Osteodystrophy is a group of diseases and secondary pathological conditions caused by local metabolic disorders. Accompanied by increased resorption of bone tissue. The cause of osteodystrophy can be diseases of the digestive system, endocrine diseases, kidney diseases, vitamin deficiency, poisoning, metabolic disorders and local blood supply disorders. It can be manifested by pain, pathological fractures, and bone deformation. The diagnosis is made on the basis of examination, X-ray data and other studies. Treatment is more often conservative.
ICD 10
M80-M85
Meaning
Osteodystrophy is a syndrome that occurs in a number of diseases of various genesis. It is caused by local trophic disorders, as a result of which the structure of bone tissue changes or bone tissue resolves and is replaced by fibrous. It is manifested by a decrease in bone strength, as a result of which deformities and pathological fractures may occur. It can develop in diseases accompanied by metabolic disorders and diseases resulting from local circulatory disorders in certain areas of the bones.
Symptomatic osteodystrophy caused by metabolic disorders can be detected in people of any gender and age. The course depends on the cause of development and the success of treatment of the underlying disease. Osteodystrophy of an angioedema character affects mainly children and adolescents, differs in a cyclical course and in most cases ends in recovery. With unfavorable development, long-term consequences are possible in the form of residual deformities, early arthrosis, osteochondrosis, etc. Treatment of osteodystrophy is carried out by orthopedists.
Classification
Currently, in orthopedics and traumatology, there are several options for systematization of osteodystrophy: by etiology, by the nature of pathological changes, by localization, etc. Taking into account the causes of all osteodystrophy are divided into endogenous and exogenous. Exogenous osteodystrophy is caused by the impact of adverse external factors: the ingestion of toxins (chemical poisoning, Kashin-Beck disease, etc.), lack or excess of vitamins in food (rickets, scurvy, other vitamin deficiencies and hypervitaminoses).
The cause of the development of exogenous osteodystrophy are severe kidney diseases (renal osteodystrophy), endocrine diseases (parathyroid, pituitary and thyrotoxic osteodystrophy), some diseases of the gastrointestinal tract (intestinal, gastric, pancreatic and hepatic osteodystrophy), as well as local osteodystrophy due to local blood supply disorders. The group of endogenous osteodystrophy includes osteodystrophy in renal tubular acidosis, vitamin-D-resistant and vitamin-D-dependent rickets, blastomatous reticulosis, de Toni-Debre-Fanconi syndrome, etc. The subgroup of endogenous angioedema osteodystrophy includes osteochondropathies, Zudek atrophy, bone cysts, progressive osteolysis, osteodystrophy of bones that occurs when nerves and blood vessels are damaged.
Taking into account the nature of the pathological process, there are three forms of osteodystrophy: osteomalacia, osteoporosis, as well as osteochondrosis and osteosclerosis. Osteomalacia is accompanied by a decrease in the amount of minerals while maintaining the protein structure of the bone. With osteoporosis, the protein matrix of the bone is destroyed, its architecture is disrupted, and the mineral density of bone tissue decreases. In osteochondrosis and osteosclerosis, there is a local increase in mineralization and deposition of bone-like tissue (calcinates) in tendons and periarticular tissues.
Systemic osteodystrophy
The main feature of secondary (systemic) osteodystrophy is the absence of neoplasm or primary inflammatory process. The variety of reasons for which this syndrome develops causes a significant variability of pathological changes. A common feature in the morphological picture of osteodystrophy is a change in the bone structure. At the same time, full-fledged bone elements are absorbed and replaced by new tissue, which differs from normal by certain structural features.
With osteodystrophy caused by intestinal or liver diseases, widespread osteoporosis is observed, osteomalacia is possible. With a lack of vitamin A, a violation of periosteal and enchondral bone formation is detected, early closure of the growth zones is observed, resulting in stunting. Hypervitaminosis A is accompanied by hyperostosis of the diaphysis of long tubular bones. With vitamin deficiency, collagen formation is disrupted, osteoporosis develops, in children it is most pronounced in metaphysical zones, in adults – on the border of the cartilaginous and bony parts of the ribs.
With thyrotoxicosis, there is an acceleration of metabolism, which causes increased bone restructuring with the development of osteoporosis and frequent pathological fractures. With thyrotoxicosis, there is a lack of vitamin D, bone tissue is partially replaced by osteoid, which can lead to the development of osteomalacia. With congenital hypothyroidism, age-related bone restructuring slows down, a large number of interstitial plates remain in adults, germinal zones close early, which causes a decrease in bone strength and the development of dwarfism.
Among the toxic lesions, osteodystrophy, developing due to the action of fluoride or lead, is of the greatest clinical importance. Especially strongly lead salts affect children’s bones – the deposition of salts in metaphysics causes severe osteosclerosis. Fluoride intoxication can also provoke osteosclerosis or bone rarification in combination with periosteal hyperostosis.
Diagnosis of osteodystrophy is based on the identification of characteristic radiological changes. With osteomalacia, parathyroid osteodystrophy, hypothyroidism, renal osteodystrophy and rickets, widespread osteoporosis is detected. With pituitary dwarfism, hypothyroidism, childhood scurvy and rickets, epichondral growth disorders are detected. With acromegaly, hyperostosis is detected. With parathyroid osteodystrophy and rickets, zones of Loozer rearrangement are revealed. To clarify the causes of osteodystrophy, consultations of appropriate specialists are prescribed: therapist, gastroenterologist, nephrologist, endocrinologist and conduct special studies.
Osteochondropathy
Angioedeurotic osteodystrophy (osteochondropathy) is a large group of diseases characterized by the defeat of a certain bone (or several bones) and the stages of the pathological process. The cause of the development of such osteodystrophy is local blood supply disorders caused by congenital, traumatic or metabolic factors. The disease usually manifests itself in adolescence, during the period of active growth and practically does not occur in adults.
Various bones can be affected, including the femoral head (Perthes disease), tuberosity of the tibia (Osgood-Schlatter disease), phalanges of the fingers (Timann disease), wrist bones (Kinbeck disease), tarsal bones (Iselin disease), talus bone (Haglund-North disease), patella (patella Sinding-Larsen), the head of the shoulder (Gass disease), the apophyses of the vertebrae (Scheuermann disease), the vertebral bodies (Calve disease), the metatarsal bones of the foot (Koehler II disease) and the navicular bone of the foot (Koehler I disease).
All angioedema osteodystrophy occurs in stages. Initially, there are areas of bone necrosis, pain and dysfunction appear. Then the destroyed area of bone tissue “subsides”, a compression fracture occurs. Then the affected areas dissolve, are replaced by osteoclasts and granulation tissue. All types of osteochondropathy last 2-4 years and end in recovery. In the absence of treatment, it is possible to preserve the residual deformation, which in the future may cause the development of early deforming arthrosis.
Other osteodystrophy
Progressive osteolysis (essential osteolysis, spontaneous absorption, disappearing bone disease) is a rare disease accompanied by resorption of one or more bones. The cause of the development has not been clarified, the autoimmune nature of the disease is assumed. Normally formed bones undergo resorption: small and long tubular bones, vertebrae, sternum, pelvic bones, shoulder blade, ribs, collarbones, jaws and bones of the base of the skull. It is accompanied by pain, dysfunction, deformities and pathological fractures. The radiography of the affected segment reveals a characteristic picture of “melting bone”. Treatment is symptomatic.
Solitary and aneurysmal bone cyst is a disease in which a cavity forms in the bone tissue. It is caused by a local violation of blood supply and activation of bone-destroying enzymes. It develops in childhood and adolescence, while solitary cysts are more often detected in boys, and aneurysmal cysts in girls. X-rays reveal a structureless focus of rarefaction, which is subsequently replaced by sclerosed bone tissue. It proceeds in stages, lasts for several years, ends with recovery. In the absence of treatment, residual shortening and deformities of the limbs are possible. Aneurysmal cysts in the vertebral region can be complicated by compression of the spinal cord and nerve roots. Treatment is symptomatic.