The relationship between OPLL and metabolic disorders

Junfeng Wang , Ziheng Wei , Qingjie Kong , Yanqing Sun , Zhichao Zhang , Haiyuan Yang , Xiongsheng Chen

Bone Research ›› 2025, Vol. 13 ›› Issue (1) : 90

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Bone Research ›› 2025, Vol. 13 ›› Issue (1) : 90 DOI: 10.1038/s41413-025-00446-9
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review-article

The relationship between OPLL and metabolic disorders

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Abstract

Ossification of the posterior longitudinal ligament (OPLL) is a degenerative disease characterized by progressive ectopic bone formation process, which can lead to severe neurological impairments and reduced quality of life. While the etiology of OPLL is generally considered multifactorial, there is no consensus regarding these contributing factors including genetic, endocrine, biomechanical, immune and lifestyle factors. Through accumulating evidence from multidisciplinary investigations, the pathophysiological connection between OPLL and endocrine-metabolic dysregulation is becoming increasingly clear. Nevertheless, comprehensive understanding of the relationship between the two is hindered by several problems, such as methodological limitations and inadequate mechanistic studies. This review takes a deep dive into the possible factors contributing to OPLL from all aspects of metabolism, including glucose metabolism, lipid metabolism, bone and mineral metabolism, leptin, vitamin, growth hormone/IGF-1 and sex hormones, highlighting their potential roles in the onset and progression of OPLL. Clarifying the etiology of OPLL and elucidating the underlying pathogenesis are crucial for advancing both early intervention strategies and therapeutic approaches in clinical management. Therefore, the endocrine and metabolic disorders in OPLL patients should become a focus of future research.

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Junfeng Wang, Ziheng Wei, Qingjie Kong, Yanqing Sun, Zhichao Zhang, Haiyuan Yang, Xiongsheng Chen. The relationship between OPLL and metabolic disorders. Bone Research, 2025, 13(1): 90 DOI:10.1038/s41413-025-00446-9

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References

[1]

Boody BS, Lendner M, Vaccaro AR. Ossification of the posterior longitudinal ligament in the cervical spine: a review. Int. Orthop., 2019, 43: 797-805.

[2]

Le HV, Wick JB, Van BW, Klineberg EO. Ossification of the posterior longitudinal ligament: pathophysiology, diagnosis, and management. J. Am. Acad. Orthop. Surg., 2022, 30: 820-830.

[3]

Fujimori T. et al.. Prevalence, concomitance, and distribution of ossification of the spinal ligaments: results of whole spine CT scans in 1500 Japanese patients. Spine, 2016, 41: 1668-1676.

[4]

Tsuji T. et al.. Epidemiological survey of ossification of the posterior longitudinal ligament by using clinical investigation registration forms. J. Orthop. Sci., 2016, 21: 291-294.

[5]

Choi BW, Song KJ, Chang H. Ossification of the posterior longitudinal ligament: a review of literature. Asian Spine J., 2011, 5: 267-276.

[6]

Yan L. et al.. The pathogenesis of ossification of the posterior longitudinal ligament. Aging Dis., 2017, 8: 570-582.

[7]

Liang H. et al.. Epidemiology of ossification of the spinal ligaments and associated factors in the Chinese population: a cross-sectional study of 2000 consecutive individuals. BMC Musculoskelet. Disord., 2019, 20. 253

[8]

Velan GJ, Currier BL, Clarke BL, Yaszemski MJ. Ossification of the posterior longitudinal ligament in vitamin D-resistant rickets: case report and review of the literature. Spine, 2001, 26: 590-593.

[9]

Fujimori T. et al.. Ossification of the posterior longitudinal ligament of the cervical spine in 3161 patients: a CT-based study. Spine, 2015, 40: E394-E403.

[10]

Chang H, Song KJ, Kim HY, Choi BW. Factors related to the development of myelopathy in patients with cervical ossification of the posterior longitudinal ligament. J. Bone Jt. Surg. Br., 2012, 94: 946-949.

[11]

Matsunaga S, Komiya S, Toyama Y. Risk factors for development of myelopathy in patients with cervical spondylotic cord compression. Eur. Spine J., 2015, 24: 142-149.

[12]

Matsunaga S. et al.. Radiographic predictors for the development of myelopathy in patients with ossification of the posterior longitudinal ligament: a multicenter cohort study. Spine (Philos. Pa 1976), 2008, 33: 2648-2650.

[13]

Matsunaga S. et al.. Pathogenesis of myelopathy in patients with ossification of the posterior longitudinal ligament. J. Neurosurg., 2002, 96: 168-172

[14]

Tetreault L. et al.. A systematic review of classification systems for cervical ossification of the posterior longitudinal ligament. Glob. Spine J., 2019, 9: 85-103.

[15]

Koda M. et al.. Comparison of clinical outcomes between laminoplasty, posterior decompression with instrumented fusion, and anterior decompression with fusion for K-line (-) cervical ossification of the posterior longitudinal ligament. Eur. Spine J., 2016, 25: 2294-2301.

[16]

Yang H. et al.. Implications of different patterns of “double-layer sign” in cervical ossification of the posterior longitudinal ligament. Eur. Spine J., 2015, 24: 1631-1639.

[17]

Abiola R, Rubery P, Mesfin A. Ossification of the posterior longitudinal ligament: etiology, diagnosis, and outcomes of nonoperative and operative management. Glob. Spine J., 2016, 6: 195-204.

[18]

Ng BW, Tan JA, Sabri S, Baharuddin A, Muhamad Ariffin MH. Surgical management of cervical ossification of posterior longitudinal ligament: the treatment algorithm and outcome. Cureus, 2023, 15: e36517

[19]

An HS, Al-Shihabi L, Kurd M. Surgical treatment for ossification of the posterior longitudinal ligament in the cervical spine. J. Am. Acad. Orthop. Surg., 2014, 22: 420-429.

[20]

Smith ZA, Buchanan CC, Raphael D, Khoo LT. Ossification of the posterior longitudinal ligament: pathogenesis, management, and current surgical approaches. A Rev. Neurosurg. Focus, 2011, 30: E10.

[21]

Lee CH. et al.. Are there differences in the progression of ossification of the posterior longitudinal ligament following laminoplasty versus fusion? A meta-Analysis. Spine, 2017, 42: 887-894.

[22]

Onari K. et al.. Long-term follow-up results of anterior interbody fusion applied for cervical myelopathy due to ossification of the posterior longitudinal ligament. Spine, 2001, 26: 488-493.

[23]

Sato R. et al.. Ossification of the posterior longitudinal ligament of the cervical spine: histopathological findings around the calcification and ossification front. J. Neurosurg. Spine, 2007, 7: 174-183.

[24]

Kimura A. et al.. Possible involvement of vitamin K insufficiency in the progression of cervical ossification of the posterior longitudinal ligament. Sci. Rep., 2025, 15. 2608

[25]

Saetia K, Cho D, Lee S, Kim DH, Kim SD. Ossification of the posterior longitudinal ligament: a review. Neurosurg. Focus, 2011, 30: E1.

[26]

Kawaguchi Y. Biomarkers of ossification of the spinal ligament. Glob. Spine J., 2019, 9: 650-657.

[27]

Cai GD. et al.. Multiplex analysis of serum hormone and cytokine in patients with cervical cOPLL: towards understanding the potential pathogenic mechanisms. Growth Factors, 2017, 35: 171-178.

[28]

Katsumi K. et al.. Predictive biomarkers of ossification progression and bone metabolism dynamics in patients with cervical ossification of the posterior longitudinal ligament. Eur. Spine J., 2023, 32: 1282-1290.

[29]

Li H, Jiang LS, Dai LY. Hormones and growth factors in the pathogenesis of spinal ligament ossification. Eur. Spine J., 2007, 16: 1075-1084.

[30]

Kobashi G. et al.. High body mass index after age 20 and diabetes mellitus are independent risk factors for ossification of the posterior longitudinal ligament of the spine in Japanese subjects: a case-control study in multiple hospitals. Spine, 2004, 29: 1006-1010.

[31]

Bai XC. et al.. Oxidative stress inhibits osteoblastic differentiation of bone cells by ERK and NF-kappaB. Biochem. Biophys. Res. Commun., 2004, 314: 197-207.

[32]

Bai XC. et al.. Reactive oxygen species stimulates receptor activator of NF-kappaB ligand expression in osteoblast. J. Biol. Chem., 2005, 280: 17497-17506.

[33]

Mody N, Parhami F, Sarafian TA, Demer LL. Oxidative stress modulates osteoblastic differentiation of vascular and bone cells. Free Radic. Biol. Med., 2001, 31: 509-519.

[34]

Morita K. et al.. Reactive oxygen species induce chondrocyte hypertrophy in endochondral ossification. J. Exp. Med., 2007, 204: 1613-1623.

[35]

Chen NX, Duan D, O’Neill KD, Moe SM. High glucose increases the expression of Cbfa1 and BMP-2 and enhances the calcification of vascular smooth muscle cells. Nephrol. Dial. Transpl., 2006, 21: 3435-3442.

[36]

Li YM. et al.. Effects of high glucose on mesenchymal stem cell proliferation and differentiation. Biochem. Biophys. Res. Commun., 2007, 363: 209-215.

[37]

Han YS. et al.. High dose of glucose promotes chondrogenesis via PKCalpha and MAPK signaling pathways in chick mesenchymal cells. Cell Tissue Res., 2004, 318: 571-578.

[38]

Balint E, Szabo P, Marshall CF, Sprague SM. Glucose-induced inhibition of in vitro bone mineralization. Bone, 2001, 28: 21-28.

[39]

Inaba M. et al.. Influence of high glucose on 1,25-dihydroxyvitamin D3-induced effect on human osteoblast-like MG-63 cells. J. Bone Miner. Res., 1995, 10: 1050-1056.

[40]

Ishida Y, Kawai S. Characterization of cultured cells derived from ossification of the posterior longitudinal ligament of the spine. Bone, 1993, 14: 85-91.

[41]

Nam DC, Lee HJ, Lee CJ, Hwang SC. Molecular pathophysiology of ossification of the posterior longitudinal ligament (OPLL). Biomol. Ther., 2019, 27: 342-348.

[42]

Li H, Jiang LS, Dai LY. High glucose potentiates collagen synthesis and bone morphogenetic protein-2-induced early osteoblast gene expression in rat spinal ligament cells. Endocrinology, 2010, 151: 63-74.

[43]

Shingyouchi Y, Nagahama A, Niida M. Ligamentous ossification of the cervical spine in the late middle-aged Japanese men. Its relation to body mass index and glucose metabolism. Spine, 1996, 21: 2474-2478.

[44]

Singh M, Kuharski M, Balmaceno-Criss M, Diebo BG, Daniels A. Hyperlipidemia, obesity, and diabetes, and risk of ossification of the posterior longitudinal ligament. World Neurosurg., 2024, 188: e642-e647.

[45]

Akune T. et al.. Insulin secretory response is positively associated with the extent of ossification of the posterior longitudinal ligament of the spine. J. Bone Jt. Surg. Am., 2001, 83: 1537-1544.

[46]

Okano T. et al.. Orthotopic ossification of the spinal ligaments of Zucker fatty rats: a possible animal model for ossification of the human posterior longitudinal ligament. J. Orthop. Res., 1997, 15: 820-829.

[47]

Olesen P, Nguyen K, Wogensen L, Ledet T, Rasmussen LM. Calcification of human vascular smooth muscle cells: associations with osteoprotegerin expression and acceleration by high-dose insulin. Am. J. Physiol. Heart Circ. Physiol., 2007, 292: H1058-H1064.

[48]

White MF, Kahn CR. The insulin signaling system. J. Biol. Chem., 1994, 269: 1-4.

[49]

Xiao G. et al.. Bone morphogenetic proteins, extracellular matrix, and mitogen-activated protein kinase signaling pathways are required for osteoblast-specific gene expression and differentiation in MC3T3-E1 cells. J. Bone Miner. Res., 2002, 17: 101-110.

[50]

Li H, Liu D, Zhao CQ, Jiang LS, Dai LY. Insulin potentiates the proliferation and bone morphogenetic protein-2-induced osteogenic differentiation of rat spinal ligament cells via extracellular signal-regulated kinase and phosphatidylinositol 3-kinase. Spine, 2008, 33: 2394-2402.

[51]

Aubert CE. et al.. Association of peripheral neuropathy with circulating advanced glycation end products, soluble receptor for advanced glycation end products and other risk factors in patients with type 2 diabetes. Diabetes Metab. Res. Rev., 2014, 30: 679-685.

[52]

Yamagishi S, Fujimori H, Yonekura H, Tanaka N, Yamamoto H. Advanced glycation endproducts accelerate calcification in microvascular pericytes. Biochem. Biophys. Res. Commun., 1999, 258: 353-357.

[53]

Kume S. et al.. Advanced glycation end-products attenuate human mesenchymal stem cells and prevent cognate differentiation into adipose tissue, cartilage, and bone. J. Bone Miner. Res., 2005, 20: 1647-1658.

[54]

Yoshimura N. et al.. Prevalence and progression of radiographic ossification of the posterior longitudinal ligament and associated factors in the Japanese population: a 3-year follow-up of the ROAD study. Osteoporos. Int., 2014, 25: 1089-1098.

[55]

Yokosuka K. et al.. Immunohistochemical demonstration of advanced glycation end products and the effects of advanced glycation end products in ossified ligament tissues in vitro. Spine, 2007, 32: E337-E339.

[56]

Doi T. et al.. Noninvasive skin autofluorescence of advanced glycation end products for detecting ossification of the posterior longitudinal ligament in the thoracic spine. Spine, 2023, 48: E40-E45.

[57]

Endo T. et al.. Strong relationship between dyslipidemia and the ectopic ossification of the spinal ligaments. Sci. Rep., 2022, 12. 22617

[58]

Fukada S. et al.. Dyslipidemia as a novel risk for the development of symptomatic ossification of the posterior longitudinal ligament. Spine J., 2023, 23: 1287-1295.

[59]

Zhang R, Yang Q, Wang Y, Zhao Y. Investigation of the association between hyperlipidemia and ossification of the posterior longitudinal ligament through two-sample mendelian randomization analysis. Spine, 2025, 50: 163-171.

[60]

Endo T. et al.. Close association between non-alcoholic fatty liver disease and ossification of the posterior longitudinal ligament of the spine. Sci. Rep., 2021, 11. 17412

[61]

Parisi V. et al.. The lipid theory in the pathogenesis of calcific aortic stenosis. Nutr. Metab. Cardiovasc. Dis., 2015, 25: 519-525.

[62]

Bundy K, Boone J, Simpson CL. Wnt signaling in vascular calcification. Front. Cardiovasc. Med., 2021, 8. 708470

[63]

Hu L, Chen W, Qian A, Li YP. Wnt/beta-catenin signaling components and mechanisms in bone formation, homeostasis, and disease. Bone Res., 2024, 12: 39.

[64]

He X, Semenov M, Tamai K, Zeng X. LDL receptor-related proteins 5 and 6 in Wnt/beta-catenin signaling: arrows point the way. Development, 2004, 131: 1663-1677.

[65]

Karner CM, Long F. Wnt signaling and cellular metabolism in osteoblasts. Cell Mol. Life Sci., 2017, 74: 1649-1657.

[66]

Alekos NS, Moorer MC, Riddle RC. Dual effects of lipid metabolism on osteoblast function. Front. Endocrinol., 2020, 11. 578194

[67]

Borrell-Pages M, Romero JC, Badimon L. LRP5 deficiency down-regulates Wnt signalling and promotes aortic lipid infiltration in hypercholesterolaemic mice. J. Cell Mol. Med., 2015, 19: 770-777.

[68]

Albanese, I., Khan, K., Barratt, B., Al-Kindi, H. & Schwertani, A. Atherosclerotic calcification: Wnt is the hint. J. Am. Heart Assoc.7, e007356 (2018).

[69]

Tsuji T. et al.. Metabolite profiling of plasma in patients with ossification of the posterior longitudinal ligament. J. Orthop. Sci., 2018, 23: 878-883.

[70]

Hamazaki K. et al.. Mead acid (20:3n-9) and n-3 polyunsaturated fatty acids are not associated with risk of posterior longitudinal ligament ossification: results of a case-control study. Prostaglandins Leukot. Ess. Fat. Acids, 2015, 96: 31-36.

[71]

Adams JE, Davies M. Paravertebral and peripheral ligamentous ossification: an unusual association of hypoparathyroidism. Postgrad. Med. J., 1977, 53: 167-172.

[72]

Soehle M, Casey AT. Cervical spinal cord compression attributable to a calcified intervertebral disc in a patient with X-linked hypophosphatemic rickets: case report and review of the literature. Neurosurgery, 2002, 51: 239-242.

[73]

Okazaki T. et al.. Ossification of the paravertebral ligaments: a frequent complication of hypoparathyroidism. Metabolism, 1984, 33: 710-713.

[74]

Kashii M. et al.. Circulating sclerostin and dickkopf-1 levels in ossification of the posterior longitudinal ligament of the spine. J. Bone Miner. Metab., 2016, 34: 315-324.

[75]

Taguchi, T. in OPLL: Ossification of the Posterior Longitudinal Ligament (eds Kazuo Yonenobu, Kozo Nakamura, & Yoshiaki Toyama) 29–31 (Springer, 2006).

[76]

Sasaki K. et al.. Bone turnover markers in patients with ossification of the posterior longitudinal ligament in the thoracic spine. Spine, 2024, 49: E100-E106.

[77]

Takuwa Y. et al.. Calcium metabolism in paravertebral ligamentous ossification. Acta Endocrinol., 1985, 109: 428-432

[78]

Seichi A, Hoshino Y, Ohnishi I, Kurokawa T. The role of calcium metabolism abnormalities in the development of ossification of the posterior longitudinal ligament of the cervical spine. Spine (Philos. Pa 1976), 1992, 17: S30-S32.

[79]

Yamauchi T, Taketomi E, Matsunaga S, Sakou T. Bone mineral density in patients with ossification of the posterior longitudinal ligament in the cervical spine. J. Bone Miner. Metab., 1999, 17: 296-300.

[80]

Fujita R. et al.. High whole-body bone mineral density in ossification of the posterior longitudinal ligament. Spine J., 2023, 23: 1461-1470.

[81]

Silva BC, Bilezikian JP. Parathyroid hormone: anabolic and catabolic actions on the skeleton. Curr. Opin. Pharm., 2015, 22: 41-50.

[82]

Horie S. et al.. Factors associated with bone metabolism in patients with cervical ossification of the posterior longitudinal ligament accompanied with diffuse idiopathic skeletal hyperostosis. Sicot J., 2018, 4: 7.

[83]

Kawaguchi Y. et al.. Increase of the serum FGF-23 in ossification of the posterior longitudinal ligament. Glob. Spine J., 2019, 9: 492-498.

[84]

Fukumoto S, Yamashita T. FGF23 is a hormone-regulating phosphate metabolism–unique biological characteristics of FGF23. Bone, 2007, 40: 1190-1195.

[85]

Mackenzie NC. et al.. Altered bone development and an increase in FGF-23 expression in Enpp1-/- mice. PLoS One, 2012, 7: e32177.

[86]

Ikegawa S. Genomic study of ossification of the posterior longitudinal ligament of the spine. Proc. Jpn. Acad. Ser. B Phys. Biol. Sci., 2014, 90: 405-412.

[87]

Marie PJ, Miraoui H, Severe N. FGF/FGFR signaling in bone formation: progress and perspectives. Growth Factors, 2012, 30: 117-123.

[88]

Wang W, Kong L, Zhao H, Jia Z. Ossification of the transverse atlantal ligament associated with fluorosis: a report of two cases and review of the literature. Spine, 2004, 29: E75-E78.

[89]

Reddy KVS, Mudumba VS, Tokala IM, Reddy DR. Ossification of posterior longitudinal ligament and fluorosis. Neurology, 2018, 66: 1394-1399

[90]

Sohn S, Chung CK. Increased bone mineral density and decreased prevalence of osteoporosis in cervical ossification of the posterior longitudinal ligament: a case-control study. Calcif. Tissue Int., 2013, 92: 28-34.

[91]

Matsui H, Yudoh K, Tsuji H. Significance of serum levels of type I procollagen peptide and intact osteocalcin and bone mineral density in patients with ossification of the posterior longitudinal ligaments. Calcif. Tissue Int., 1996, 59: 397-400.

[92]

Niu CC. et al.. Correlation of blood bone turnover biomarkers and Wnt signaling antagonists with AS, DISH, OPLL, and OYL. BMC Musculoskelet. Disord., 2017, 18. 61

[93]

Ishihara C. et al.. The efficacy of biochemical markers in patients with ossification of posterior longitudinal ligament of the spine. Spinal Cord., 2000, 38: 211-213.

[94]

Westendorf JJ, Kahler RA, Schroeder TM. Wnt signaling in osteoblasts and bone diseases. Gene, 2004, 341: 19-39.

[95]

Piters E, Boudin E, Van Hul W. Wnt signaling: a win for bone. Arch. Biochem. Biophys., 2008, 473: 112-116.

[96]

Baron R, Kneissel M. WNT signaling in bone homeostasis and disease: from human mutations to treatments. Nat. Med., 2013, 19: 179-192.

[97]

Li X. et al.. Sclerostin binds to LRP5/6 and antagonizes canonical Wnt signaling. J. Biol. Chem., 2005, 280: 19883-19887.

[98]

Mao B. et al.. Kremen proteins are Dickkopf receptors that regulate Wnt/beta-catenin signalling. Nature, 2002, 417: 664-667.

[99]

Dong J, Xu X, Zhang Q, Yuan Z, Tan B. Dkk1 acts as a negative regulator in the osteogenic differentiation of the posterior longitudinal ligament cells. Cell Biol. Int., 2020, 44: 2450-2458.

[100]

Senolt L. et al.. Low circulating Dickkopf-1 and its link with severity of spinal involvement in diffuse idiopathic skeletal hyperostosis. Ann. Rheum. Dis., 2012, 71: 71-74.

[101]

Aeberli D, Schett G, Eser P, Seitz M, Villiger PM. Serum Dkk-1 levels of DISH patients are not different from healthy controls. Jt. Bone Spine, 2011, 78: 422-423.

[102]

Maeda K, Takahashi N, Kobayashi Y. Roles of Wnt signals in bone resorption during physiological and pathological states. J. Mol. Med., 2013, 91: 15-23.

[103]

Simonet WS. et al.. Osteoprotegerin: a novel secreted protein involved in the regulation of bone density. Cell, 1997, 89: 309-319.

[104]

Fay, L. Y. et al. Comparative study of the cytokine profiles of serum and tissues from patients with the ossification of the posterior longitudinal ligament. Biomedicines11, 2021 (2023).

[105]

DiGiovanna JJ, Helfgott RK, Gerber LH, Peck GL. Extraspinal tendon and ligament calcification associated with long-term therapy with etretinate. N. Engl. J. Med., 1986, 315: 1177-1182.

[106]

Pennes DR, Martel W, Ellis CN. Retinoid-induced ossification of the posterior longitudinal ligament. Skelet. Radio., 1985, 14: 191-193.

[107]

Ishida Y, Kawai S. Effects of bone-seeking hormones on DNA synthesis, cyclic AMP level, and alkaline phosphatase activity in cultured cells from human posterior longitudinal ligament of the spine. J. Bone Miner. Res., 1993, 8: 1291-1300.

[108]

Kodama T, Matsunaga S, Taketomi E, Sakou T. Retinoid and bone metabolic marker in ossification of the posterior longitudinal ligament. Vivo, 1998, 12: 339-344

[109]

Endo T. et al.. Association between Vitamin A intake and disease severity in early-onset heterotopic ossification of the posterior longitudinal ligament of the spine. Glob. Spine J., 2022, 12: 1770-1780.

[110]

Weston AD, Chandraratna RA, Torchia J, Underhill TM. Requirement for RAR-mediated gene repression in skeletal progenitor differentiation. J. Cell Biol., 2002, 158: 39-51.

[111]

Shimono K. et al.. Potent inhibition of heterotopic ossification by nuclear retinoic acid receptor-gamma agonists. Nat. Med., 2011, 17: 454-460.

[112]

Willems BA, Vermeer C, Reutelingsperger CP, Schurgers LJ. The realm of vitamin K dependent proteins: shifting from coagulation toward calcification. Mol. Nutr. Food Res., 2014, 58: 1620-1635.

[113]

Yamada K. et al.. High serum levels of menatetrenone in male patients with ossification of the posterior longitudinal ligament. Spine, 2003, 28: 1789-1793.

[114]

Schmidt RF, Goldstein IM, Liu JK. Ossified ligamentum flavum causing spinal cord compression in a patient with acromegaly. J. Clin. Neurosci., 2013, 20: 1599-1603.

[115]

Kamakura D. et al.. Acromegaly presenting with myelopathy due to ossification of posterior longitudinal ligament: a case report. BMC Musculoskelet. Disord., 2021, 22. 353

[116]

Ikegawa S. et al.. Increase of serum growth hormone-binding protein in patients with ossification of the posterior longitudinal ligament of the spine. Spine, 1993, 18: 1757-1760.

[117]

Goto K. et al.. Involvement of insulin-like growth factor I in development of ossification of the posterior longitudinal ligament of the spine. Calcif. Tissue Int., 1998, 62: 158-165.

[118]

Chaput CD, Siddiqui M, Rahm MD. Obesity and calcification of the ligaments of the spine: a comprehensive CT analysis of the entire spine in a random trauma population. Spine J., 2019, 19: 1346-1353.

[119]

Zhao Y, Xiang Q, Lin J, Jiang S, Li W. High body mass index is associated with an increased risk of the onset and severity of ossification of spinal ligaments. Front. Surg., 2022, 9. 941672

[120]

Katsumi K. et al.. Natural history of the ossification of cervical posterior longitudinal ligament: a three dimensional analysis. Int. Orthop., 2018, 42: 835-842.

[121]

Takahata M. et al.. Adipokine dysregulation as an underlying pathology for diffuse ectopic ossification of spinal posterior longitudinal ligament in patients with obesity. Spine J., 2025, 25: 80-90.

[122]

Ikeda Y. et al.. Association between serum leptin and bone metabolic markers, and the development of heterotopic ossification of the spinal ligament in female patients with ossification of the posterior longitudinal ligament. Eur. Spine J., 2011, 20: 1450-1458.

[123]

Iida M. et al.. Substitution at codon 269 (glutamine –> proline) of the leptin receptor (OB-R) cDNA is the only mutation found in the Zucker fatty (fa/fa) rat. Biochem. Biophys. Res. Commun., 1996, 224: 597-604.

[124]

Fan D, Chen Z, Chen Y, Shang Y. Mechanistic roles of leptin in osteogenic stimulation in thoracic ligament flavum cells. J. Biol. Chem., 2007, 282: 29958-29966.

[125]

Zheng B. et al.. Increased osteogenesis in osteoporotic bone marrow stromal cells by overexpression of leptin. Cell Tissue Res., 2015, 361: 845-856.

[126]

Lamghari M, Tavares L, Camboa N, Barbosa MA. Leptin effect on RANKL and OPG expression in MC3T3-E1 osteoblasts. J. Cell Biochem., 2006, 98: 1123-1129.

[127]

Jiang H. et al.. Leptin accelerates the pathogenesis of heterotopic ossification in rat tendon tissues via mTORC1 signaling. J. Cell Physiol., 2018, 233: 1017-1028.

[128]

Feng B. et al.. Roles and mechanisms of leptin in osteogenic stimulation in cervical ossification of the posterior longitudinal ligament. J. Orthop. Surg. Res., 2018, 13: 165.

[129]

Chen S. et al.. Combined use of leptin and mechanical stress has osteogenic effects on ossification of the posterior longitudinal ligament. Eur. Spine J., 2018, 27: 1757-1766.

[130]

Okada Y, M. M., Fujita, L., Furufu, T., Yuji, M. & Tabe, S. Association of ossification of the spinal ligaments and sex hormones. Orthop. MOOK, 12–25 (1987).

[131]

Wada A. Affinity of estrogen binding in the cultured spinal ligament cells: an in vitro study using cells from spinal ligament ossification patients]. Nihon Seikeigeka Gakkai Zasshi, 1995, 69: 440-449

[132]

Ogata N. et al.. Association of bone metabolism regulatory factor gene polymorphisms with susceptibility to ossification of the posterior longitudinal ligament of the spine and its severity. Spine, 2002, 27: 1765-1771.

[133]

Morisu M. Influence of foods on the posterior longitudinal ligament of the cervical spine and serum sex hormones. Nihon Seikeigeka Gakkai Zasshi, 1994, 68: 1056-1067

[134]

Liang L, Yu JF, Wang Y, Wang G, Ding Y. Effect of estrogen receptor beta on the osteoblastic differentiation function of human periodontal ligament cells. Arch. Oral. Biol., 2008, 53: 553-557.

[135]

Shu L. et al.. Estrogen modulates cytokine expression in human periodontal ligament cells. J. Dent. Res., 2008, 87: 142-147.

[136]

Fruhbeck G, Salvador J. Relation between leptin and the regulation of glucose metabolism. Diabetologia, 2000, 43: 3-12.

[137]

Niswender KD, Schwartz MW. Insulin and leptin revisited: adiposity signals with overlapping physiological and intracellular signaling capabilities. Front. Neuroendocrinol., 2003, 24: 1-10.

[138]

Hegyi K, Fulop K, Kovacs K, Toth S, Falus A. Leptin-induced signal transduction pathways. Cell Biol. Int., 2004, 28: 159-169.

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