scholarly journals Osteoporosis in Skin Diseases

2020 ◽  
Vol 21 (13) ◽  
pp. 4749 ◽  
Author(s):  
Maria Maddalena Sirufo ◽  
Francesca De Pietro ◽  
Enrica Maria Bassino ◽  
Lia Ginaldi ◽  
Massimo De Martinis
Keyword(s):  
Bone Resorption ◽  
Bone Formation ◽  
Skin Diseases ◽  
Public Health Problem ◽  
Bone Fragility ◽  
Skeletal Disease ◽  
Metabolic Bone ◽  
Systemic Treatments ◽  
Increased Risk ◽  
Skeletal Homeostasis

Osteoporosis (OP) is defined as a generalized skeletal disease characterized by low bone mass and an alteration of the microarchitecture that lead to an increase in bone fragility and, therefore, an increased risk of fractures. It must be considered today as a true public health problem and the most widespread metabolic bone disease that affects more than 200 million people worldwide. Under physiological conditions, there is a balance between bone formation and bone resorption necessary for skeletal homeostasis. In pathological situations, this balance is altered in favor of osteoclast (OC)-mediated bone resorption. During chronic inflammation, the balance between bone formation and bone resorption may be considerably affected, contributing to a net prevalence of osteoclastogenesis. Skin diseases are the fourth cause of human disease in the world, affecting approximately one third of the world’s population with a prevalence in elderly men. Inflammation and the various associated cytokine patterns are the basis of both osteoporosis and most skin pathologies. Moreover, dermatological patients also undergo local or systemic treatments with glucocorticoids and immunosuppressants that could increase the risk of osteoporosis. Therefore, particular attention should be paid to bone health in these patients. The purpose of the present review is to take stock of the knowledge in this still quite unexplored field, despite the frequency of such conditions in clinical practice.

scholarly journals Osteoblasts in osteoporosis: past, emerging, and future anabolic targets

2011 ◽  
Vol 165 (1) ◽  
pp. 1-10 ◽  
Author(s):  
Pierre J Marie ◽  
Moustapha Kassem
Keyword(s):  
Bone Resorption ◽  
Bone Loss ◽  
Bone Formation ◽  
Bone Matrix ◽  
Bone Fragility ◽  
Osteoblastic Cell ◽  
Medline Search ◽  
Cell Functions ◽  
Age Related ◽  
Increased Risk

ObjectiveAge-related bone loss is associated with significant changes in bone remodeling characterized by decreased trabecular and periosteal bone formation relative to bone resorption, resulting in bone fragility and increased risk of fractures. Prevention or reversal of age-related decrease in bone mass and increase in bone fragility has been based on inhibition of bone resorption using anticatabolic drugs. The current challenge is to promote osteoblastogenesis and bone formation to prevent age-related bone deterioration.MethodsA limited number of approved therapeutic molecules are available to activate bone formation. Therefore, there is a need for anabolic drugs that promote bone matrix apposition at the endosteal, endocortical, and periosteal envelopes by increasing the number of osteoblast precursor cells and/or the function of mature osteoblasts. In this study, we review current therapeutics promoting bone formation and anabolic molecules targeting signaling pathways involved in osteoblastogenesis, based on selected full-text articles searched on Medline search from 1990 to 2010.Results and discussionWe present current therapeutic approaches focused on intermittent parathyroid hormone and Wnt signaling agonists/antagonists. We also discuss novel approaches for prevention and treatment of defective bone formation and bone loss associated with aging and osteoporosis. These strategies targeting osteoblastic cell functions may prove to be useful in promoting bone formation and improving bone strength in the aging population.

scholarly journals Relation of Sociodemographics and Personal Hygiene on Different Childhood Dermatoses

2015 ◽  
Vol 13 (1) ◽  
pp. 29-33
Author(s):  
E Gauchan ◽  
A Kumar ◽  
G BK ◽  
P Thapa ◽  
J Pun
Keyword(s):  
Socioeconomic Status ◽  
Low Socioeconomic Status ◽  
Skin Disease ◽  
Skin Diseases ◽  
Public Health Problem ◽  
Personal Hygiene ◽  
Cross Sectional ◽  
Dermatology Department ◽  
Low Socioeconomic ◽  
Increased Risk

Background Skin diseases in children contribute to significant morbidity and psychological distress. Infective dermatoses are one of the major dermatoses in children. Low socioeconomic status, overcrowding and poor personal hygiene has been linked to skin diseases.Objective To find out the prevalence of infectious skin disease in children, rate of transmissible skin disease and association of sociodemographic factors and personal hygiene on infective childhood dermatoses.Method This was a cross-sectional study conducted in the Pediatric and Dermatology Department, Manipal Teaching Hospital, Pokhara, Nepal. A total of 226 patients were examined over a period of one year. Relation of sociodemographics, crowding and personal hygiene on skin disease were assessed.Result The most common category was Infections and Infestations (51.3%) followed by Dermatitis (27.9%) . Transmissible skin disease was seen in 49.6%. Low socioeconomic status and overcrowding were associated with increased risk for infective dermatoses.Conclusion Skin disease in children constitutes a public health problem. Improving the socioeconomic status and personal hygiene can help to reduce the incidence of skin disease in children.Kathmandu University Medical Journal Vol.13(1) 2015; 29-33

scholarly journals Cortical bone adaptation and mineral mobilization in the subterranean mammalBathyergus suillus(Rodentia: Bathyergidae): effects of age and sex

PeerJ ◽  
2018 ◽  
Vol 6 ◽  
pp. e4944 ◽  
Author(s):  
Germán Montoya-Sanhueza ◽  
Anusuya Chinsamy
Keyword(s):  
Bone Resorption ◽  
Bone Loss ◽  
Bone Formation ◽  
Strong Support ◽  
Bone Adaptation ◽  
Medullary Cavity ◽  
Bone Modeling ◽  
Terrestrial Mammals ◽  
Skeletal Homeostasis ◽  
Subterranean Mammal

The patterns of bone modeling and mineral mobilization (skeletal homeostasis) among mammals other than humans and laboratory rodents are still poorly known. In this study we assessed the pattern of bone formation and bone resorption in the femur of a wild population of Cape dune molerats,Bathyergus suillus(n= 41) (Bathyergidae), a solitary subterranean mammal with a marked extended longevity among rodents, and which also lives in a naturally deficient state of vitamin D. In order to determine ontogenetic and sex effects on histomorphometric parameters of transversal undecalcified bone sections, two-way ANOVA, linear mixed-effects model and regression statistical analyses were performed. During ontogeny,B. suillusincreased their cross sectional area, cortical area and cortical thickness, and most importantly, they showed scarce endosteal bone resorption which resulted in a retained medullary cavity size during ontogeny. This resulted in a positively imbalanced bone modeling, where bone formation considerably surpasses bone loss by almost 100-fold in adulthood. This differs markedly from other terrestrial mammals with relatively thin cortical walls. Regarding bone loss and remodeling, three main processes involving intracortical resorption were observed: modeling-related bone loss in early postnatal growth; secondary osteon formation occurring in both sexes; and subendosteal secondary reconstruction observed only in females. The latter is accompanied by females having six-fold more relative bone loss than males, which is evidenced by the development of enlarged resorption cavities (RCs) distributed circumferentially around the medullary cavity. Males have smaller, more circular and randomly distributed RCs. In general, our data indicate no age-related decline in mineral content inB. suillus, and provides strong support for a pattern of sexual dimorphism in skeletal homeostasis, similar to that occurring in humans and other mammals, with females losing more bone throughout aging as compared to males due to reproductive factors. Interestingly as well, despite the high mechanical loads experienced during burrow construction, bone remodeling inB. suillusis kept at very low levels throughout their lifespan, and dense Haversian tissue never forms. This study represents the first comprehensive assessment of skeletal homeostasis in a subterranean mammal, and it enables a better understanding of the complex processes governing the acquisition and maintenance of bone properties in this species with extraordinary fossorial adaptations.

The effect of monthly ibandronate on bone mineral density and bone turnover markers in patients with haemophilia A and B and increased risk for fracture

2013 ◽  
Vol 110 (08) ◽  
pp. 257-263 ◽  
Author(s):  
Timoleon-Achilleas Vyzantiadis ◽  
Maria Charizopoulou ◽  
Fotini Adamidou ◽  
Spyridon Karras ◽  
Dimitrios Goulis ◽  
...  
Keyword(s):  
Bone Mineral Density ◽  
Bone Resorption ◽  
Bone Formation ◽  
Bone Mineral ◽  
Tartrate Resistant Acid Phosphatase ◽  
Haemophilia A ◽  
Mineral Density ◽  
Risk Of Fracture ◽  
Increased Risk ◽  
Turnover Markers

SummaryHaemophilia A and B have been associated with increased prevalence of low bone mineral density (BMD). However, no study has so far evaluated the effects of anti-osteoporotic therapy on BMD in haemophilia. The primary endpoint of this prospective study was to estimate the effect of 12-month therapy of oral ibandronate 150 mg/ month on BMD in patients with haemophilia A and B. Secondary endpoint was its effect on turnover markers (BTM) of bone resorption [serum C-terminal telopeptide of type 1 collagen (sCTX), tartrate-resistant acid phosphatase band 5b] and bone formation (osteocalcin and bone-specific alkaline phosphatase. Ten adult patients with T-score < −2.5 SD or Z-score < −2 and/or increased risk of fracture according to FRAX model were included. All received 1,000 mg/day calcium carbonate with 800 IU/d cholecalciferol. Males with haemophilia A (n=7) or B (n=3) (mean age 43.5 ± 13.5 years) were studied. Ibandronate resulted in an increase in lumbar BMD (from 0.886 ± 0.169 to 0.927 ± 0.176 g/cm2, 4.7%, p=0.004). No change in BMD of total hip (from 0.717 ± 0.128 to 0.729 ± 0.153 g/cm2, p=0.963) or femoral neck (0.741 ± 0.135 to 0.761 ± 0.146 g/cm2, p=0.952) was noticed. Ibandronate led to a decrease in sCTX (from 0.520 ± 0.243 to 0.347 ± 0.230 ng/ml, −29.9%, p=0.042). No change was observed in other BTM. Ibandronate was generally well-tolerated. In conclusion, ibandronate significantly improved BMD in lumbar spine and reduced bone resorption in adults with haemophilia at increased risk of fracture. Its effect on hip BMD and bone formation markers was not significant.

scholarly journals A pragmatic window of opportunity to minimise the risk of MRONJ development in individuals with osteoporosis on Denosumab therapy: a hypothesis

2021 ◽  
Vol 17 (1) ◽  
Author(s):  
Giuseppina Campisi ◽  
Rodolfo Mauceri ◽  
Francesco Bertoldo ◽  
Vittorio Fusco ◽  
Alberto Bedogni
Keyword(s):  
Tooth Extraction ◽  
Oral Surgery ◽  
Metastatic Cancer ◽  
Bone Fragility ◽  
Osteonecrosis Of The Jaw ◽  
Time Interval ◽  
Dental Surgery ◽  
Metabolic Bone ◽  
Increased Risk

Abstract Denosumab is associated with the development of medication-related osteonecrosis of the jaw (MRONJ), an uncommon but severe oral side effect with a higher prevalence in metastatic cancer patients than in patients with metabolic bone fragility. Although several oral triggers can initiate MRONJ, invasive oral treatments and tooth extraction still remain the most common precipitating event. In general, tooth extraction and oral surgery should be avoided in patients at increased risk of MRONJ, while extraction of non-restorable teeth should be performed based on specific risk reduction protocols to eliminate dental/periodontal infections, still protecting from MRONJ onset. Based on the different pharmacological activity of denosumab and nitrogen-containing bisphosphonates, it is likely that the MRONJ risk profile of patients with osteoporosis could somewhat vary. We hypothesize the chance to maximize the pharmacokinetic of denosumab 60 mg (Prolia®) and identify a time interval in which invasive oral treatments can ideally take place without restrictions in patients with metabolic bone fragility, We propose that dental surgery (e.g. tooth extraction) may be safely performed without additional intra or peri-operative procedures in osteoporosis patients using denosumab provided that careful case selection, adequate communication among specialists, planning of a delayed dosing window (1-month deferral) and rigorous postoperative follow-up are granted. Graphical abstract

scholarly journals PTH Protects Osteocytes From Oxidative Stress and Cellular Senescence

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A239-A239
Author(s):  
Yuhei Uda ◽  
Roberto Santos ◽  
Alejandro Kochen ◽  
Carly Newell ◽  
Tim Y Huang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Bone Resorption ◽  
Bone Loss ◽  
Bone Formation ◽  
Cellular Senescence ◽  
Intracellular Ros ◽  
Antioxidant Function ◽  
Skeletal Homeostasis ◽  
In Cells

Abstract Age-induced osteoporosis is characterized by a progressive decline in bone formation and increase in bone resorption with uncoupled activities of osteoblasts and osteoclasts. Parathyroid hormone (PTH) is used in the clinic to treat osteoporosis due to its anabolic actions on bone via binding to the PTH receptor (PPR). The receptor is highly expressed in cells of the osteoblastic lineage, including osteocytes. Osteocytes are the most abundant cells in bone and serve as a key regulator of bone remodeling. Despite the significant role of PPR signaling in skeletal homeostasis, its function in osteocytes during aging remains unclear. We have gathered preliminary data demonstrating that mice lacking PPR predominantly in osteocytes (Dmp1-PPRKO) have marked age-induced bone loss due to increased bone resorption and suppressed bone formation. These mice, with aging, develop characteristics of skeletal senescence: a decrease in osteoprogenitors and an increase in bone marrow adiposity and p16Ink4a/Cdkn2a expression in bone. Since senescence of cells in the bone microenvironment has been reported as a cause of age-induced bone loss, we hypothesized that PPR signaling protects osteocytes from senescence. To test this hypothesis, we generated osteocytes (Ocy454-12H), in which the PPR expression was ablated using CRISPR/Cas9 technique. Ocy454-12H-PPRKO and Ocy454-12H-PPRCtrl cells were treated with PTH followed by an exposure to hydrogen peroxide (H2O2). High levels of intracellular reactive oxygen species (ROS), including H2O2, promote protein and DNA oxidation, resulting in cell death and senescence. PTH treatment significantly suppressed the increase in H2O2-induced cell death, measured by resazurin-based assays, in PPRCtrl but not in PPRKO cells. We analyzed intracellular ROS levels using a fluorescent probe and found that PTH treatment significantly suppressed the increase in ROS upon H2O2 exposure, suggesting an antioxidant function of PTH in osteocytes. To further investigate if PTH prevents osteocytes from oxidative stress-induced senescence, we examined senescence-associated β-galactosidase (SA β-gal) activity in cells that were treated with PTH followed by an exposure to low doses of H2O2. Compared to untreated and PPRKO groups, treatment with PTH significantly decreased the number of SA β-gal positive cells, demonstrating that PPR signaling protects osteocytes, and possibly other osteoblastic cells, from H2O2-induced cellular senescence. PTH treatment reduced mRNA expression of p21/Cdkn1a. Taken together these results demonstrate that PPR signaling is important to protect osteocytes from cellular senescence.

scholarly journals Osteoporosis and the Potential of Cell-Based Therapeutic Strategies

2020 ◽  
Vol 21 (5) ◽  
pp. 1653 ◽  
Author(s):  
Iratxe Macías ◽  
Natividad Alcorta-Sevillano ◽  
Clara I. Rodríguez ◽  
Arantza Infante
Keyword(s):  
Metabolic Bone Disease ◽  
Public Health Problem ◽  
Bone Fragility ◽  
Molecular Evidence ◽  
Major Public Health Problem ◽  
Low Bone Mass ◽  
Metabolic Bone ◽  
Decrease Bone Resorption ◽  
Potential Use

Osteoporosis, the most common chronic metabolic bone disease, is characterized by low bone mass and increased bone fragility. Nowadays more than 200 million individuals are suffering from osteoporosis and still the number of affected people is dramatically increasing due to an aging population and longer life, representing a major public health problem. Current osteoporosis treatments are mainly designed to decrease bone resorption, presenting serious adverse effects that limit their safety for long-term use. Numerous studies with mesenchymal stem cells (MSCs) have helped to increase the knowledge regarding the mechanisms that underlie the progression of osteoporosis. Emerging clinical and molecular evidence suggests that inflammation exerts a significant influence on bone turnover, thereby on osteoporosis. In this regard, MSCs have proven to possess broad immunoregulatory capabilities, modulating both adaptive and innate immunity. Here, we will discuss the role that MSCs play in the etiopathology of osteoporosis and their potential use for the treatment of this disease.

scholarly journals The roles of miRNA, lncRNA and circRNA in the development of osteoporosis

2020 ◽  
Vol 53 (1) ◽  
Author(s):  
Yang Yang ◽  
Wang Yujiao ◽  
Wang Fang ◽  
Yuan Linhui ◽  
Guo Ziqi ◽  
...  
Keyword(s):  
Environmental Factors ◽  
Bone Fragility ◽  
Circular Rnas ◽  
Therapeutic Approaches ◽  
Control Of Gene Expression ◽  
Metabolic Bone ◽  
Increased Risk ◽  
Non Coding Rnas ◽  
Genetic And Environmental Factors

Abstract Osteoporosis is a common metabolic bone disease, influenced by genetic and environmental factors, that increases bone fragility and fracture risk and, therefore, has a serious adverse effect on the quality of life of patients. However, epigenetic mechanisms involved in the development of osteoporosis remain unclear. There is accumulating evidence that epigenetic modifications may represent mechanisms underlying the links of genetic and environmental factors with increased risk of osteoporosis and bone fracture. Some RNAs, such as microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), have been shown to be epigenetic regulators with significant involvement in the control of gene expression, affecting multiple biological processes, including bone metabolism. This review summarizes the results of recent studies on the mechanisms of miRNA-, lncRNA-, and circRNA-mediated osteoporosis associated with osteoblasts and osteoclasts. Deeper insights into the roles of these three classes of RNA in osteoporosis could provide unique opportunities for developing novel diagnostic and therapeutic approaches to this disease.

scholarly journals Effects of Incretin-Related Diabetes Drugs on Bone Formation and Bone Resorption

2021 ◽  
Vol 22 (12) ◽  
pp. 6578
Author(s):  
Hideki Kitaura ◽  
Saika Ogawa ◽  
Fumitoshi Ohori ◽  
Takahiro Noguchi ◽  
Aseel Marahleh ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Bone Resorption ◽  
Bone Formation ◽  
Current Knowledge ◽  
Osteoclast Differentiation ◽  
Glucose Absorption ◽  
Dipeptidyl Peptidase 4 ◽  
Increased Risk ◽  
Glucagon Like Peptide 1

Patients with type 2 diabetes have an increased risk of fracture compared to the general population. Glucose absorption is accelerated by incretin hormones, which induce insulin secretion from the pancreas. The level of the incretin hormone, glucagon-like peptide-1 (GLP-1), shows an immediate postprandial increase, and the circulating level of intact GLP-1 is reduced rapidly by dipeptidyl peptidase-4 (DPP-4)-mediated inactivation. Therefore, GLP-1 receptor agonists and DPP-4 inhibitors are effective in the treatment of type 2 diabetes. However, these incretin-related diabetic agents have been reported to affect bone metabolism, including bone formation and resorption. These agents enhance the expression of bone markers, and have been applied to improve bone quality and bone density. In addition, they have been reported to suppress chronic inflammation and reduce the levels of inflammatory cytokine expression. Previously, we reported that these incretin-related agents inhibited both the expression of inflammatory cytokines and inflammation-induced bone resorption. This review presents an overview of current knowledge regarding the effects of incretin-related diabetes drugs on osteoblast differentiation and bone formation as well as osteoclast differentiation and bone resorption. The mechanisms by which incretin-related diabetes drugs regulate bone formation and bone resorption are also discussed.

scholarly journals Changes in Bone Metabolism and Structure in Primary Hyperparathyroidism

2020 ◽  
Vol 47 (4) ◽  
pp. 75-80
Author(s):  
I. Yankova ◽  
A. Shinkov ◽  
R. Kovatcheva
Keyword(s):  
Bone Resorption ◽  
Primary Hyperparathyroidism ◽  
Bone Formation ◽  
Bone Metabolism ◽  
Cortical Bone ◽  
Mineral Density ◽  
Trabecular Microarchitecture ◽  
Duration Of Action ◽  
Increased Risk ◽  
Stimulation Of

AbstractParathyroid hormone (PTH) is a key regulator of bone turnover. Depending on the duration of action, the hormone causes catabolic and anabolic effects by binding with specific receptors (PTHR1) in the bone. Various cells expressing PTHR1 on their surface are involved in the process – osteoblasts, osteocytes, bone marrow stromal cells, T-lymphocytes and macrophages. In physiological conditions PTH balances the bone metabolism. Intermittent pharmacological doses of PTH lead to the prevalence of bone formation and are used in the treatment of osteoporosis. Persistently elevated levels of PTH stimulate bone resorption by impacting mainly the cortical bone. New imaging and analysis techniques show that high PTH levels can also have an adverse effect on trabecular microarchitecture. Primary hyperparathyroidism (PHPT) is a disease characterized by increased bone metabolism, decreased bone mineral density (BMD), inadequate osteoid mineralization and an increased risk of fractures. Prolonged overproduction of PTH leads to stimulation of bone resorption and defects in bone formation, mainly causing loss of cortical bone mass, while in the trabecular bone predominate demineralization processes. One explanation of these findings is the enhanced stimulation of RANKL expression by osteoblasts with decreased OPG expression and bone formation at the same time.

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