ArticleAnnals of pediatric endocrinology & metabolism2019
Skeletal mineralization: mechanisms and diseases.
Article in Annals of pediatric endocrinology & metabolism, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.
- Clinical characteristics of pediatric tumor-induced osteomalacia: a systematic review and individual patient data analysis.Frontiers in endocrinology · 2026Pooled it
- Pathophysiology and Molecular Signalling in Osteoporosis: Linking Risk Factors to Bone Loss.Journal of cellular and molecular medicine · 2026Review
- Hypophosphatasia in childhood: Diagnosis to management.Osteoporosis and sarcopenia · 2025Review
- Article
- Molecular roles in membrane receptor signaling pathways and cascade reactions in chondrocytes: a review.Journal of molecular histology · 2025Review
- Sox10 is required for systemic initiation of bone mineralization.Development (Cambridge, England) · 2025Article
- Comprehensive treatment approaches for skeletal deformities in hypophosphatasia: a case study ofFrontiers in pediatrics · 2025Article
- Stanniocalcin 1 and 1,25-dihydroxyvitamin DExperimental & molecular medicine · 2024Article
- Biomarkers and Biochemical Indicators to Evaluate Bone Metabolism in Preterm Neonates.Biomedicines · 2024Article
- Diagnostic and New Therapeutic Approaches to Two Challenging Pediatric Metabolic Bone Disorders: Hypophosphatasia and X-linked Hypophosphatemic Rickets.Current pediatric reviews · 2024Review
- The association of vitamin D insufficiency with the prevalence of obesity in children: implications for serum calcium levels, alkaline phosphatase activity, and bone maturation.Frontiers in nutrition · 2024Article
- Triggered metabolism of adenosine triphosphate as an explanation for the chemical heterogeneity of heterotopic ossification.Communications chemistry · 2023Article
- Convergence of Calcium Channel Regulation and Mechanotransduction in Skeletal Regenerative Biomaterial Design.Advanced healthcare materials · 2023Review
- Meclozine ameliorates bone mineralization and growth plate structure in a mouse model of X‑linked hypophosphatemia.Experimental and therapeutic medicine · 2023Article
- Not just a carrier: Clinical presentation and management of patients with heterozygous disease-causing alkaline phosphatase (ALPL) variants identified through expanded carrier screening.Molecular genetics & genomic medicine · 2023Article
- New developments in the biology of fibroblast growth factors.WIREs mechanisms of disease · 2022Review
- A rare combination of tumor-induced osteomalacia caused by sinonasal glomangiopericytoma and coexisting parathyroid adenoma: case report and literature review.BMC endocrine disorders · 2022Review
- Cellular and Molecular Alterations Underlying Abnormal Bone Growth in X-Linked Hypophosphatemia.International journal of molecular sciences · 2022Review
- Dietary calcium intake in Brazilian preschoolers and schoolchhildren: review of the literature.Revista paulista de pediatria : orgao oficial da Sociedade de Pediatria de Sao Paulo · 2022Review
- How Do Extracellular Vesicles Play a Key Role in the Maintenance of Bone Homeostasis and Regeneration? A Comprehensive Review of Literature.International journal of nanomedicine · 2022Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Skeletal mineralization is initiated in matrix vesicles (MVs), the small extracellular vesicles derived from osteoblasts and chondrocytes. Calcium and inorganic phosphate (Pi) taken up by MVs form hydroxyapatite crystals, which propagate on collagen fibrils to mineralize the extracellular matrix. Insufficient calcium or phosphate impairs skeletal mineralization. Because active vitamin D is necessary for intestinal calcium absorption, vitamin D deficiency is a significant cause of rickets/osteomalacia. Chronic hypophosphatemia also results in rickets/osteomalacia. Excessive action of fibroblast growth factor 23 (FGF23), a key regulator of Pi metabolism, leads to renal Pi wasting and impairs vitamin D activation. X-linked hypophosphatemic rickets (XLH) is the most common form of hereditary FGF23-related hypophosphatemia, and enhanced FGF receptor (FGFR) signaling in osteocytes may be involved in the pathogenesis of this disease. Increased extracellular Pi triggers signal transduction via FGFR to regulate gene expression, implying a close relationship between Pi metabolism and FGFR. An anti-FGF23 antibody, burosumab, has recently been developed as a new treatment for XLH. In addition to various forms of rickets/osteomalacia, hypophosphatasia (HPP) is characterized by impaired skeletal mineralization. HPP is caused by inactivating mutations in tissue-nonspecific alkaline phosphatase, an enzyme rich in MVs. The recent development of enzyme replacement therapy using bone-targeting recombinant alkaline phosphatase has improved the prognosis, motor function, and quality of life in patients with HPP. This links impaired skeletal mineralization with various conditions, and unraveling its pathogenesis will lead to more precise diagnoses and effective treatments.
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