Sex Differences in Destructive Periodontal Disease: Exploring the Biologic Basis

“…In the periodontal literature, it has been shown that males are more prone to periodontal infection than females (22). Elevation of LPS binding protein, CD14 and TLR-4 in males, was noted as a plausible explanation for the gender difference (23). …”

Section: Discussionmentioning

confidence: 99%

Sexual Dimorphism in Periapical Inflammation and Bone Loss from Mitogen-activated Protein Kinase Phosphatase-1 Deficient Mice

McAbee¹,

Li²,

Yu³

et al. 2012

Journal of Endodontics

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Introduction Mitogen Activating Protein (MAPK) kinase phosphatase-1 (MKP-1) has been shown to be a key negative regulator of the MAP kinase pathways of the innate immune system. The impact of MKP-1 in an endodontic model has yet to be studied. Thus, the purpose of this study was to determine the role of MKP-1 in a bacterial-driven model of pathological endodontic bone loss. Methods Pulps were exposed in both lower 1st molars of 10-week old mkp-1+/+ and mkp-1−/− mice and left open to the oral environment for either 3 or 8 weeks. At sacrifice, mandibles were harvested and scanned by microcomputed tomography (μCT) to determine periapical bone loss. Histopathological scoring was then performed on the samples to determine the amount of inflammatory infiltrate within the periapical microenvironment. Results Significant bone loss and inflammatory infiltrate were found in all experimental groups when compared to control. No statistical difference was found between mkp-1+/+ and mkp-1−/− at either time point with respect to bone loss or inflammatory infiltrate. At 8 weeks, male mkp-1−/− mice were found to have significantly more bone loss and inflammatory infiltrate when compared to female mkp-1−/− mice. There was also a significant correlation between an increase in bone loss and increase in inflammatory infiltrate. Conclusions A sexual dimorphism exists in the periapical inflammatory process, where male mkp-1−/− mice have more inflammation than female mkp-1−/− mice. The increase in inflammatory infiltrate correlates to more bone loss in the male mice.

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“…In smokers it was reported early onset of disease (7, 8) and increased rates of disease progression (9). Furthermore, clinical investigations have demonstrated that cigarette smoking may hamper the healing outcome following surgical and nonsurgical periodontal therapy (10, 11).…”

Section: Introductionmentioning

confidence: 99%

Comparative Analysis of Smoking Influence on Periodontal Tissue in Subjects with Periodontal Disease

Petrović

Kesić²,

Obradoviç³

et al. 2013

Mater Sociomed

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The aim of the study:The aim of the study was clinical and cytological examination of gingival changes in smokers and non-smokers. Further, specific goals of this study were health promotion in patient, particularly in smokers.Methods:The anamnesis was taken and clinical examination was conducted on the patients who came on Dental Clinic. During the clinical examination, plaque index (Pl)16, gingival index Löe-Silness (Gi) and the community periodontal index of treatment needs (CPITN)17 were done. After diagnosis was established, participants divided into group I –smokers, and group II – non-smokers. The gingival smears were taken for cytological analysis, dried on air, and stained by haematoxylin-eosin method.Results:The values of gingival index (GI)- Löe-Silness and periodontal index (CPITN) were higher in the group of smokers, but plaque index was also higher with statistically significant difference of their values between examined group, with maximum level of significance (p<0,001). The size of nucleus (area, Ferret’s diameter and perimeter) was higher in the group of smokers, but differences were not statistically significant. In the group of non-smokers density of nucleus was higher than in non-smokers group, but difference was not statistically significant.Conclusion:The values of examined indices showed higher values in smokers group. This finding could show that the level of oral hygiene is higher in the non smokers group. The size of nucleus (area, Ferret’s diameter and perimeter) was higher in the group of smokers, but differences were not statistically significant. Teamwork of many different speciality experts is required for better periodontal health of smokers.

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Sex Differences in Destructive Periodontal Disease: Exploring the Biologic Basis

Abstract: Differential gene regulation, particularly in sex steroid-responsive genes, may contribute to a sexual dimorphism in susceptibility to destructive periodontal disease.

Cited by 94 publications

References 169 publications

Association of periodontitis with insulin resistance, β-cell function, and impaired fasting glucose before onset of diabetes

Association of periodontitis with insulin resistance, β-cell function, and impaired fasting glucose before onset of diabetes

Sexual Dimorphism in Periapical Inflammation and Bone Loss from Mitogen-activated Protein Kinase Phosphatase-1 Deficient Mice

Comparative Analysis of Smoking Influence on Periodontal Tissue in Subjects with Periodontal Disease

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Sex Differences in Destructive Periodontal Disease: Exploring the Biologic Basis

Abstract: Differential gene regulation, particularly in sex steroid-responsive genes, may contribute to a sexual dimorphism in susceptibility to destructive periodontal disease.

Cited by 94 publications

References 169 publications

Association of periodontitis with insulin resistance, &beta;-cell function, and impaired fasting glucose before onset of diabetes

Association of periodontitis with insulin resistance, &beta;-cell function, and impaired fasting glucose before onset of diabetes

Sexual Dimorphism in Periapical Inflammation and Bone Loss from Mitogen-activated Protein Kinase Phosphatase-1 Deficient Mice

Comparative Analysis of Smoking Influence on Periodontal Tissue in Subjects with Periodontal Disease

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Product

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Association of periodontitis with insulin resistance, β-cell function, and impaired fasting glucose before onset of diabetes

Association of periodontitis with insulin resistance, β-cell function, and impaired fasting glucose before onset of diabetes