The Musculoskeletal System

Human musculoskeletal system

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Aged muscles are more prone to injury and take longer to repair and recover. This slower recovery may be due to a reduction in the number of progenitor satellite cells — undifferentiated stem cells that can develop into new muscle cells or myocytes — combined with progressive cellular senescence Bougea et al, Calcium phosphate crystals form the bone matrix and give bones their rigidity. Insufficient levels of calcium or vitamin D essential for calcium absorption can lead to a reduction in bone density and increase predisposition to osteoporosis and fractures.

In older people, the gut absorbs less calcium and vitamin D levels tend to decrease, which reduces the amount of calcium available for the bones. Collagen provides anchorage for the calcium phosphate crystals, knitting the bone together to prevent fractures. Some people have genes leading to faulty collagen production, which results in brittle bone disease osteogenesis imperfecta.

Like muscle, bone is a dynamic tissue continuously being deposited and broken down. This state of flux is mediated by the two major bone cell types:.

Learning About Your Musculoskeletal System

Osteoblasts are more active when the bones are under the stress imposed by the weight of an upright, active body. In young mobile adults, osteoblasts and osteoclasts work at a similar rate and bone density is maintained. Inactivity means a decrease in osteoblast activity that ultimately results in reduced bone density Nigam et al, The age-related loss of skeletal muscle mass contributes to the reductions in load both weight and contractile force on the bones, which compounds decalcification.

It is therefore essential that older people keep as mobile and active as possible. Increases continue in both sexes until around the age of 30 when peak bone strength and density is achieved National Institutes of Health, Bone density decreases as middle age approaches. Women are at particular risk of bone demineralisation and osteoporosis as they gradually lose the osteo-protective effects of oestrogen pre and post menopause.

In a year study, women lost 1. Bone loss in both sexes continues into old age, and year-olds have approximately half the bone mass they had at its peak in young adulthood Lau and Adachi, ; Kloss and Gassner, The age-related loss of calcium from the skeleton commonly leads to the bones taking on the porous, sponge-like appearance indicative of osteoporosis.

There are two recognised forms of this Lau and Adachi, :. The vertebrae are particularly vulnerable to osteoporosis and may develop micro-fractures resulting in them collapsing under the weight of the body and becoming compressed and deformed. This contributes to the stooping curvature of the spine often seen in older age Fig 2.

The age-related decrease in bone density is associated with an increased risk of fracture in many bones including the femur, ribs, vertebrae and bones of the upper arm and forearm. Osteoporosis is linked not only to a loss of inorganic mineral content, but also with a loss of collagen and changes to its structure. As collagen helps to hold bones together, this further increases the risk of fracture Boskey and Coleman, ; Bailey, The risk of fracture is compounded by a lack of mobility, for example, due to a prolonged stay in hospital Nigam et al, Not only are fractures more common in old age, but healing takes much longer Lau and Adachi, This region is particularly vulnerable to fracture, as the two femoral necks support the weight of the upright body.

Costache and Costache found that femoral neck fractures — which are serious and potentially life-threatening injuries — become more frequent after the age of 60 years and that women are more affected than men. The articular cartilages in synovial joints play the role of shock absorbers, as well as ensuring the correct spacing and smooth gliding of bones during joint movement.

Osteoarthritis is the most common arthropathy joint pathology in the world. In the UK, around 8. This places a great burden on health services as many patients will require expensive joint surgery, particularly to the knee, hip and lumbar spine.

The outer portion of a joint capsule is composed of elastic ligaments that bind the joint together, preventing dislocation while allowing free movement. With age, changes to the collagen and elastin components of ligaments decrease their elasticity Freemont and Hoyland, , resulting in stiffness and reduced mobility.

Although there are many risk factors associated with the disease including genetic predisposition, gender, obesity and previous joint injury , age is by far the greatest. Many factors influence how our bones and skeletal muscles age; genetics, environmental factors and lifestyle all play a role, so there is much individual variation. Preserving the structural and functional integrity of the musculoskeletal system is essential to maintain good health and slow down the progression to frailty. Programmed cell death apoptosis plays a role in bone loss and sarcopenia.

Performing a regional examination of the musculoskeletal system (‘REMS’)

The apoptotic pathways involved may be attenuated by exercise, calorific restriction and anti-oxidants such as carotenoids and oleic acid Musumeci et al, Recent studies have shown that calorific restriction can slow down, and sometimes even reverse, age-related changes in neuromuscular junctions, thereby providing a potential mechanism for reducing sarcopenia.

Drugs that mimic the effects of calorific restriction and exercise — such as metformin an oral hypoglycaemic used to treat diabetes and resveratrol an anti-inflammatory and anti-oxidant — could be used instead of reducing food intake. Stokinger et al have reported some success with these drugs, particularly resveratrol, in animal models. Increasing the intake of calcium, vitamin D and lean protein can increase bone density and provide amino acids for muscle growth. This may offset the reduction in the efficiency of nutrient absorption seen in older age.

We know that, in younger adults, increasing protein intake can enhance protein synthesis in skeletal muscles, but this seems to work less well in older people.

THE CHANGES OF PREGNANCY

Hormone replacement therapy HRT improves bone health in older people: oestrogen HRT and testosterone replacement therapy TRT are proven to increase bone density in women and men, respectively, thereby reducing the risk of fracture. The effects of HRT on muscle physiology are less well investigated. TRT has been shown to increase lean muscle mass in men and appears to negate some of the effects of ageing on muscles occurring during the andropause; however, in women, HRT with either oestrogen or oestrogen plus progesterone does not have the same anabolic effect Fragala et al, Women can use TRT, but they may be reluctant to do so because of unwanted effects such as facial and body hair growth and deepening of the voice.

Unless regularly used and placed under load, muscle fibres and neuromuscular junctions degenerate, resulting in disuse atrophy Kwan, Moderate exercise helps to maintain lean muscle mass, increase bone density and reduce fat accumulation. Exercise also increases the number of mitochondria in muscle fibres, enhancing energy release, metabolism and muscle power. In people who remain physically active, the efficiency of mitochondria in releasing energy appears to be maintained until at least the age of 75 Cartee et al, Progressive resistance training is considered to be the most effective method to increase bone density and promote muscle growth in older people with sarcopenia.

Bailey AJ Changes in bone collagen with age and disease.

Introduction to the Biology of the Musculoskeletal System

Journal of Musculoskeletal and Neuronal Interactions ; 2: 6, Journal of Dental Research ; 12, Bougea et al An age-related morphometric profile of skeletal muscle in healthy untrained women. Journal of Clinical Medicine ; 5: pii, E Cartee GD et al Exercise promotes healthy aging of skeletal muscle. Cell Metabolism ; 6, Choi SJ Age-related functional changes and susceptibility to eccentric contraction-induced damage in skeletal muscle cell.

Integrative Medicine Research ; 5: 3, Cleasby ME et al Insulin resistance and sarcopenia: mechanistic links between common co-morbidities. Journal of Endocrinology ; 2, RR Costache C, Costache D Femoral neck fractures.

The Musculoskeletal System

Daly RM et al Gender specific age-related changes in bone density, muscle strength and functional performance in the elderly: a year prospective population-based study. BMC Geriatrics ; Fragala MS et al Muscle quality in aging: a multi-dimensional approach to muscle functioning with applications for treatment.

Sports Medicine ; 5, Journal of Pathology ; 2, Hanna F et al Factors influencing longitudinal change in knee cartilage volume measured from magnetic resonance imaging in healthy men. It is important to introduce yourself, explain to the patient what you are going to do, gain verbal consent to examine, and ask the patient to let you know if you cause them any pain or discomfort at any time. In all cases it is important to make the patient feel comfortable about being examined. A good musculoskeletal examination relies on patient cooperation, in order for them to relax their muscles, if important clinical signs are not to be missed.

The examination should always start with a visual inspection of the exposed area at rest. Compare one side with the other, checking for symmetry. You should look specifically for skin changes, muscle bulk, and swelling in and around the joint. Look also for deformity in terms of alignment and posture of the joint. Using the back of your hand, feel for skin temperature across the joint line and at relevant neighbouring sites.

Any swellings should be assessed for fluctuance and mobility. The hard bony swellings of osteoarthritis should be distinguished from the soft, rubbery swellings of inflammatory joint disease. Tenderness is an important clinical sign to elicit — both in and around the joint. Identifying inflammation of a joint synovitis relies on detecting the triad of warmth, swelling and tenderness. The full range of movement of the joint should be assessed.

Compare one side with the other. As a general rule both active movements where the patient moves the joint themselves and passive movements where the examiner moves the joint should be performed. If there is a loss of active movement, but passive movement is unaffected, this may suggest a problem with the muscles, tendons or nerves rather than in the joints, or it may be an effect of pain in the joints. In certain instances joints may move further than expected — this is called hypermobility.

It is important to elicit a loss of full flexion or a loss of full extension as either may affect function. A loss of movement should be recorded as mild, moderate or severe. The quality of movement should be recorded, with reference to abnormalities such as increased muscle tone or the presence of crepitus.

It is important to make a functional assessment of the joint — for example, in the case of limited elbow flexion, does this make it difficult for the patient to bring their hands to their mouth? For the purposes of this handbook and the accompanying DVD the REMS examination has been divided into seven areas, each of which is described in detail below. However, it should be remembered that this is an artificial division and that one group of joints may need to be examined in conjunction with another group e. The positive and significant negative findings of the REMS examination are usually documented longhand in the notes.

You may find it helpful to document joint involvement on a homunculus such as the one shown below. The total number of tender and swollen joints can be used for calculating disease activity scores — these are useful in monitoring disease severity and response to treatment over time.

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