with clinical attachment loss were higher in CKD+CP. The glutathione peroxidase was significantly higher in CP group (p=0.001) and significantly correlated with periodontal parameters. Conclusion:The oxidative stress marker glutathione peroxidase was higher in CP, followed by the CKD groups. This could pave a strong link of oxidative stress as a risk factor for chronic periodontitis, as well as chronic kidney disease.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 90%

A Cross-Sectional Study of Serum Glutathione Peroxidase: An Antioxidative Marker in Chronic Periodontitis and Chronic Kidney Disease

Palathingal¹,

Mahendra²,

Annamalai³

et al. 2022

Cureus

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“…This response can be regulated positively or negatively by a number of factors such as local and systemic diseases, medications, systemic hormones, local cytokines including interleukin (IL)-1, IL-6, and IL-10, growth factors, mediators of bone metabolism (RANK) [7, 8], and genetic polymorphisms [9]. Although pathogens are the known etiological agents in peri-implant inflammatory disease, subsequent progression and disease severity can be attributed to differences in the host response to pathogenic microorganisms, as observed in other infectious diseases [10].…”

Section: Introductionmentioning

confidence: 99%

Polymorphisms of Il-10 (-1082) and RANKL (-438) Genes and the Failure of Dental Implants

Ribeiro

Melo

Neto

et al. 2017

International Journal of Dentistry

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Background. Genetic polymorphisms in certain cytokines and chemokines have been investigated to understand why some individuals display implant flaws despite having few risk factors at the time of implant. Purpose. To investigate the association of genetic polymorphisms in interleukin- (IL-) 10 [-1082 region (A/G)] and RANKL [-438 region (A/G)] with the failure of dental implants. Materials and Methods. This study included 90 partially edentulous male and female patients who were rehabilitated with a total of 245 Straumann dental implants. An implant was considered a failure if any of the following occurred: mobility, persistent subjective complaint, recurrent peri-implant infection with suppuration, continuous radiolucency around the implant, probing depth ≥ 5 mm, and bleeding on probing. Buccal mucosal cells were collected for analysis of RANKL438 and IL-10. Results. The implant success rate in this population was 34.4%. The mutant allele (G) in RANKL had an incidence of 52.3% and mutant allele (A) in IL-10 was observed in 37.8%. No statistically significant difference was detected between the failure of the implant and the genotypes and allelic frequencies. Conclusion. No association was detected between the genetic polymorphisms of RANKL (-438) and IL-10 (-1082) and the failure of dental implants in the population studied.

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“…Heterozygosity for Lys3Asn was observed at a higher frequency in CP patients/controls (46/43%) (Wagner et al 2007). No association between polymorphism OPG-223 (C/T) and chronic periodontal disease in a Brazilian population was observed recently by Baioni et al (2008), while Park et al (2008) revealed that the TG haplotype of T950C and G1181C polymorphisms in the OPG gene may be useful genetic markers for the prediction of AP. The previous-mentioned studies have suggested that excess RANKL shifts the balance of bone metabolism in the direction of catabolism and causes periodontal bone resorption.…”

Section: Mechanisms Of Alveolar Bone Destructionmentioning

confidence: 93%

Particular Aspects of Periodontal Disease Pathogenesis

Dumitrescu¹,

Tanaka²

2010

Etiology and Pathogenesis of Periodontal Disease

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Analysis of the association of polymorphism in the osteoprotegerin gene with susceptibility to chronic kidney disease and periodontitis

Cited by 14 publications

References 69 publications

A Cross-Sectional Study of Serum Glutathione Peroxidase: An Antioxidative Marker in Chronic Periodontitis and Chronic Kidney Disease

A Cross-Sectional Study of Serum Glutathione Peroxidase: An Antioxidative Marker in Chronic Periodontitis and Chronic Kidney Disease

Polymorphisms of Il-10 (-1082) and RANKL (-438) Genes and the Failure of Dental Implants

Particular Aspects of Periodontal Disease Pathogenesis

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