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Osteoporosis is a common complication of chronic liver disease that results from an imbalance between bone formation and resorption, leading to decreased bone mass. The mechanisms of bone loss differ depending on the type of liver disease and can involve reduced bone formation and increased resorption. While the exact factors are not fully understood, research has provided insight into potential pathogenic mechanisms involved in liver disease-associated osteoporosis.

Health & Medicine

Contents Prevalence. Introduction: Pathophysiology: Risk factors. 1 2 3 4 5 Key points..

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Osteopenia refers to decreased bone mass. Osteoporosis refers to osteopenia (reduced bone strength/mass) that is severe enough to increase the risk of fracture. According to WHO, osteoporosis is defined as bone mineral density that falls 2.5 standard deviation below mean for young healthy adult of same sex and race. Osteoporosis associated fractures : These are adulthood fractures of any bones (chiefly hip and vertebral fractures) in the setting of trauma less than or equal to fall from standing height with exception of fingers, toes, face and skull. Drugs associated with osteoporosis Alcohol Glucocorticoids Anticoagulants Anticonvulsants Chemotherapy Excess thyroxine Endocrine disorders Cushing syndrome Hyperparathyroidism Thyrotoxicosis Diabetes mellitus (both type I and II) Acromegaly CATEGORIZATION OF OSTEOPOROSIS A.Primary Idiopathic Postmenopausal Senile/age related B. Secondary (Diseases) Hypogonadal state, endocrine disorders, nutritional and gastrointestinal disorders, rheumatologic disorders, hematological disorders/malignancy, inherited disorders and others. Usually asymptomatic until fracture occurs Vertebral and hip fracture common by simple fall Loss of height due to multiple vertebral fracture and other deformities like lordoisis, kyphoscoliosis. Fracture of femur neck, pelvis or spine causes deep vein thrombosis and pulmonary embolism, pneumonia. INVESTIGATIONS FOR OSTEOPOROSIS DXA (Dual energy X-ray absorptiometry) Quantitative CT Ultrasound Urea, creatinine and electrolytes Liver function test and albumin Renal function test Full blood count, ESR Serum calcium and phosphate Serum vitamin D and alkaline phosphate Serum PTH Thyroid function test Testosterone, estrogen and gonadotropins Serum cortisol Bone biopsy Plain radiography not diagnostic Following non pharmacological approaches are taken: Exercise Appropriate calcium and vitamin D intake (Calcium 1000mg/day and vitamin D 800 IU/daily) Cessation of smoking Limit/ Quit alcohol intake Get up and go exercise Hip protectors to reduce the risk of fracture. Pharmacological agents Bisphosphonates ( decrease osteoclast activity) Postmenopausal hormone replacement therapy Denusumab (anti- RANKL antibody) Anti- sclerostin antibodies Cathepsin k antibodies

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The Mechanisms of Treatments for Osteoporosis Heather Drew 05/19/12 The Mechanisms of Treatments for Osteoporosis Heather Drew 05/19/12 Introduction The cost of aging is one debt that we all share. Advances in the fields of healthcare and biomedical research have allowed us to extend our lives as much as is currently possible and yet we still battle with many age-related illnesses. Age is a major risk factor for detrimental morphological changes that the body undergoes as well as the onset of cancer or degenerative diseases (Kohlmeier, Lynn Kohlmeier, 1998). One set of collective physical markers that are indicative of the aging process, frailty, is characterized by the loss and dysfunction of skeletal bone and muscle (Lauretani F et al, 2003). Frailty not only increases the risk of both acute and chronic disease but is also a predictor of mortality. Osteoporosis itself is the manifestation of altered cellular senescence and other age-related factors and contributes greatly to frailty and increased risk of bone fracture. By studying the molecular mechanisms that dictate the cycle of bone formation and resorption, scientists have been able to identify novel methods that may used to counter frailty and ultimately osteoporosis. Background Osteoporosis is an age-related disease of the bone that is characterized by reduced bone mineral density, disruption of the microarchitecture of osseous tissue, and alterations in bone-related proteins (Raisz L, 2005). These changes lead to frailty of the bones and increase the risk of disease and mortality. Osteoporosis occurs when there is a disruption of bone tissue homeostasis, or, the balance between bone resorption and bone formation (Poole KE, Compston JE, 2006). As seen in Figure 1 and Figure 2, this balance largely depends on the development of osteoblasts and osteoclasts. Both cell types are derived from bone marrow progenitors; osteoblasts differentiating from mesenchymal lineage and osteoclasts from hematopoietic cells. The production of such progenitor cells has been shown to be regulated by cytokines (such as interleukin-6 and interleukin-11) as well as sex steroids (such as estrogen). This indicates that both inflammatory response as well as hormonal changes such as menopause may lead to an increased risk of osteoporosis (Raisz L, 2005). In regards to the affect of aging on this cycle, cellular senescence may decrease the ability of the bone marrow to form osteoblast precursors leading to a loss in bone formation and increase in fractures. The large amount and variety of regulatory factors that play key rolls in the homeostasis of bone formation has led to multiple drug targets and therapies that may possibly be able to combat the detrimental effects of osteoporosis. Lining Cells Osteoclasts Osteoblasts Osteocytes Mononuclear Cells Mesenchymal Stem Cells Hematopoietic Stem Cells Fig. 1. Schematic outline of the bone remodeling system. In the bone tissue, osteoclasts play a major role ...

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