MATERIALS AND METHODS: A cross-sectional comparative study was performed on subjects from multiple dental centres in Malaysia using a questionnaire covering sociodemographics, OHRQoL using the Malaysian Oral Health Impact Profile questionnaire, OHIP-14(M) and self-reported symptoms. Participants with severe CP were age-and gender-matched with periodontally healthy/mild periodontitis (HMP) participants based on inclusion and exclusion criteria. Full mouth periodontal examination was performed on participants. Outcome measures were OHIP-14(M) prevalence of impact and severity of impact scores.
RESULTS: One hundred and thirty (130) participants comprising 65 severe CP and 65 HMP participants were included in the study. Prevalence of impact on OHRQoL was significantly higher in the severe CP than HMP group, with an odds ratio of 3. Mean OHIP-14(M) score was significantly higher in the severe CP (18.26 ± 10.22) compared to HMP (11.28± 8.09) group. The dimensions of psychological discomfort and functional limitation, and factors such as 'discomfort due to food stuck' and 'felt shy' were impacted more in severe CP compared to HMP group (p < 0.05). When compared with the HMP group, generalised severe CP participants showed higher prevalence of impact on OHRQoL [OR=5] (p < 0.05) compared to localised severe CP [OR=2] (p = 0.05). Participants who had experienced self-reported symptoms had statistically significant impacts on OHRQoL.
CONCLUSIONS: Severe CP had a greater impact on OHRQoL compared to HMP. Impacts were mainly for functional limitation and psychological discomfort dimensions. When considering extent of disease, the impact on OHRQoL was mostly in generalised severe CP subgroup.
MATERIALS AND METHODS: Gingival tissue samples of healthy (n = 5), PD with RA (n = 5) and PD without RA (n = 5) were collected. Specimens were formalin fixed, paraffin embedded and sectioned at 4 μm. The tissue sections were analysed for the presence of citrullinated and carbamylated proteins by immunohistochemistry. Semi-quantitative analysis was performed to quantify and compare the protein abundance between groups.
RESULTS: The number of cells containing citrullinated and carbamylated proteins with higher intensity was markedly increased in gingival tissues from PD with or without RA in comparison with healthy controls.
CONCLUSION: Inflamed gingival tissue is a potential source of citrullinated and carbamylated proteins other than synovial tissues. The extent to which the local accumulation of these proteins contributes to the pathogenesis of RA needs further elucidation.
CLINICAL RELEVANCE: If PD is a potential source of post-translationally modified proteins, untreated PD should not be taken lightly in the context of RA. Hence, addressing gingival inflammation should be viewed as an important preventive measure in the general population not only for the progression of periodontal disease but also reducing the risk of developing extra-oral comorbidities.
METHODS: Subjects from dental and RA clinics were screened. Complete periodontal examinations were performed. Subjects were divided into 4 groups: RA-PD, RA, PD and healthy controls (HC). Questionnaires on characteristics and Malaysian versions of Oral Health Impact Profile (OHIP-14(M)) and Health Assessment Questionnaire (HAQ-DI)) were answered.
RESULTS: A total of 187 subjects were included (29 RA-PD, 58 RA, 43 PD and 57 HC). OHIP-14(M) severity score was highest in the PD group (17.23 ± 10.36) but only significantly higher than the HC group (p
METHODS: Full mouth periodontal examination (probing pocket depth, clinical attachment levels, gingival bleeding index, visual plaque index) was conducted and serum samples obtained from 80 participants comprising RA, Pd, both RA and Pd (RAPd) and healthy individuals (HC). Erythrocyte sedimentation rates (ESR) and periodontal inflamed surface area (PISA) were obtained. Serum samples were analysed for ACPA quantification using enzyme-linked immunosorbent assay (ELISA).
RESULTS: Median levels (IU/mL) of ACPA (interquartile range, IQR) in RAPd, RA, Pd and HC groups were 118.58(274.51), 102.02(252.89), 78.48(132.6) and 51.67(91.31) respectively. ACPA levels were significantly higher in RAPd and RA as compared to HC group (p RA > Pd > HC. However, lack of any significant correlation between the serum ACPA levels with the clinical Pd and RA parameters warrants further studies to investigate the causal link between RA and Pd for such a trend. Further studies involving more inflammatory biomarkers might be useful to establish the causal link between Pd in the development and progression of RA or vice versa.