We are the witnesses of a significant change in perceiving osteoporosis. For the last 15 years osteoporosis has been determined as a disease characterized by low bone mass, microarchitectural deterioration of bone tissue and an increased propensity to fractures. Decreased bone mineral density with T-score = –2,5, has been considered the main criterion for diagnosis of osteoporosis and DXA measurement the best tool to find the disease.

Epidemiological studies have revealed, however, that approximately ľ of all fractures appear in persons with normal or only slightly reduced BMD (T-score> –2,5). It became clear, that low bone mass is one of multiple skeletal and extraskeletal factors influencing bone fragility.

Osteoporosis is defined currently as a multifactoral disease characterized by an increased risk of bone fracture resulting from any reason. The main task for a physician is to find out persons in danger for low trauma fracture. Several clinical factors have been found to increase independently the risk of bone fracture. These are: advanced age, prior fragility fracture, family history of hip fracture, low BMI, low bone mass, glucocortycoid treatment, rheumatoid arthritis, smoking, and alcohol abuse. Determination of number of risk factors together with population risk allows to calculate absolute 10-year fracture risk in any individual patient.

Bone mineral density assessed with the method of DXA should be regarded as one of several significant parameters influencing bone fragility. X-ray pictures are performed in order to diagnose vertebral fractures, which multiply the risk of further fractures.

Osteoporosis is most often found in postmenopausal women but older men are also at increased risk of fragility fractures. They account for about 30% of all hip fractures. Clinical disorders that increase fracture risk in men are the same as in women, however hypogonadism seems to be the best-characterized risk factor for male osteoporosis.

Apart from the well known clinical risk factors many diseases and biochemical disturbances are suggestive to increase fracture risk, dependently or independently from BMD. Some of them are are described in detail in this issue of the journal.

Rheumatoid arthritis, that is found in 1% of adult population, leads to both primary and secondary osteoporosis. Pro-inflammatory cytokines, especially TNFα and IL-1 stimulate osteoclast differentiation and bone mass loss through direct and indirect mechanisms. Glucocorticoids used in most cases of active rheumatoid arthritis inhibit the inflammatory process and restore joint mobility. On the other hand, however, they inhibit bone formation, stimulate bone resorption and lead to muscle weeknes. All these factors seem to participate in a significant increase in the number of skeletal fractures. It was shown that as much as 30% to 50% of patients taking glucocorticoids experience fractures. This prevalence is much higher than expected from BMD measurements.

Gastrointestinal tract along with the liver and the pancreas play an important role in maintaining calcium homeostasis. It was found that both total and partial gastrectomy, bariatric surgery, achlorhydria, pernicious anemia, sprue, short-bowel syndrome, and non-specific inflammatory bowel diseases result in a decrease in BMD and an increase in the number of osteoporotic fractures.

In patients with kidney insufficiency phosphate retention, deterioration of renal hydroxylation of vitamin D, excessive response of parathyroid glands to hypocalcemia and resistance of the skeleton to the influence of parathormone are observed. Renal osteodystrophy may present as high-turnover or adynamic bone disease together with symptoms of osteoporosis, osteomalacia and aluminium osteopathy. A significant role in the pathogenesis of the disease seem to play disturbances in a function of sodium-dependent phosphate transporter 2, phosphatonins, α-Klotho protein, RANKL/RANK and osteoprotegerin