Diagnosis of osteoporosis in osteoarthritis

The improvement of specific and sensitive biochemical markers reflecting the overall rate of bone formation and resorption in recent years has significantly improved the noninvasive assessment of bone metabolism in various metabolic bone diseases. As is known, biochemical markers are divided into markers of bone formation and bone resorption.

The most promising bone resorption markers include pyridinoline (Pyr) and deoxypyridinoline (D-Pyr) - two indivisible pyridine compounds formed as a result of post-translational modification of collagen molecules, present in native collagen and not involved in its resynthesis. In rheumatic joint diseases, these markers are considered as sensitive and specific laboratory indicators of not only bone resorption, but also joint destruction. Thus, according to experimental studies, in rats with adjuvant arthritis, an increase in the excretion of pyridinoline in the urine is observed already during the first 2 weeks after induction of the disease, correlating with clinical signs of inflammation. The level of deoxypyridinoline in the urine increases later and is more closely associated with a decrease in bone mineral density. It is noteworthy that the introduction of collagenase inhibitors is associated with a decrease in the excretion of pyridinoline and deoxypyridinoline.

Urinary pyridinoline and deoxypyridinoline levels are significantly higher in children than in adults; they typically increase by 50-100% during menopause. In patients with osteoporosis, their urinary concentrations (especially deoxypyridinoline) correlate with the rate of bone turnover measured by calcium kinetics and bone histomorphometry.

In patients with osteoarthrosis, the increase in urinary excretion of pyridinoline and deoxypyridinoline is expressed to a lesser extent than in rheumatoid arthritis, and correlates less strongly with the severity of clinical manifestations. No relationship was noted between the severity of radiographic changes (according to the Kellgren-Lawrence scale) and the levels of these markers.

Of the bone formation markers, osteocalcin should be mentioned. R. Emkey et al. (1996) found that intra-articular administration of corticosteroids leads to a significant decrease in the concentration of osteocalcin in the blood the day after the injection, followed by normalization within 2 weeks (with the clinical effect lasting for 4 weeks), and no significant changes in the concentration of pyridinoline in the urine were noted. These results indicate that intra-articular administration of corticosteroids causes only transient inhibition of bone tissue formation and does not affect the resorption process.

Determination of laboratory markers of bone metabolism increases the efficiency of instrumental assessment of the risk of osteoporosis (primarily densitometric methods). Repeated measurements of bone markers during treatment can improve the quality of monitoring of patients with osteoporosis.

Practical recommendations for the use of biochemical markers of bone metabolism for the diagnosis of osteopenic conditions:

• Serum osteocalcin and bone isoenzyme of alkaline phosphatase are currently the most sensitive markers of bone formation in osteoporosis.
• The most sensitive markers of bone resorption are urinary excretion of pyridinoline compounds and terminal fragments of type I collagen using immunoassay or high-pressure liquid chromatography.
• Before drawing a conclusion about the clinical significance of the studied laboratory markers of bone metabolism, a thorough assessment of each clinical situation and the characteristics of the therapy is necessary.
• Increased bone turnover is associated with a high rate of bone loss. Laboratory markers of bone formation and/or resorption may help identify individuals with initially normal bone mass among patients with osteoarthritis who are at increased risk of developing osteopenia (especially in the early stages of the disease).
• Elevated levels of bone resorption markers are associated with an increased risk of vertebral and hip fractures, independent of bone mass. Thus, combined assessment of bone mass and bone turnover markers is useful for selecting treatment targets for patients with osteoarthritis at highest fracture risk (taking into account other risk factors).
• Bone markers are convenient for assessing the effectiveness of antiresorptive therapy for rapid (3-6 months) screening of patients who do not respond to treatment, since the effect of therapy on bone metabolism is detected earlier than changes in bone mass detected densitometrically.

The main disadvantage of currently used laboratory methods is that they reflect only the state of bone tissue metabolism at the time of the study, without providing direct information on the quantitative parameters of the bone tissue state (i.e., it is impossible to establish a diagnosis of osteoporosis or osteopenia based on the use of laboratory test results alone). It should also be noted that, unlike some metabolic bone diseases (Paget's disease, renal osteodystrophy), which are characterized by significant changes in bone metabolism, in osteoporosis against the background of osteoarthrosis, minor changes in the rate of bone remodeling over a long period can often lead to significant loss of bone mass. This may explain the fact that the data obtained using standard markers (total alkaline phosphatase activity, hydroxyproline level, etc.) in patients with osteoporosis are within normal limits in most time intervals. Therefore, it is necessary to develop more specific and sensitive markers of bone metabolism. Thus, the requirements for an ideal bone resorption marker are as follows: it should be a degradation product of bone matrix components that is not found in other tissues, is not absorbed by the body during new bone formation, and is not affected by endocrine factors when determining its level in the blood.

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