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    Fast Facts: Postmenopausal Osteoporosis
    Fast Facts: Postmenopausal Osteoporosis
    Fast Facts: Postmenopausal Osteoporosis
    Ebook86 pages47 minutes

    Fast Facts: Postmenopausal Osteoporosis

    By E. Dennison and M. Clynes

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    About this ebook

    Fractures resulting from osteoporosis are increasingly common in postmenopausal women, resulting in substantial bone-associated morbidities, and increased mortality and healthcare costs. Despite well-established treatment guidelines, there is an urgent need to improve the recognition of women at high risk for fracture and their treatment. 'Fast Facts: Postmenopausal Osteoporosis' provides an overview of current clinical guidelines and addresses the reasons cited for suboptimal fracture prevention. Finally, but importantly, best practice regarding patient support is described. This concise educational resource is ideal for any primary care practitioner involved in the diagnosis and treatment of patients with postmenopausal osteoporosis. Table of Contents: • Age-related changes affecting bone • Epidemiology • Screening and estimating risk • Diagnosis and assessment • Pharmacological management • Non-pharmacological management • Patient support
    LanguageEnglish
    PublisherS. Karger
    Release dateNov 30, 2021
    ISBN9783318069723
    Fast Facts: Postmenopausal Osteoporosis

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      Book preview

      Fast Facts - E. Dennison

      Introduction

      Osteoporosis is a disease of the skeleton, characterized by a loss of bone mass and microarchitectural deterioration of bone tissue. With an aging global population, preventing and managing osteoporotic fragility fractures is becoming increasingly important because they are associated with substantial bone-associated morbidities, and increased healthcare costs and mortality.

      The hormonal changes that take place during the postmenopausal period can affect bone health. It has been estimated that postmenopausal women lose bone at a rate of 0.32–0.95% per year in the total hip region, with similar rates in the proximal femur, which contributes to increased bone fragility and greater fracture risk. However, advances in osteoporosis management over the past half century have included the widespread availability of new pharmacological therapies and osteoporosis is no longer considered an inevitable consequence of aging.

      This first edition of Fast Facts: Postmenopausal Osteoporosis places particular emphasis on current clinical guidelines and the need for improved fracture prevention. Concise, up-to-date guidance is provided for accurate diagnosis and risk stratification, alongside a discussion of best practice in terms of patient support. This handbook is an essential resource for primary and secondary care providers across the healthcare spectrum.

      The process of bone formation is similar in all individuals, but the resulting skeleton is influenced by multiple factors and can vary considerably as a result. Peak bone mass is achieved in early adulthood, followed by a period of stability before a gradual decline in later life, with alterations in bone density and structure.

      Bone structure

      Bone is made up of an organic matrix, inorganic mineral and a cellular component. The matrix comprises a system of type I collagen (95%) and non-collagenous proteins, including proteoglycan, osteonectin, sialoprotein, osteocalcin and bone morphogenic proteins. The inorganic mineralized component of bone is formed from calcium phosphate laid down in an organized manner as calcium hydroxyapatite crystals ([Ca3(PO4)2]Ca(OH)2).

      There are two macroscopic forms of bone: cortical bone and trabecular bone (Figure 1.1). Cortical bone is the solid, tightly packed, ordered, hard layer found around the outside of long bones. It accounts for approximately 80% of the total bone mass in an adult skeleton. Trabecular bone is a more irregular and porous network of rods and plates, which form a three-dimensional mesh; it accounts for the remaining 20% of total bone mass. Trabecular bone has a surface area about ten times greater than that of cortical bone. This greater surface area contributes to the higher rate of turnover in trabecular bone than cortical bone.

      Bone remodeling. Knowledge of this process is useful to understand how bone mass can be altered by events such as the menopause, and therapeutic interventions. Skeletal remodeling in bone ‘multicellular’ units begins with bone dissolution/resorption and ends with new bone formation (Figure 1.2). Resorption is carried out by osteoclasts while new bone is formed by osteoblasts, which produce several bone matrix proteins and synthesize a lattice for subsequent mineralization. It is thought that osteoclasts can sense changes in gravitational forces and loading, and in this way initiate signals that activate osteoblasts and osteoclasts.

      Figure 1.1 Structure of cortical and trabecular bone.

      In adulthood, each remodeling cycle is balanced, with resorption equaling formation. However, changes in systemic hormones such as during menopause or changes to dietary intake can cause remodeling cycles to become imbalanced, and over several cycles this can result in significant bone loss. These imbalances are almost always a result of greater bone resorption relative to bone formation. The net result is bone loss and a reduction in mechanical strength, leading to diminished bone quality and quantity.

      Peak bone mass. Total bone mineral content increases during childhood until the epiphyseal growth plates close and skeletal mineralization and growth are complete. Peak bone mass is defined as the amount of bony tissue present at the end of skeletal maturation and is important in determining the risk of osteoporotic fracture occurrence in the future. It has been estimated that a 10%

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