Deoxypyridinoline EIA is a urinary assay that provides a quantitative measure of the excretion of deoxypyridinoline (DPD) crosslinks as an indicator of bone resorption. Elevated levels of urinary DPD indicate elevated bone resorption in individuals. Measurement of DPD is intended for use as an aid in monitoring bone resorption changes in postmenopausal women receiving hormonal or bisphosphonate antiresorptive therapies and in individuals diagnosed with osteoporosis.
Storage
Store kit at 2°C to 8°C. Do not freeze. Store unused reagents at 2°C to 8°C.
Precision
Within-run precision was determined for ≥ 21 replicates of 3 samples on 2 plates from each of 3 kit lots (6 plates total). Between-run precision was determined for 3 samples run in 9 separate plates from each of 3 kit lots (27 plates total). Samples shown below represent a range of nmol/L values. For a female with a creatinine of 4.5 mmol/L, samples 1 through 3 represent low normal, high normal, and elevated resorption (2.4 nmol/mmol, 6.7 nmol/mmol, and 38.8 nmol/mmol, respectively).
Sensitivity
The minimum detection limit of the DPD EIA is 1.1 nmol/L, determined by the upper 3 SD limit in a zero standard study.
General Description
Approximately 90% of the organic matrix of bone is type I collagen, a triple helical protein.1 Type I collagen of bone is crosslinked by specific molecules which provide rigidity and strength. Crosslinks of mature type I collagen in bone are the pyridinium crosslinks, pyridinoline (PYD) and deoxypyridinoline (DPD).1,2 DPD is formed by the enzymatic action of lysyl oxidase on the amino acid lysine.3 DPD is released into the circulation during the bone resorption process.2-5 DPD is excreted unmetabolized in urine and is unaffected by diet,6 making it suitable for assessing resorption. Bone is constantly undergoing a metabolic process called remodeling. This includes a degradation process, bone resorption, mediated by the action of osteoclasts, and a building process, bone formation, mediated by the action of osteoblasts.2,7 Remodeling is required for the maintenance and overall health of bone and is tightly coupled; that is, resorption and formation are in balance.7 In abnormal states of bone metabolism this process becomes uncoupled and, when resorption exceeds formation, this results in a net loss of bone.7 The measurement of specific degradation products of bone matrix provide analytical data of the rate of bone metabolism.2,4,5 Osteoporosis is a metabolic bone disease characterized by abnormal bone remodeling. It is a systemic skeletal disease characterized by low bone mass and microarchitectural deterioration of bone tissue, with a consequent increase in susceptibility to fractures.8 The most common type of osteoporosis occurs in postmenopausal women as a result of the estrogen deficiency produced by the essation of ovarian function.7 Restoration of premenopausal estrogen levels by replacement therapy prevents bone loss and osteoporosis.7-10 Estrogens and a class of compounds known as bisphosphonates are antiresorptive therapies which can be used to prevent bone loss or treat osteoporosis.7-12 Osteoporosis can also result from attaining an inadequate peak bone mass during the growing years, an age-related imbalance of bone remodeling with a net excess of resorption, and a number of clinical conditions and therapies which induce bone loss or bone remodeling imbalances.7 These include endocrine diseases such as hypo-gonadism, hyperthyroidism, hyperparathyroidism, and hypercortisolism; gastrointestinal diseases related to nutrition and mineral metabolism; connective tissue diseases; multiple myeloma; chronic immobilization, alcoholism, or tobacco use; and chronic therapy with heparin or corticosteroids.7 Other diseases characterized by abnormal bone remodeling include Paget's disease and cancers metastatic to bone.3
Citations
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Background
Pyridinoline (PYD) and deoxypyridinoline (DPD) are irreducible metabolites of mature collagen of the extracellular matrix in bone, which enter the blood circulation and are excreted directly into the urine without hepatic degradation; they are sensitive indicators of bone resorption, and have been used in recent years for the diagnosis of bone metabolic diseases. PYD is mainly concentrated in bone and cartilage, and DPD has a more restricted distribution than PYD, being found almost exclusively in dentin and bone. They are both specific components of mature collagen and are released from collagen molecules when hydroxylysine oxidase acts on mature collagen. Measurement of urinary PYD and DPD is a sensitive indicator of collagen degradation and bone resorption. PYD and DPD are present in blood and urine in both free and peptide-bound forms, with the free form accounting for 40% of the urine and the peptide-bound form accounting for 60%, and in most cases their concentrations in the urine are highly correlated.
Figure 1. Structures of PYD and DPD (Source: Benarba B, et al. 2014)
PYD and DPD have unique advantages in sensitivity and specificity as biochemical markers of bone resorption due to their distribution and metabolism. Firstly, pyridinoline crosslinks are formed only in extracellular collagen fibers and originate as mature matrix degradation products rather than newly formed collagen, and they are not further metabolized to other products. Second, PYD is derived from type I and type II collagen of bone and cartilage, whereas DPD is found almost exclusively in type I collagen, making its measurement more specific than other bone resorption indicators. Furthermore, cross-linking of pyridinoline was not affected by dietary intake.
Clinically they are commonly used in bone metabolic diseases such as osteoporosis, arthritis, cancer, and hyperthyroidism. Urinary PYD and DPD levels were significantly higher in postmenopausal osteoporosis patients than in premenopausal women, and PYD and DPD decreased to premenopausal levels after 6 months of oral estrogen therapy; therefore, PYD and DPD may be useful indicators for screening high-risk groups for osteoporosis and for monitoring the efficacy of estrogen. In cancer patients with or without bone metastases, urinary PYD and DPD were higher than in the normal control population, with cancer patients with bone metastases having higher urinary PYD and DPD levels than cancer patients without bone metastases. This suggests the possibility that both of these indicators could be a sensitive indicator of advanced tumors and perhaps serve as a prognostic marker for bone metastasis of cancer.
Alternative Names
DPD ELISA Kit
References
1. Benarba B, et al. Response of Bone Resorption Markers to Aristolochia longa Intake by Algerian Breast Cancer Postmenopausal Women. Adv Pharmacol Sci. 2014;2014:820589.
2. Eastell R, et al. DIAGNOSIS OF ENDOCRINE DISEASE: Bone turnover markers: are they clinically useful? Eur J Endocrinol. 2018 Jan;178(1):R19-R31.
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References
First use of the RANKL antibody denosumab in Osteogenesis Imperfecta Type VI
JOURNAL OF MUSCULOSKELETAL & NEURONAL INTERACTIONS
Osteogenesis imperfecta (OI) is a genetically heterogeneous disease leading to bone fragility. OI-VI is an autosomal-recessive form caused by mutations in SERPINF1. There is experimental evidence suggesting that loss of functional SERPINF1 leads to an activation of osteoclasts via the RANK/RANKL pathway. Patients with OI-VI show a poor response to bisphosphonates. We report on four children with OI-VI who had shown continuously elevated urinary bone resorption markers during previous treatment with bisphosphonates. We treated these children with the RANKL antibody denosumab to reduce bone resorption. Intervention and results: Denosumab (1 mg/kg body weight) was injected s.c. every 3 months. There were no severe side effects. Markers of bone resorption decreased to the normal range after each injection. N-terminal Propeptide of collagen 1 was measured in the serum during the first treatment cycle and decreased also. Urinary deoxypyridinoline/creatinine was monitored in a total of seven treatment cycles and indicated that bone resorption reached the pre-treatment level after 6-8 weeks. Conclusion: This was the first use of denosumab in children with OI-VI. Denosumab was well tolerated, and laboratory parameters provided evidence that the treatment reversibly reduced bone resorption. Therefore, denosumab may be a new therapeutic option for patients with OI-VI.
Effects of Ovariectomy on Bone Metabolism and Bone Mineral Density in Spontaneously Diabetic Torii-Lepr(fa) Rats
The Spontaneously Diabetic Torii-Lepr(fa) (SDT-fa/fa) rat is a new model of obese type 2 diabetes. The female SDT-fa/fa rat shows obesity, hyperglycemia and hyperlipidemia from a young age. However, it is not known whether diabetes and estrogen deficiency can lead to bone abnormalities in the female SDT-fa/fa rat. The objective of the present study was to investigate the effects of ovariectomy (OVX) on bone metabolism and bone mineral density (BMD) in the female SDT-fa/fa rat. Female Sprague-Dawley rats were used as control animals. The BMDs of the whole tibia and fifth lumbar (L5) vertebral body were analyzed at 30 weeks after OVX. Serum osteocalcin, a bone formation marker, and urine deoxypyridinoline (DPD), a bone resorption marker, were sequentially analyzed before and at 5,15 and 30 weeks after OVX. Serum osteocalcin and urine DPD levels were lower in SDT-fa/fa rats than in control rats before OVX. Both serum osteocalcin and urine DPD levels were elevated in control rats 5-30 weeks after OVX, but only the urine DPD levels were elevated in SDT-fa/fa rats 5-30 weeks after OVX. SDT-fa/fa rats showed a decrease in the BMDs of the whole tibia and L5 vertebral body compared with control rats. OVX decreased the BMDs of the whole tibia and L5 vertebral body in control rats, but not in SDT-fa/fa rats. These data suggest that estrogen deficiency is not a risk factor for bone loss in type 2 diabetes mellitus.
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Figure 1. Structures of PYD and DPD
