The global epidemiology of atopic dermatitis (AD) in the current decade (2009–2019) has not been extensively reported. Epidemiological studies play an important role in presenting the risk factors of AD, as detailed prevalence and incidence data could demonstrate the burden of disease in the population of adults, adolescents, and children in different geographical regions. Thus, the primary objective of this review was to assess and summarize the epidemiological studies of the prevalence and incidence of AD in different age groups, focusing on data from studies published for 2009 to 2019. After a thorough literature search, six countries were identified from African, Asian, and European regions respectively, who published studies on AD. In contrast, only two studies were identified from Australia and New Zealand, three countries from North America and two from South America published AD studies, respectively. The highest prevalence of AD from included studies was noted among Swedish children with 34%, while the lowest prevalence was in Tunisian children with 0.65%; studies reporting incidence data were far less numerous. A common trend in the prevalence of AD was that children would have a higher prevalence as compared to adolescents and adults. The severity and morbidity of the disease showed variance with age, sex, socioeconomic characteristics, geographical location, and ethnicity. Environmental factors played an important role as causative agents in AD. The risk factors that were proven to cause and induce AD were skin barrier impairments due to FLG mutation, changes in the environment, and diet. FLG mutation may impair the skin barrier function by disruption of pH and hydration maintenance of the skin. Lastly, there were only a few studies on the incidence of AD in the 21st century. Therefore, epidemiological studies on childhood and adulthood AD in different continents are still needed, especially on the incidence of AD during adulthood.

Aging is a universal process that can cause diminished function of organs and various diseases. The most striking consequences of aging can be seen visibly on the skin, which acts as a barrier against various external insults. Aging of the skin consists of intrinsic and extrinsic processes that work in concert and influence each other. Intrinsic aging involves biochemical degenerative processes that gradually takes place with age. Extrinsic aging are biochemical processes driven by external influences that lead to aging. There are significant morphological changes at all levels in aged skin that have a profound effect on the characteristics of the skin. Even though skin is subjected to damage by external insults, it is equipped with a healing capability in order to restore its normal structure and function. However, aging has a significant impact on the skin’s healing function by prolonging the inflammatory phase and increasing the production of reactive oxygen species (ROS). This shifts the healing process towards having more protein degradation, which can lead to chronic wound healing with an abundance of complications.

Sclerostin has emerged as an important regulator of bone mass. We have shown that sclerostin can act by targeting late osteoblasts/osteocytes to inhibit bone mineralization and to upregulate osteocyte expression of catabolic factors, resulting in osteocytic osteolysis. Here we sought to examine the effect of exogenous sclerostin on osteocytes in trabecular bone mechanically loaded ex vivo. Bovine trabecular bone cores, with bone marrow removed, were inserted into individual chambers and subjected to daily episodes of dynamic loading. Cores were perfused with either osteogenic media alone or media containing human recombinant sclerostin (rhSCL) (50 ng/ml). Loaded control bone increased in apparent stiffness over time compared with unloaded bone, and this was abrogated in the presence of rhSCL. Loaded bone showed an increase in calcein uptake as a surrogate of mineral accretion, compared with unloaded bone, in which this was substantially inhibited by rhSCL treatment. Sclerostin treatment induced a significant increase in the ionized calcium concentration in the perfusate and the release of β-CTX at several time points, an increased mean osteocyte lacunar size, indicative of osteocytic osteolysis, and the expression of catabolism-related genes. Human primary osteocyte-like cultures treated with rhSCL also released β-CTX from their matrix. These results suggest that osteocytes contribute directly to bone mineral accretion, and to the mechanical properties of bone. Moreover, it appears that sclerostin, acting on osteocytes, can negate this effect by modulating the dimensions of the lacunocanalicular porosity and the composition of the periosteocyte matrix.

Peer reviewed article authored by (Aw MS, Khalid KA, Gulati K, Atkins GJ, Pivonka P, Findlay DM, Losic D). Read article or submit your manuscript for publishing.

Histological Evaluation of Hydroxyapatite Granules with and without Platelet-Rich Plasma versus an Autologous Bone Graft: Comparative study of biomaterials used for spinal fusion in a New Zealand white rabbit model