Journal of Bone Research and Reports

Description

Patients with HIV now live longer and have better quality of life, but they are more likely to develop chronic conditions like osteoporosis. The high pervasiveness of bone demineralization among more youthful and more seasoned HIV contaminated patients has been portrayed in different examinations and deficiency of bone mineral thickness is related with expanded paces of bone fractures. The most widely recognized breaks are those of the vertebrae, hip and wrist. Mortality rates have also increased following vertebral fractures, which cause significant complications such as back pain, height loss, and kyphosis. The management of a hip fracture almost always necessitates major surgical intervention, and mortality rates can be as high as 30% in the first year alone. Therefore, HIV/AIDS patients' future health depends on early detection and treatment of osteopenia/osteoporosis. Low muscle strength, decreased walking speed, weight loss, a lack of physical activity, and falls and fractures are all symptoms of frailty, a major geriatric syndrome. It is more common in older people and raises the risk of negative health outcomes like reduced quality of life, disability, recurrent hospitalizations, and death.

Endocrine Disrupting Chemicals

Reliably, studies have examined a hypothetical connection between sarcopenia, an age related decline in muscle strength and mass, and the mind boggling pathogenesis of fragility and its significant results However, the literature has not been able to determine whether this association is limited to muscle mass or strength. Individually, sarcopenia and severe osteoporosis/osteoporosis were associated with frailty in community-dwelling elderly women, but neither of these associations reached statistical significance. On the other hand, the likelihood of frailty was significantly increased when sarcopenia and severe osteopenia/osteoporosis were present. Antiresorptive medications are still the primary treatment for osteoporosis. Recombinant Lingzhi-8 ability to inhibit osteoclast in vitro and bone resorption in vivo was the subject of this study. Osteopenia and osteoporosis are more common in HIV-infected patients, making them a major global public health issue. Fragility fractures caused by osteoporosis are also common. It is still up for debate whether antiretroviral therapy leads to a decrease in Bone Mineral Density (BMD), and there are only a few studies on women.

The connection between BMD and antiretroviral treatment is examined in this cross-sectional study of HIV-infected women before they reach menopause. By lowering morbidity and mortality, highly active antiretroviral therapy  has significantly improved HIV-infected patients' outcomes. However, a number of metabolic abnormalities, including lipodystrophy, hypertriglyceridemia, hypercholesterolemia, diabetes mellitus, osteopenia, osteoporosis, and osteonecrosis, are linked to the continued use of these treatments. Bone Mineral Density (BMD) loss's pathogenic mechanisms are still poorly understood. BMD loss may be caused by HIV alone, according to a number of studies. It is still up for debate, and BMD loss may be influenced by Protease Inhibitors (PI).Lipodystrophy and BMD loss have been linked, but the connection is also contentious. Fractures with fragility result in significant costs to society, both directly and indirectly, as well as a decline in quality of life. The most predictable side effect of this anti-inflammatory is secondary osteoporosis caused by glucocorticoids. By interfering with Wnt/-catenin signalling, glucocorticoids are one of the primary mechanisms by which they cause such negative effects on bone.

Antisclerostin Antibodies

The main negative regulator of the Wnt signalling pathways proformative and antiresorptive roles in the skeleton is sclerostin, which is encoded by the Sost gene. It was hypothesized that high endogenous glucocorticoid levels would cause osteopenia if genetic manipulation partially inactivated sclerostin function. The effects on bone mass and structure were examined by crossing Sost-deficient mice with an established mouse model of excessive glucocorticoids. High glucocorticoid levels led to low bone mass, which was not remedied by sost haploinsufficiency. Intriguingly, sporadic, sudden, unprovoked, and non-convulsive death was the primary symptom of glucocorticoid excess and Sost deficiency. Peracute hemopericardium and cardiac tamponade were found to be the cause after extensive histopathological examination of a variety of tissues. Results from these preclinical studies are directly applicable to on-going clinical trials looking into the use of antisclerostin antibodies to treat osteoporosis. They specifically draw attention to the possibility of an increased cardiovascular risk and may help improve the classification of patients who might otherwise benefit from treatment with antisclerostin antibodies. The adrenal glands produce and secrete glucocorticoids, which are anti-inflammatory molecules that have a significant impact on the physiological functioning of several systems, including stress adaptation, metabolism, and immune response regulation. The hypothalamic–pituitary–adrenal axis, which is influenced by numerous factors such as neuro-inflammation, physical stress, circadian rhythm, and negative feedback, is the GCs' signalling axis.

GC-Induced Osteoporosis (GIO) is the most predictable side effect and the most common cause of secondary osteoporosis. The suppression of bone formation is central to the pathogenesis of GIO. Osteocytes are the other key players in GIO because GCs induce their apoptosis. This is likely achieved by the GC-mediated disruption of the osteocyte–lacunar–canalicular network, essential for osteocyte viability and maintenance of the bone's material properties. These changes may explain the impairment of the biomechanical properties in the surrounding bone16 and may account for the loss of bone strength that occurs before the loss of bone mineral density. Oste Endocrine Disrupting Chemicals (EDCs) are linked to this disease, which is very common in industrialized regions. One of these EDCs is di isononyl phthalate, which is mostly used as a plasticizer in flexible PVC products. Despite the fact that exposure to DINP is known to be harmful to humans, there have been no studies on how it affects osteopenia.