Fig. 27.1
Crosstalk among SNS, fat tissue, bone, and skeletal muscle
27.2 Osteo-metabolic Disorders in Elderly: Osteoporosis and Osteomalacia
27.2.1 Osteoporosis
27.2.1.1 Definition
Osteoporosis is a systemic skeletal disease characterized by a generalized decrease in bone density and deterioration of the microarchitecture of bone tissue that predispose to skeletal fragility resulting in increased risk of fractures [27].
From an operational point of view, the WHO defined osteoporosis when the bone mineral density (BMD) is less than 2.5 standard deviations than the mean peak bone mass of healthy young adults [27], based on a BMD measured by dual-energy X-ray absorptiometry (DXA). The normal BMD corresponds to a T-score ≥ −1; osteopenia is defined as a T-score between −1 and −2.5; severe osteoporosis as a T-score ≤ −2.5 with a fracture.
27.2.1.2 Epidemiology
The incidence of osteoporosis increases with aging affecting most of the population over 80 years old. It is estimated that about one out of two women over the age of 50 will sustain a fragility fracture [28]. In the Italian people aged over 50, the incidence of hip fractures is more than 90,000, and vertebral fracture was detected in over 20% of people over 65 in both men and women [29].
27.2.1.3 Physiopathology
Primary or idiopathic osteoporosis includes juvenile, postmenopausal, and senile osteoporosis.
Secondary osteoporosis instead includes all clinical conditions in which the bone involvement is not the main pathologic finding, but the bone is one of the targets of primary disease or related treatments, especially those that include the use of glucocorticoids.
The main pathogenetic factor of postmenopausal osteoporosis is the estrogen depletion that worsens the age-related bone loss occurring from the age of 40 [30]. Senile osteoporosis comes from the combination of various factors: tissue aging, hormone depletion, nutritional disorders, and decrease in physical activity.
Secondary osteoporosis is caused by several diseases such as endocrine disorders and hematologic, gastrointestinal, rheumatic, and kidney diseases or by the use of medications such as glucocorticoids, anticoagulants, and other drugs [31].
Male osteoporosis can be considered primary only in 40% of cases [32], whereas most frequently it is secondary to other conditions, such as hypogonadism, alcoholism, multiple myeloma, hyperparathyroidism, malabsorption, and corticosteroid use [33], but also to androgen deprivation therapy for prostate cancer [34].
27.2.1.4 Risk of Falls and Fragility Fractures in Older Patients
Fall is the most important risk factor for fragility fractures, and the risk of falling increases exponentially with aging. The risk factors of falling can be categorized as intrinsic or extrinsic. The first ones include the physiological decline in age-related postural control mechanisms [35] and appendicular muscle strength, medications (diuretics, antiarrhythmics, antidepressants), orthostatic hypotension, and comorbidities. Neurological diseases, such as Parkinson’s disease, cerebellar disorders, peripheral neuropathy, myelopathy secondary to cervical spondylosis, epilepsy, and stroke, increase the risk of falling.
Extrinsic risk factors include environmental issues, such as low or soft chairs, carpets, slippery surfaces, raised thresholds, stairs (especially the first and last step), inadequate lighting, unsuitable shoes, clutter, and wires. The reduction of the risk of falling is the main target of a non-pharmacological approach for the prevention of osteoporotic fractures [36].
Fragility fractures occur when a mechanical stress applied to the bone exceeds its strength. They result from a “low-energy” trauma due to mechanical forces equivalent to a fall from a standing height or less, which would not ordinarily cause a fracture.
27.2.1.5 Treatment of Primary and Secondary Osteoporosis
In order to reduce the risk of fragility fractures, a preventive strategy can be taken which is essentially based on exercise and lifestyle [37]. The National Osteoporosis Foundation (NOF) suggested the use of different prevention measures that include an adequate calcium and vitamin D intake, constant and regular physical activity, smoking cessation, alcoholism identification and treatment, and fall prevention. Physical activity is strongly recommended as an effective strategy to reduce the risk of osteoporosis and fracture through its beneficial effects on bone, muscle, and risk of falling [38].
The estimated risk necessary to establish the threshold of the pharmacological intervention is based on both the BMD and clinical fracture risk factors. Integrated assessment of multiple risk factors can be done through algorithms validated as the FRAX®.
The drugs commonly used for the treatment of osteoporosis and their related evidence are shown in Tables 27.1 and 27.2.
Table 27.1
Level of evidence for pharmacological treatment in postmenopausal osteoporosis
Drugs | Target of therapy | |||
---|---|---|---|---|
Hip fracture | Vertebral | Non-vertebral | BMD | |
Alendronate | 1 | 1 | 1 | 1 |
Ibandronate | 1 | 1 | 1 | |
Risedronate | 1 | 1 | 1 | 1 |
Zoledronate | 1 | 1 | 1 | 1 |
Teriparatide | 1 | 1 | 1 | |
Raloxifene | 1 | 1 | ||
Bazedoxifene | 1 | 1 | ||
Denosumab | 1 | 1 | 1 | 1 |
Table 27.2
Level of evidence for pharmacological treatment in male osteoporosis
Drugs | Target of therapy | |||
---|---|---|---|---|
Hip fracture | Vertebral | Non-vertebral | BMD | |
Alendronate | 2 | 1 | ||
Risedronate | 2 | 1 | ||
Zoledronate | 2 | 1 | 2 | 1 |
Teriparatide | 1 | 1 | ||
Denosumab | 1 | 1 |
27.2.2 Osteomalacia
27.2.2.1 Definition
Osteomalacia is a metabolic bone disorder characterized by the presence of a normal bone mass, with reduced mineral content for an inadequate mineralization of the organic matrix. Patients with osteomalacia may complain of bone pain and muscle weakness and present vertebral deformity and/or pseudofractures (Looser-Milkman striae) [39].
27.2.2.2 Epidemiology
Nowadays, osteomalacia is a fairly rare disease. According to the National Institutes of Health (NIH), its incidence is less than 1/1000 [39].
27.2.2.3 Pathophysiology
Osteomalacia is linked to a reduced availability or to an altered metabolism of vitamin D or to alterations of the renal tubular reabsorption of phosphorus. The most common causes of osteomalacia are shown in Table 27.3 [40].
Table 27.3
Common causes of osteomalacia
Vitamin D deficiency | • Inadequate oral intake • Inadequate exposure to sunlight • Intestinal malabsorption |
Abnormal vitamin D metabolism | • Liver disease • Renal disease • Medication |
Hypophosphatemia | • Low oral phosphate intake • Excess renal phosphate loss |
Inhibition of mineralization | • Bisphosphonate • Aluminum • Fluoride |
Hypophosphatasia | Inherited autosomal disorder |
27.2.2.4 Treatment
For the treatment of osteomalacia, it is essential to identify and promptly treat the underlying cause to prevent the occurrence of fractures; furthermore it is necessary to adopt simple corrective measures regarding nutrition and sun exposure. We should encourage patients to have a higher nutritional intake (oily fish, cod liver oil, egg yolk, mushrooms, cereals, and margarine enriched of vitamin D). Early pharmacological treatment is mandatory, consisting of 50–125 μg per day of calcifediol, or 5000–10,000 IU per day of cholecalciferol for 1–2 months, with a maintenance therapy of 20 μg per day of calcifediol, or 800 IU per day of cholecalciferol.
27.3 Physiatric Approach to Older Patients with Osteo-metabolic Disorders
27.3.1 Background
The global rehabilitative approach has a key role in all stages of these diseases, from prevention to functional recovery after a fragility fracture. The pivotal element of rehabilitation is the therapeutic exercise. Several studies and international guidelines suggested that this intervention is effective in increasing bone mass during skeletal growth, maintaining what has been achieved in adult life, reducing bone loss in the elderly and the risk of fractures.
In the elderly, exercise can enhance cortical thickness and strength in overloaded bone tissue. These effects might result from a diminished loss of endocortical bone and/or an increase in tissue density rather than an increase in bone size (due to periosteal apposition), even if also in elderly a progressive widening of the outer diameter occurs. These geometrical adaptations are able to increase the mechanical resistance to the compression load [44].
Two types of physical exercises are suitable for elderly: aerobic activities (walking, stair climbing, jogging, tennis, tai chi, gymnastics, dancing) and resistance exercises (where joints move against an external force given by weights, machines, or the own body weight).
The most common aerobic training in older people is walking that could be effective in maintaining BMD when combined with high-impact activities, such as jogging or stepping [45].
Therapeutic exercise could exert, through the improvement of the muscle performance, an indirect effect on bone health. However, aging is characterized by a progressive decline in aerobic exercise capacity due to the reduction in cardiovascular efficiency and skeletal muscle function caused by a decrease of mitochondrial number and activity [46]. Aerobic training stimulates the synthesis of mitochondria in the skeletal muscle with a consequent reduction of the oxidative stress and the enhancement of muscular performance [47].
Several studies suggest that the muscle strengthening produces a significant increase in femoral neck BMD [48]. Furthermore, improvement in muscle strength and performance, due to resistance exercise, might reduce the risk of falls.
At a cellular level, strengthening exercises increase the transverse diameter of type I and type II muscle fibers and of the entire lean mass, with relative increase in muscle strength [49]. Fast-velocity resistance exercises (i.e., performing a concentric phase as quickly as possible followed by an eccentric 2-second contraction phase) [50] have shown to cause a greater recruitment of motor units in type II muscle fibers counteracting atrophy in aging [51].
There is a general consensus that older people should perform moderate-intensity aerobic exercises for a minimum of 30 min 5 days a week or high-intensity aerobic activity for a minimum of 20 min 3 days per week [45]. Moderate-intensity aerobic exercise is intended, from an absolute scale, as the activity that takes place at an intensity of 3.0–5.9 times the intensity at rest or, from a relative scale based on individual’s capacity (ranging from 0 to 10), an intensity of 5 or 6 times the intensity at rest. High-intensity aerobic exercise is the activity that takes place at an intensity of at least 6 times the intensity at rest on an absolute scale, an exercise intensity of 7 or 8 times the intensity at rest based on individual’s capacity. Aerobic exercise should be performed for at least 10 consecutive minutes [52].
Bodyweight exercises or training with equipment is also useful, but should be performed slowly, with 1–3 series for each type of exercise, spacing 1–3 min of rest, for 2–3 days/week [52]. Strengthening exercises are safe, feasible, and effective to induce muscle hypertrophy and to increase strength and should be performed as soon as possible in order to prevent the progression of skeletal fragility and sarcopenia. General principles of the prescription of therapeutic exercise in osteoporotic patients have been proposed by a specific task force of the NOF [53] (Table 27.4).
Table 27.4
General principles of therapeutic exercise in patients with osteoporosis
Specificity | Specific to the individual patient; specific to one or more physiological goals (bone strength, muscle strength, flexibility, cardiovascular fitness); specific to the anatomical site |
Progression | Gradual increases in duration, intensity, and frequency; applied loads must remain below bone and connective tissue injury threshold, but be high enough to provide a greater than current activity stimulus to the organ system (muscle, heart, or connective tissue) |
Reversibility | Positive effects of exercise will be slowly lost if the program is discontinued |
Initial values
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