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Hand Augmentation Using Injectable Fillers
Published in Neil S. Sadick, Illustrated Manual of Injectable Fillers, 2020
Sachin M. Shridharani, Teri N. Moak, Trina G. Ebersole, Grace M. Tisch
Extrinsic factors of skin aging include sun exposure or photodamage, environmental or chemical exposure, and smoking. These largely manifest in the superficial skin layers of the hand as dyschromia, thinning of the epidermis, and textural changes related to dryness and roughness (1,10). Intrinsic factors of skin aging, however, affect deeper soft tissue planes, causing decreased skin elasticity, loss of collagen, loss of volume, and increased dermal vascularity, resulting in the presence of thinner, lax skin with notable rhytides (1,2). Volume loss is principally the result of fat loss in the hand (10). The progression of lipoatrophy causes a pronounced appearance of underlying hand structures such as veins, tendons, and joints (1,4,10). Bone remodeling and muscle atrophy exacerbate this process, leading to the characteristic skeletonized appearance of the aged hand (4). Other underlying conditions such as rheumatologic disease or skin cancers can accelerate the aged appearance of the hand as well (10).
A screening model for osteoporosis using dermal skin thickness and bone densitometry
Published in Barry G. Wren, Progress in the Management of the Menopause, 2020
M. P. Brincat, R. Galea, Y. Muscat Baron
The quality of bone is not easy to assess, although it can be reliably quantified by measurement of bone density. The diagnosis of osteoporosis and its response to hormone replacement therapy is therefore rather difficult2. Postmenopausal osteoporosis is increasingly considered to be due to accelerated collagen loss3–5, similarly to the effect of the menopause on organs of mesodermal origin (skin dermis, cardiovascular system and bladder trigone). Collagen loss from the skin has been shown to correlate with bone mass6–8. Brincat and co-workers have shown that hormone replacement therapy increases the collagen content in both bone and skin in postmenopausal women, compared with age-matched controls6. Skin thickness, similarly to bone mass and skin collagen, has been shown to increase in postmenopausal women treated with estrogen6,9. The mode of action of hormone replacement therapy in increasing bone mass has not been clearly defined, and the pathology of postmenopausal osteoporotic fracture requires further investigation. Any additional information relating to the quality of bone, rather than simply its quantity, would thereby aid in determining who is likely to have strong bones and therefore less likely to incur fracture.
Infection-driven periodontal disease
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
Thomas E. Van Dyke, Mike Curtis
The early lesion of periodontitis is a more mature leukocyte infiltrate in which neutrophils no longer dominate. The absolute number of neutrophils does not decline, but the main infiltrating cell types are lymphocytes with increasing numbers of lymphoblasts and a few peripheral plasma cells. Mononuclear phagocytes and macrophages also accumulate and maintain a proinflammatory phenotype contributing to the chronicity of the lesion. Collagen loss may reach 80%, and there is loss of fibroblasts and matrix. An exudate forms and flows through the gingival sulcus.
Skin, hair and beyond: the impact of menopause
Published in Climacteric, 2022
C. C. Zouboulis, U. Blume-Peytavi, M. Kosmadaki, E. Roó, D. Vexiau-Robert, D. Kerob, S. R. Goldstein
Skin atrophy due to collagen loss is more pronounced in menopausal women [15–17]. In early menopause, skin collagen levels decrease fairly rapidly with a collagen reduction of approximately 30% in the first 5 years, followed by a further decline of 2% per year for the next 15 years [17]. A steady depletion of collagen and reduced skin thickness with yearly reductions of 2.1% and 1.1%, respectively, was observed in menopausal women [18].
Vitamin D deficiency and its relationship with cardiac iron and function in patients with transfusion-dependent thalassemia at Chiang Mai University Hospital
Published in Pediatric Hematology and Oncology, 2018
Prapai Dejkhamron, Karn Wejaphikul, Tuanjit Mahatumarat, Suchaya Silvilairat, Pimlak Charoenkwan, Suwit Saekho, Kevalee Unachak
Cardiac function in patients with thalassemia is relatively complex. Patients with Transfusion-dependent thalassemia usually have a mild chronic anemia despite regular transfusion, subsequently resulting in hyperdynamic circulation characterized by increased cardiac output, increased left ventricular dimensions. Cardiac iron overload is therefore hardly found in isolation, but is part of the complexity.18 Iron overload induces oxidative damage by generating reactive oxygen species and results in mitochondrial dysfunction and heart failure.19 Other causes of cardiac dysfunction in Transfusion-dependent thalassemia are hypothyroidism and nutritional deficiencies, eg, vitamin D, vitamin C, thiamine, carnitine, selenium, zinc deficiencies.20 In our study, hypothyroidism was not identified in these patients (data not shown). Vitamin D deficiency could contribute in an impaired cardiac function since chronic heart failure was also well described in Vitamin D deficiency.21 Vitamin D deficiency also results in increased inflammation and inflammatory cytokines which lead to collagen loss, fibrosis, and further increased oxidative stress.22 This could also be the link between Vitamin D deficiency and cardiac dysfunction in patients with Transfusion-dependent thalassemia. There were conflicting findings regarding vitamin D status and cardiac iron overload. Wood et al reported that Vitamin D deficiency may be associated with increased cardiac iron uptake and ventricular dysfunction in patients with thalassemia major.10 Moreover, Ambarwati et al demonstrated an association between vitamin D and left ventricular function and iron overload in children with thalassemia major.3 However, Noetzli et al tried to reproduce the association between Vitamin D deficiency and cardiac iron status by performing a prospective study three years later. Noetzli et al was not able to replicate the correlations between vitamin D deficiency and cardiac iron and cardiac function.11 Our results were in alignment with this prospective study which did not demonstrate the correlations between vitamin D deficiency and cardiac iron and cardiac function.11 In our study, patients with cardiac iron deposition had tendency for low D-25OH; however, the correlation between D-25OH and cardiac function was not identified. This could be due to the multifactorial effects on cardiac function in patients with thalassemia.