Synovium and capsule

Author(s):  
Floris P. J. G. Lafeber ◽  
Nick J. Besselink ◽  
Simon C. Mastbergen

Synovium is an integrated tissue of the diarthrodial joints that interacts with all the other joint tissues and specifically is important in nourishment and lubrication of the articular cartilage, removal of waste products, and immunological surveillance. Chronic as well as recurrent low-grade synovial inflammation definitely contributes to progression and symptoms of certain patients with osteoarthritis. Low-grade inflammation may even be causative in the disease. The challenge is that osteoarthritis is a heterogeneous disorder with inflammation not only of the synovial tissue but with its mediators also present in cartilage and bone. Therefore, despite the presence of inflammatory mediators, in some cases synovitis may be seen as a bystander and not as a driving force in pathogenesis. Future research must be directed toward defining the risk-to-benefit ratio for (systemic) anti-inflammatory therapy, especially when targeting mediators of low-grade inflammation.

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Satoshi Niijima ◽  
Michiaki Nagai ◽  
Satoshi Hoshide ◽  
Mami Takahashi ◽  
Masahisa Shimpo ◽  
...  

Background: Recently, several studies have reported that long sleep duration was independently associated with increased aortic stiffness. On the other hand, high-sensitive C-reactive protein (hs-CRP) was associated with increased aortic stiffness. In this study, the relationships among self-reported sleep duration, hs-CRP and pulse wave velocity (PWV) were investigated in the Japanese at high-risk of cardiovascular disease. In addition, we investigated whether antihypertensive treatment moderated these relationships or not. Methods: Among 4310 patients with one or more cardiovascular risks recruited for the Japan Morning Surge-Home Blood Pressure Study, brachial-ankle PWV and hs-CRP measurement were performed in the 2304 patients (64.7 years old, male 49.6%). A self-administered questionnaire included items on daily sleep duration was used. Results: According to the sleep duration (6h or less,6h to 8h,8h or more per night), significant associations of sleep duration were observed with PWV (1594 vs 1644 vs 1763 cm/s, p<0.0001).In the multiple regression analysis adjustment for confounders including age body mass index, total cholesterol, HbA1c and clinic systolic blood pressure (SBP), long sleep duration (8h or more per night) (B: 29, 95%CI: 1.0-56, p<0.05) and log hs-CRP (B: 25, 95%CI: 3.1-48, p<0.05) were significantly positively associated with PWV. A significant interaction was found between long sleep duration and antihypertensive agent non-use for PWV (p<0.05). Especially, in the group without calcium channel blockers (CCBs), long sleep duration was significantly associated with PWV (p<0.01), while a marginal significant synergetic relationship was observed between long sleep duration and log hs-CRP for PWV (p=0.07). On the other hand, there were no significant interactions between long sleep duration and angiotensin receptor blockers non-use. Conclusions: Long sleep duration and hs-CRP were significant indicators of increased PVW in the high-risk Japanese population. In those without CCBs, long sleep duration served as a strong determinant for arterial stiffness, marginally interacted by low-grade inflammation. CCBs use might be important not to aggravate artery remodeling caused by long sleep duration.


2020 ◽  
Vol 13 ◽  
pp. 117863882097902
Author(s):  
Hunter S Waldman ◽  
Matthew J McAllister

High-stress occupations (ie, firefighters, military personnel, police officers, etc.) are often plagued by cardiometabolic diseases induced by exposure to chronic stressors. Interrupted sleep cycles, poor dietary patterns, lack of physical activity, and smoke exposure along with simultaneous psychological stressors promote chronic low-grade inflammation and excessive oxidative stress. Collectively, these data suggest that practical interventions which might mitigate the underlying pathologies of these cardiometabolic diseases are warranted. Ketones, specifically R-βHB, modulates intracellular signaling cascades such as the cellular redox ratios of NAD+/NADH, the activity of NAD dependent deacetylases SIRT1 and SIRT3, and promotes a robust mitochondrial environment which favors reductions in oxidative stress and inflammation. To date, the literature examining R-βHB as a signaling metabolite has mostly been performed from endogenous R-βHB production achieved through nutritional ketosis or cell culture and mouse models using exogenous R-βHB. To the authors knowledge, only 1 study has attempted to report on the effects of exogenous ketones and the mitigation of oxidative stress/inflammation. Therefore, the scope of this review is to detail the mechanisms of R-βHB as a signaling metabolite and the role that exogenous ketones might play in mitigating diseases in individuals serving in high-stress occupations.


2014 ◽  
pp. 693-704 ◽  
Author(s):  
C. B. O’LEARY ◽  
A. C. HACKNEY

The biosynthesis and metabolism of testosterone and cortisol are altered by the high levels of adipose tissue and the constant state of low-grade inflammation of obesity. Resistance exercise (REx) has become one of the main lifestyle interventions prescribed to obese individuals due to its ability to positively influence body composition and some biomarkers, such as cholesterol and insulin resistance. Yet, little research has been done in obese examining the effects of REx on the testosterone and blood cortisol responses, two integral hormones in both exercise and obesity. The obese testosterone response to REx and whether or not it is blunted compared to lean individuals remains elusive. Conflicting findings concerning the blood cortisol response have also been reported, likely due to variance in REx protocol and the level of obesity in the participants in studies. Comparatively, both of these hormones have been extremely well studied in untrained lean males, which could be used as a basis for future research in obese males. However, without this endocrinological information, it is unknown if the current acute REx prescriptions are appropriate for eliciting a favorable acute endocrinological response, and ultimately, a positive chronic adaptation in obese males.


Nutrients ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 3091
Author(s):  
Matheus Thomaz Nogueira Silva Lima ◽  
Michael Howsam ◽  
Pauline M. Anton ◽  
Carine Delayre-Orthez ◽  
Frédéric J. Tessier

Chronic Low-Grade Inflammation (CLGI) is a non-overt inflammatory state characterized by a continuous activation of inflammation mediators associated with metabolic diseases. It has been linked to the overconsumption of Advanced Glycation End-Products (AGEs), and/or macronutrients which lead to an increase in local and systemic pro-inflammatory biomarkers in humans and animal models. This review provides a summary of research into biomarkers of diet-induced CLGI in murine models, with a focus on AGEs and obesogenic diets, and presents the physiological effects described in the literature. Diet-induced CLGI is associated with metabolic endotoxemia, and/or gut microbiota remodeling in rodents. The mechanisms identified so far are centered on pro-inflammatory axes such as the interaction between AGEs and their main receptor AGEs (RAGE) or increased levels of lipopolysaccharide. The use of murine models has helped to elucidate the local and systemic expression of CLGI mediators. These models have enabled significant advances in identification of diet-induced CLGI biomarkers and resultant physiological effects. Some limitations on the translational (murine → humans) use of biomarkers may arise, but murine models have greatly facilitated the testing of specific dietary components. However, there remains a lack of information at the whole-organism level of organization, as well as a lack of consensus on the best biomarker for use in CLGI studies and recommendations as to future research conclude this review.


2016 ◽  
Vol 101 (11) ◽  
pp. 1043-1047 ◽  
Author(s):  
Kammi K Schmeer ◽  
Aimee Yoon

BackgroundFamily socioeconomic status (SES) is an important source of child health disparities in the USA. Chronic stress is one way SES may impact children's physiology with implications for later health inequalities. These processes may work differently across childhood due to differences in exposure and susceptibility to stressors at different ages. We assess associations between family SES and one biomarker of chronic stress exposure—low-grade inflammation detected by elevated C reactive protein (CRP)—and evaluate differences in the associations by child age.MethodsWe used nationally representative data from the National Health and Nutrition Examination Survey and Tobit regression models to estimate SES associations with CRP and the moderating effects of age for children age 2–18 years. Our sample was limited to CRP ≤10 mg/l to focus on low-grade inflammation (N=13 165).ResultsChildren whose parent had less than a high school degree had 35% higher CRP than those with a college graduate parent; and, poor children had 24% higher CRP than those with high family income, net of controls. When children's body mass index was accounted for, low education and poverty associations were reduced to 19% and 15%, respectively. Child age interactions were negative and significant for both parental education and family income.ConclusionsThis study provides new evidence that SES is associated with low-grade inflammation in children, and that these associations may be particularly strong during early and mid-childhood. Future research should further our understanding of stressors related to low family SES that may lead to immune system dysregulation during childhood.


2020 ◽  
Vol 9 (1) ◽  
Author(s):  
Helena C. Kaltenegger ◽  
Linda Becker ◽  
Nicolas Rohleder ◽  
Dennis Nowak ◽  
Matthias Weigl

Abstract Background With the dynamic advancement of digitalization, working environments are changing and risk for employee stress may be increasing. Work stress has been associated with a dysregulation of inflammatory processes as a component of immune function. Systemic low-grade inflammation is discussed as a key player in the relation between stress exposure and chronic illness, such as cardiovascular diseases. The objective of this investigation will be to evaluate the association of working conditions including digital technology use and systemic inflammation among employees. Methods We designed and registered a study protocol for a systematic review of randomized controlled trials and prospective non-randomized studies (e.g., cohort, interrupted time series, or before-after studies). We will include studies conducted among adult workers reporting associations of working conditions and inflammatory activity. The outcome will be biomarkers of systemic low-grade inflammation on cell, plasma molecule and intracellular level, such as C-reactive protein, or different types of leukocytes, cytokines, etc. Literature searches will be conducted in several electronic databases (from January 1982 onwards), including PubMed/MEDLINE, Embase, PsycINFO, Web of Science, and CENTRAL. Two reviewers will independently screen all retrieved records, full-text articles, and extract data. The study methodological quality (or bias) will be appraised using appropriate tools. Our results will be described qualitatively. Random effects meta-analysis will be conducted, if feasible and appropriate. Additional analyses will be performed to explore potential sources of heterogeneity. Discussion This systematic review and meta-analysis will provide a synthesis of studies evaluating the association of working conditions and systemic inflammation. We anticipate our findings to identify knowledge gaps in the literature that future research should address. Moreover, results of our review may provide implications for corporate and public policy action for employee health promotion and prevention of occupational stress. Systematic review registration PROSPERO ID: CRD42020166887


2021 ◽  
Vol 8 (3) ◽  
pp. 193-201
Author(s):  
Brandt D. Pence ◽  
◽  

<abstract> <p>Aging is the strongest contributor to the development and severity of many chronic and infectious diseases, primarily through age-related increases in low-grade inflammation (inflammaging) and decreases in immune function (immunosenescence). Metabolic reprogramming in immune cells is a significant contributor to functional and phenotypic changes in these cells, but little is known about the direct effect of aging on immunometabolism. This review highlights several recent advances in this field, focusing on mitochondrial dysfunction, NAD+ metabolism, and therapeutic reprogramming in aged monocytes and macrophages. Perspectives on opportunities for future research in this area are also provided. Targeting immunometabolism is a promising strategy for designing therapeutics for a wide variety of age-related diseases.</p> </abstract>


Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 469-P
Author(s):  
MILOS MRAZ ◽  
ANNA CINKAJZLOVA ◽  
ZDENA LACINOVÁ ◽  
JANA KLOUCKOVA ◽  
HELENA KRATOCHVILOVA ◽  
...  

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