Osteomalacia is a systemic decrease in bone strength due to insufficient mineralization of bone tissue. As a result, the bones become excessively flexible. Pathology is manifested by pain in the bones, deformities and pathological fractures. Hypotrophy and hypotension of muscles are characteristic, gait and posture disorders are possible. The diagnosis is established on the basis of anamnesis and objective examination, the results of radiography and other studies. Treatment is more often conservative, surgical correction is performed for deformities.
M83 Osteomalacia in adults
Osteomalacia is a systemic disease of the skeleton, accompanied by a decrease in the strength of bone tissue. Osteomalacia is observed mainly in childhood and the elderly, it is very rare during pregnancy. Women suffer 10 times more often than men. In children, limb bones are usually affected, in pregnant women – pelvic bones, in the elderly – vertebrae.
The cause of the disease is disorders of mineral metabolism due to a lack of vitamins, phosphoric acid and calcium salts in the body. Less often, pathology develops due to impaired excretory function of the kidneys (renal osteodystrophy), chronic and progressive kidney diseases (chronic interstitial nephritis, polycystic kidney disease, hydronephrosis, abnormalities of kidney development).
Taking into account the time of occurrence in traumatology and orthopedics, there are 4 forms of osteomalacia: children’s or youth, puerperal (in pregnant women), menopausal and senile. Young people predominate among patients with kidney pathology. In addition, cases are described when osteomalacia developed with osteopathy of starving people – nowadays in prosperous countries this pathology occurs mainly in patients with anorexia and weakened adolescent girls.
Two processes occur in parallel in human bones: the destruction of old bone tissue and the formation of a new one in combination with its mineralization. Normally, these processes are balanced, so the bones retain their strength. With osteomalacia, instead of full-fledged bone tissue, an unmineralized or poorly mineralized (containing little phosphates and calcium) osteoid is formed, which is an accumulation of collagen fibers (the backbone of the bone, a protein matrix) that give the bones elasticity. Due to the violation of the processes of formation of new bone tissue, the process of destruction of old bone also suffers, as a result of which the structure of bones is further disrupted, and their strength decreases.
Bone mineralization depends on the content of phosphates and calcium in the blood. Depending on the lack of one or another element, two forms of osteomalacia are distinguished: calcipenic and phosphoropenic. A lack of calcium can be observed with impaired absorption of calcium in the intestine, an imbalance between the process of calcium deposition in the bones and its excretion from the collapsing bone tissue, a lack of vitamin D and excessive excretion of calcium by the kidneys. The cause of calcipenic osteomalacia is congenital and acquired disorders of vitamin D synthesis due to genetic disorders, liver cirrhosis, diseases of the gastrointestinal tract, insufficient insolation, prolonged use of anticonvulsants and a vegetarian diet.
The amount of phosphates in the blood is determined by their absorption in the intestine and the rate of excretion in the kidneys. The phosphoropenic form of osteomalacia occurs due to hyperfunction of the parathyroid glands (hyperparathyroidism), lack of phosphates in food and increased secretion of phosphates by the kidneys in some tumors, hereditary metabolic disorders, kidney diseases, etc. During pregnancy and lactation, the risk of osteomalacia increases, as the body’s need for vitamin D increases, and the load on the kidneys increases, which can lead to the manifestation of various diseases and the manifestation of previously latent developmental abnormalities.
The disease begins gradually. In all four age-related forms of osteomalacia, similar symptoms are detected: decreased muscle strength and tone, vague pain in the hips and back, less often in the shoulders and chest area. Pain syndrome is observed not only during exercise, but also at rest. Bones become sensitive to pressure very early. With pressure from the sides on the iliac bones, pain appears both when pressing and when squeezing stops. Another characteristic feature of osteomalacia is the difficulty in trying to spread and lift your legs. Paresthesia often occurs.
At the initial stages of osteomalacia, skeletal deformities are absent, pathological fractures are possible. Subsequently, the pain increases, there are pronounced restrictions on movements, deformities of the limbs and other anatomical areas develop. In severe cases, the bones become waxy flexible, possible mental disorders, impaired functions of the cardiovascular system and gastrointestinal tract. Otherwise, the clinical picture of osteomalacia depends on the age of the patients. In children and adolescents with osteomalacia, tubular bones are mainly affected, with time, O-shaped legs and funnel-shaped deformity of the chest occur.
Puerperal osteomalacia, as a rule, develops during repeated pregnancy in women 20-40 years old. Less often, the first signs of the disease occur in the postpartum period and during breastfeeding. The lesion of the pelvic bones, upper thighs and lower spine is characteristic. Patients complain of pain in the legs, back, sacrum and pelvis, which increases with pressure. Duck gait is formed, sometimes osteomalacia is complicated by paresis and paralysis. Deformed (so-called osteomalacic) the pelvis makes it impossible to give birth to a child naturally, so you have to resort to cesarean section. After childbirth, the condition of patients with osteomalacia, as a rule, improves, however, in the absence or ineffectiveness of treatment, consequences in the form of severe residual deformities and concomitant disability are possible.
In the climacteric form of osteomalacia, curvature of the spine prevails, kyphosis develops. The length of the trunk gradually decreases, while there is no change in the length of the limbs, which, with pronounced pathology, causes a characteristic picture – in a sitting position, a person seems much shorter, almost a dwarf. In some cases, there is a pronounced pain syndrome that immobilizes patients. With senile osteomalacia, pathological fractures are more often observed and, less often, skeletal deformities due to bone curvature. Sometimes the presence of a large number of compression fractures of the spine causes the formation of a pronounced hump. Gait disorders (duck or mincing gait) are often observed, difficulties arise when trying to climb the stairs. Palpation of bones is painful.
The diagnosis of osteomalacia is made taking into account the X-ray picture, clinical symptoms and additional research data. In the initial stages, widespread osteoporosis is detected on X-rays. Subsequently, a plastic arc-shaped deformation is determined, which is more noticeable on radiographs of the hips and shins subjected to significant axial loads. In places where the osteoid accumulates, zones of enlightenment become visible. When an osteoid accumulates in the subcostal zone, the contours of the bone become indistinct, the cortical layer becomes layered. With a prolonged course of osteomalacia and severe osteoporosis, the cortical layer becomes thinner, the bone marrow space expands.
In the early stages, osteomalacia is differentiated from systemic osteoporosis. To do this, gamma-photon absorptiometry is performed (a study that allows you to determine the amount of calcium and phosphates in a certain area of the bone) or a pelvic bone biopsy is performed. When excluding tumor, inflammatory and systemic diseases of the skeleton, X–ray data are used, and also take into account the characteristic localization of pathological changes (damage to tubular bones in young, pelvic bones in pregnant women, spine in the elderly). When differentiating osteomalacia with Recklinghausen’s disease, the absence of Loozer’s restructuring zones is taken into account, with late rickets – the absence of signs of violation of enchondral ossification.
Pathology is treated by orthopedic traumatologists, if necessary – with the participation of nephrologists, gynecologists, endocrinologists and other specialists. Conservative therapy is carried out, including the intake of vitamin D, phosphorus and calcium, therapeutic gymnastics, massage and UV irradiation. With pronounced deformities, surgical correction is performed, but not earlier than 1-1.5 years after the start of treatment, since repeated deformities are often observed in patients with osteomalacia during early surgical interventions.
With osteomalacia that occurred during pregnancy, drugs containing a large amount of trace elements and vitamin D are also prescribed. If therapy is ineffective, termination of pregnancy is indicated, after childbirth – sterilization and termination of breastfeeding. With a favorable course, a caesarean section is performed and it is recommended not to breastfeed the baby.
Prognosis and prevention
The prognosis for life with the timely start of treatment is favorable in most cases, disability is possible due to severe deformities of the pelvis and spine. In the absence of treatment, patients with osteomalacia die from concomitant diseases and complications from internal organs. Prevention includes timely detection and treatment of diseases that may cause the development of pathology.
- Vitamin D metabolism, rickets, and osteomalacia. Berry JL, Davies M, Mee AP. Semin Musculoskelet Radiol. link
- Hypophosphatemic Hypovitaminosis D Induces Osteomalacia in the Adult Female Rat. Durup D, Diaz-delCastillo M, Morgenlykke J, Jensen LT, Frandsen E, Abelson KSP, Pedersen L, Lykkesfeldt J, Ding M, Jørgensen NR, Syberg S, Petersen S, Heegaard AM. Endocrinology. link
- Nutritional rickets & osteomalacia: A practical approach to management. Uday S, Högler W. Indian J Med Res. link