Inflammatory and bone turnover markers in a cross‐sectional and prospective study of acute Charcot osteoarthropathy

Petrova, Nina L.; Dew, Tracy; Musto, Rebecca; Sherwood, Roy; Bates, Maureen; Moniz, C.; Edmonds, M.

doi:10.1111/dme.12590

Cited by 58 publications

(78 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…OCN is also used as a biomarker of skeletal development, and increased serum OCN level is associated with increased bone mineral density during osteoporosis treatment [48,49]. However, in our study, elevated OCN levels were accompanied by decreased BMD.…”

Section: Discussioncontrasting

confidence: 64%

Glucose metabolic abnormality is associated with defective mineral homeostasis in skeletal disorder mouse model

Zou

Xiong

Lai

et al. 2015

Sci. China Life Sci.

View full text Add to dashboard Cite

Bone was reported as a crucial organ for regulating glucose homeostasis. In this study, we found that Phex mutant mice (PUG), a model of human X-linked hypophosphatemic rickets (XLH), displayed metabolic abnormality in addition to abnormal phosphate homeostasis, skeletal deformity and growth retardation. Glucose tolerance was elevated with enhanced insulin sensitivity in PUG, though circulating insulin level decreased. Interestingly, bone mineral density defects and glucose metabolic abnormality were both rescued by adding phosphorus-and calcium-enriched supplements in daily diet. Serum insulin level, glucose tolerance and insulin sensitivity showed no differences between PUG and wild-type mice with rescued osteocalcin (OCN) following treatment. Our study suggested that OCN is a potential mediator between mineral homeostasis and glucose metabolism. This investigation brings a new perspective on glucose metabolism regulation through skeleton triggered mineral homeostasis and provides new clues in clinical therapeutics of potential metabolic disorders in XLH patients. glucose metabolism, mineral homeostasis, bone, Phex, X-linked hypophosphatemic rickets Citation:Zou JH, Xiong XW, Lai BB, Sun M, Tu X, Gao X. Glucose metabolic abnormality is associated with defective mineral homeostasis in skeletal disorder mouse model. [5,6]. In the past decades, bone was studied as an endocrinal organ [7,8]. Interactions between bone and energy metabolism aroused extensive interests and concerns [911]. Phex is mainly expressed in osteoblasts and odontoblasts [1214] and its mutations lead to reduced 1,25-(OH) 2 D 3 and elevated circulating FGF23 (fibroblast growth factor 23) [1517]. 1,25-(OH) 2 D 3 and its receptor could influence expression of uncoupling protein (UCP) in adipocytes [18,19]. In vitro studies demonstrate that the role of 1,25-(OH) 2 D 3 in lipid metabolism is regulator of peroxisome proliferator-activated receptor alpha (Ppara) [20]. Circulating FGF23 is also associated with fat mass and serum lipids [21]. In mouse models of XLH, like Hyp mice, decreased renal glucose reabsorption activity [22], increased glucose production in renal proximal tubules [23] and osteoblasts [24] were observed. The only known physiological substrate of PHEX protein, acidic serine aspartate-rich MEPE associated motif (ASARM peptide), could regulate glucose metabolism and insulin signaling [14]. The above findings indicate PHEXmediated association between skeletal function and energy

show abstract

Section: Discussioncontrasting

confidence: 64%

Glucose metabolic abnormality is associated with defective mineral homeostasis in skeletal disorder mouse model

Zou

Xiong

Lai

et al. 2015

Sci. China Life Sci.

View full text Add to dashboard Cite

show abstract

“…Petrova et al, have shown that serum C-terminal telopeptide, but not alkaline phosphatase, was signi cantly higher in people with Charcot osteoarthropathy at presentation than in people with diabetes [21]. The observed lack of increased levels of bone alkaline phosphatase in response to the raised Cterminal telopeptide suggests that, in people with Charcot osteoarthropathy, there may be adynamic bone, related to the presence of diabetic neuropathy, which could impair the regulation of bone remodeling [22,23].…”

Section: Discussionmentioning

confidence: 99%

Bone Markers in Charcot Neuroarthropathy

Patel

Bernstein

Grahn

et al. 2020

Preprint

View full text Add to dashboard Cite

Background There have been multiple studies evaluating the effectiveness of pharmaceuticals in the treatment of acute Charcot neuroarthropathy (CNA). The effectiveness of most pharmaceuticals historically has been based on the levels of certain biomarkers of bone turnover. Previous research has shown bone turnover markers are increased in acute phase of CNA. However, biomarkers activity in chronic phase of CNA and its utility for monitoring treatment response remains to be established. In this article, we evaluated the relationship of such biomarkers to disease severity. We hypothesized that biomarkers such as BSAP and DPD:CRT levels will be directly proportional to disease severity i.e. increased in acute CNA and decreased in chronic CNA. Hence pharmacologic treatment in acute CNA with reference to levels of such biomarkers potentially could be beneficial in clinical settings. Methods We retrospectively reviewed 41 patients diagnosed with acute and chronic CNA in our Charcot clinic. Disease severity was determined via pedal temperature difference between affected and unaffected limbs using an OMEGA Surface Temperature Scanner in conjugation with radiographic films and clinical presentation. Temperature of 2 degrees Celsius or greater is considered acute CNA, temperature less than 2 degree Celsius is considered chronic CNA. Urine and serum blood samples were collected at baseline to evaluate the levels of BSAP and DPD:CRT via immunoassays. Statistical analysis was performed via separate Mann Whitney rank sums tests to determine between-group differences in BSAP and DPD:CRT in acute versus chronic CNA. Results Bone formation marker BSAP (p = 0.46) and bone resorption marker DPD:CRT (p = 0.92) were not significantly different in acute versus chronic CNA. In acute CNA patients (n = 31) median BSAP was 11.9 (range 3.8–41.3) versus 15.2 (range 4.4–40.7) in chronic CNA patients. In acute CNA patients, median DPD:CRT was 7.8 (range 3.1–38.4) versus 8.8 (range 3.3–18.6) in chronic CNA patients. Conclusion The lack of significant between-group differences in BSAP and DPD:CRT calls into question their reliability in monitoring pharmaceuticals effectiveness in acute versus chronic CNA.

show abstract

“…Petrova et al reported elevation of serum tumor necrosis factor a and interleukin 6 in acute Charcot osteoarthropathy. 12 Baumhauer et al reported the expression of proinflammatory cytokines in bone samples collected during surgery. 3 A review by Adamopoulos and Mellins suggests an alternative pathway for osteoclastogenesis provided by the infiltrating inflammatory …”

Section: Discussionmentioning

confidence: 99%

Regrowth of the deteriorated glenoid in advanced Charcot shoulder after suboccipital decompression for syringomyelia: a case report

Makihara

Onishi

Wadano

et al. 2015

Journal of Shoulder and Elbow Surgery

View full text Add to dashboard Cite

Inflammatory and bone turnover markers in a cross‐sectional and prospective study of acute Charcot osteoarthropathy

Abstract: At the onset of acute Charcot foot, serum concentrations of tumour necrosis factor-α and interleukin-6 were elevated; however, there was a significant reduction in these markers at resolution and these markers may be useful in the assessment of disease activity.

Cited by 58 publications

References 24 publications

Glucose metabolic abnormality is associated with defective mineral homeostasis in skeletal disorder mouse model

Glucose metabolic abnormality is associated with defective mineral homeostasis in skeletal disorder mouse model

Bone Markers in Charcot Neuroarthropathy

Regrowth of the deteriorated glenoid in advanced Charcot shoulder after suboccipital decompression for syringomyelia: a case report

Contact Info

Product

Resources

About