© Springer International Publishing Switzerland 2017
Jozef Rovenský (ed.)Gerontorheumatology10.1007/978-3-319-31169-2_2424. Senile Osteoporosis
(1)
3rd Department of Internal Medicine – Department of Endocrinology and Metabolism, 1st Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic
Since 1994, osteoporosis has been defined as a progressive systemic skeletal disease characterised by low bone mass and microarchitectural deterioration of bone tissue, with a consequent increase in bone fragility and susceptibility to fracture.
The most severe complication of osteoporosis are femoral neck fractures, requiring hospitalisation, that cause the patient’s immobility and lead potentially to 10–20 % increase in patients’ mortality during the first year after fracture. The most frequent cause of femoral neck fractures are falls. A total of 80 % of them can be seen in women, and 90 % of them are sustained by individuals older than 50 years. Forearm or wrist fractures are most likely to occur in women over 65 [1].
Bone is highly metabolically active throughout life, controls the calcium level in blood, helps maintain acid–base balance, creates space for bone marrow and has mechanical functions. Bone is a tissue with active metabolic turnover associated with its remodelling [2]. Bone resorption is induced by osteoclasts activated by proteins of the tumour necrosis factor family. Membrane osteoprotegerin ligand produced by stromal cells and osteoblasts binds to specific monocyte receptors (RANK). These activated osteoclast precursors respond by increased production of osteoresorptive cytokines interleukin I and tumour necrosis factor. Antiresorptive protein is osteoprotegerin which inhibits osteoclast maturation and causes their apoptosis. Of special importance are osteocytes, modified osteoblasts, housed in lacunae and connected with each other by canaliculi, as well as with the lining cells on the bone surface [7]. Osteocytes capture bone mass deformities (microcracks) similarly as a spider sensing vibrations of insect caught in its web. As soon as they detect a deformity, it is transferred to the lining cells on the bone surface, which differentiate into osteoblasts of cells responsible for new bone formation. It should be noted in this respect that bone metabolic turnover continues also in advanced age, although at a different level than in youth and adulthood. Pathological intervention in this process leads to metabolic osteopathy.
Aetiopathogenesis of osteoporosis (OP) varies and has multiple causes. In secondary osteoporosis, the causes are known and can be found in the underlying diseases of which secondary OP is a part. These include endocrine diseases (hyperthyroidism, hypercortisolism, hyperparathyroidism, hypogonadism), hereditary diseases (osteogenesis imperfecta, homocystinuria), chronic liver disorder, long-term immobilisation, diabetes mellitus, tumour diseases and iatrogenic osteoporosis.
The term primary osteoporosis classically includes idiopathic and involutional osteoporosis. Involutional osteoporosis can be divided into postmenopausal and senile variety. In women, the dividing line between these two varieties is not quite clear, as the senile osteoporosis may directly follow the postmenopausal variety [9]. The study below is focused on senile osteoporosis only [10].
Senile osteoporosis (sometimes referred to as involutional) is characterised by patients’ age (older than 65 years), gender (male–female ratio of 2:1), type of bone loss (trabecular, cortical), fracture pattern (involvement of both axial and appendicular skeleton, with the latter prevailing; proximal femur fractures are more common), increased serum immunoreactive parathyroid hormone, decrease in intestinal absorption of calcium and lower levels of active metabolites of vitamin D. Age-related factors in aetiopathogenesis of senile osteoporosis include low intake of vitamin D and reduced capacity to synthesise vitamin D in the skin of elderly individuals. At the age of 70, the activity of enzymatic apparatus of the skin synthesising vitamin D is up to ten times lower than in young individuals. With increasing age, hydroxylation of vitamin D slows down, and resistance of target tissue to the active vitamin D metabolite calcitriol increases. Lower levels of active vitamin D metabolite lead to reduced intestinal absorption of calcium and hypocalcemia, stimulating production and release of parathyroid hormone (PTH) by parathyroid glands; the patients’ levels of immunoreactive PTH (senile secondary hyperparathyroidism) are increasing. There occurs imbalance in bone remodelling in favour of bone resorption, with marked multiplication of resorption cavities and their inadequate filling with osteoblasts. Lack of vitamin D and its active metabolites also results in reduced muscle strength, up to four times in the quadriceps, and limited neuromuscular coordination. Endocortical resorption in long bones is not compensated by periosteal bone formation.
In the ageing process, bone is also adversely affected by decrease in production of bone anabolic peptides, such as growth hormone, insulin and insulin growth factor I, and adrenal steroids, such as dehydroepiandrosterone and androstenedione.
An important factor with a negative impact on bone mass is immobilisation, even if short term, when due to insufficient stimulation of bone mechanoreceptors, bone resorption prevails over bone formation. Elderly persons have often their joint apparatus damaged by degenerative diseases limiting their mobility, ability to walk and protracting periods of immobility, which are significant risk factors for development of osteoporosis.
Of great interest is the relation between blood circulation and bone metabolism. Ischaemia caused by ligature of the femoral artery in rabbits resulted in cortical thinning and reduction of the mechanical resistance of the bone. Laroche found atherosclerotic changes in interosseous arteries that were similar to those in coronary arteries [5].
Bones receive about 5 % of cardiac output. The size and shape of the completed Haversian system depends on the size and shape of the resorption cavity created by osteoclasts. A limiting factor for centrifugal resorption is most probably the demand of most remote cells for adequate supply of oxygen and amino acids and the possibilities of removing resorption waste. Of great importance for bone cells and their metabolic activity is regional blood flow. A group of women with compression fractures of vertebral bodies exhibited a higher incidence of ischaemic heart disease or ischaemic disease of lower limbs [4]. Calcification of atherosclerotic plaques increases with increasing age of patients. In addition, a group of women with compression fractures showed a higher number of atheroplaques in the aortic arch, visible on radiographs.
Prediction of femoral neck fractures is based on analysis of risk factors. Age is an independent risk factor for fractures. Risk factors for development of senile osteoporosis develop as early as in childhood. Peak bone mass is reached between ages 25 and 30 years. In 70 % it is determined genetically, and therefore it is always necessary to take into account also family history during examination. The remaining 30 % are influenced by the lifestyle in youth, i.e. smoking drug abuse, diet and physical activity. Other factors contributing to OP development include premature or induced menopause, mainly in terms of protective effect of oestrogen on bone cell metabolism; thin or skinny figure with low muscle mass; low physical activity; sedentary lifestyle, or even immobilisation; chronic pulmonary obstructive disease; glucocorticoid treatment; and severe scoliosis. The cause is unknown, but it may be hypothesised that there is a correlation between connective tissue abnormality and development of both static and dynamic disorders of the spine [6].
24.1 Clinical Features
Clinical features largely vary. In extreme cases, osteoporosis may be quite asymptomatic and is revealed accidentally by radiographic examination. However, most frequently patients seek medical care for back pain, often pulling and nonspecific, which gets more intensive during physical activity, or prolonged sitting or standing and is eased by lying down or resting. Sudden sharp pain can be experienced after a quick movement, most often in the region of the lower and upper lumbar spine, which radiates forward into the abdomen and lower limbs. There may appear also reflex spasm of paravertebral muscles with radicular irritation. Vertebral spinous processes may be tender to palpation. Pain is caused by microfractures and later by compression fractures of vertebral bodies.
These fractures conduce to deformities of vertebral bodies, including depression of superior and inferior endplates of vertebral bodies (fish vertebrae). These changes result in graded thoracic kyphosis, absence of cervical lordosis and increased lumbar lordosis and the patient’s height loss.
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