Application of chondroprotective agents to inhibit osteodestructive processes in the subchondral bone in patients with osteoarthritis
https://doi.org/10.17749/2070-4909/farmakoekonomika.2022.126
Abstract
Background. Osteoarthritis (OA) is associated with an activation of local inflammation and involves subchondral tissue of the joint.
Objective: to conduct a systemic analysis of the publications on the association between OA and metabolic disorders in bones.
Material and methods. The authors analyzed 3,926 publications on the studies of OA and metabolic disorders in bones tissue by the method of a topologic theory of recognition selected by the request “osteoarthritis AND (bone resorption OR osteopenia OR osteoporosis)” in the database of biomedical publications PubMed/MEDLINE. The control sampling included 4,000 articles randomly selected out of 97,331 found by the request “osteoarthritis NOT bone NOT resorption NOT osteopenia NOT osteoporosis” (i.e. publications on OA that do not cover issues of bone metabolism).
Results. The associations between cartilaginous pathology and bone tissue destruction are mediated by anti-inflammatory cytokines, osteoblast and osteoclast balance impairments, steroid hormone imbalance, and carbohydrate metabolism. Bone metabolism disorders are associated with an intensification of OA-associated pain syndrome. Chondroprotective agents (chondroitin sulfate (CS), glucosamine sulfate (GS), and undenaturated collagen) block the activity of anti-inflammatory cytokines (NF-κB and toll-receptors), stimulate the activity of osteoblasts (bone tissue synthesizing cells), and decrease the excessive activity of osteoclasts (cells that degrade bone tissue).
Conclusion. Pharmaceutically standardized forms of CS and GS can be used for the normalization of bone metabolism along with safe osteoptotective means (vitamin D, calcium, etc.) in patients with OA.
About the Authors
О. А. Gromova
Federal Research Center “Informatics and Management”, Russian Academy of Sciences
Russian Federation
Russian Federation
Dr. Med. Sc., Professor, Research Supervisor,
4 Vavilov Str., Moscow, 2119333
А. М. Lila
Nasonov Research Institute of Rheumatology
Russian Federation
Russian Federation
Dr. Med. Sc., Professor, Director,
34А Kashirskoye Shosse, Moscow, 115522
I. Yu. Torshin
Federal Research Center “Informatics and Management”, Russian Academy of Sciences
Russian Federation
Russian Federation
PhD (Phys. Math.), PhD (Chem.), Senior Researcher,
4 Vavilov Str., Moscow, 2119333
I. А. Reier
Federal Research Center “Informatics and Management”, Russian Academy of Sciences
Russian Federation
Russian Federation
PhD (Tech.), Researcher,
4 Vavilov Str., Moscow, 2119333
References
1. Herrero-Beaumont G., Pérez-Baos S., Sánchez-Pernaute O., et al. Targeting chronic innate inflammatory pathways, the main road to prevention of osteoarthritis progression. Biochem Pharmacol. 2019; 165: 24–32. https://doi.org/10.1016/j.bcp.2019.02.030.
2. Gromova O.A., Torshin I.Yu., Lila A.M., et al. Standardised forms of chondroitin sulfate as a pathogenetic treatment of osteoarthritis in the context of post-genomic studies. Sovremennaya revmatologiya / Modern Rheumatology Journal. 2021; 15 (1): 136–43 (in Russ.). https://doi.org/10.14412/1996-7012-2021-1-136-143.
3. Barreto G., Manninen M., Eklund K.K. Osteoarthritis and toll-like receptors: when innate immunity meets chondrocyte apoptosis. Biology (Basel). 2020; 9 (4): 65. https://doi.org/10.3390/biology9040065.
4. Torshin I.Yu., Gromova O.A., Nechaeva G.I., et al. Systematic analysis of molecular biological mechanisms for supporting connective tissue metabolism with chondroitin sulfate. Neurology, Neuropsychiatry, Psychosomatics. 2021; 13 (1): 154–62 (in Russ.). https://doi.org/10.14412/2074-2711-2021-1-154-162.
5. Goerres G.W., Häuselmann H.J., Seifert B., et al. Patients with knee osteoarthritis have lower total hip bone mineral density in the symptomatic leg than in the contralateral hip. J Clin Densitom. 2005; 8 (4): 484–7. https://doi.org/10.1385/jcd:8:4:484.
6. Yu D., Xu J., Liu F., et al. Subchondral bone changes and the impacts on joint pain and articular cartilage degeneration in osteoarthritis. Clin Exp Rheumatol. 2016; 34 (5): 929–34.
7. Salbach J., Rachner T.D., Rauner M., et al. Regenerative potential of glycosaminoglycans for skin and bone. J Mol Med (Berl). 2012; 90 (6): 625–35. https://doi.org/10.1007/s00109-011-0843-2.
8. Fournier P., Dupuis Y. Antirachitic power of various socalled structural compounds: lactose, glucosamine, L-xylose, mannitol. C R Hebd Seances Acad Sci. 1960; 250: 3050–2 (in French).
9. Shavlovskaya O.A., Zolotovskaya I.A., Prokofyeva Y.S. Antiresorptive activity of pharmacological chondroitin sulfate in the older age group. Terapeutic Archive. 2020; 92 (12): 75–9 (in Russ.). https://doi.org/10.26442/00403660.2020.12.200448.
10. Torshin I.Yu., Rudakov K.V. On the theoretical basis of the metric analysis of poorly formalized problems of recognition and classification. Pattern Recognition and Image Analysis. 2015; 25 (4): 577–87. https://doi.org/10.1134/S1054661815040252.
11. Torshin I.Yu., Rudakov K.V. On metric spaces arising during formalization of problems of recognition and classification. Part 1: properties of compactness. Pattern Recognition and Image Analysis. 2016; 26 (2): 274–84. https://doi.org/10.1134/S1054661816020255.
12. Torshin I.Yu., Gromova O.A., Stakhovskaya L.V., et al. Analysis of 19.9 million publications from the PubMed/MEDLINE database using artificial intelligence methods: approaches to the generalizations of accumulated data and the phenomenon of “fake news”. FARMAKOEKONOMIKA. Sovremennaya farmakoekonomika i farmakoepidemiologiya / FARMAKOEKONOMIKA. Modern Pharmacoeconomics and Pharmacoepidemiology. 2020; 13 (2): 146–63 (in Russ.). https://doi.org/10.17749/2070-4909/farmakoekonomika.2020.021.
13. Stanford Biomedical Network Dataset Collection. Available at: http://snap.stanford.edu/biodata (accessed 27.12.2021).
14. The Gene Ontology Consortium. The Gene Ontology Resource: 20 years and still GOing strong. Nucleic Acids Res. 2019; 47 (D1): D330–8. https://doi.org/10.1093/nar/gky1055.
15. Maeda K., Kobayashi Y., Koide M., et al. The regulation of bone metabolism and disorders by Wnt signaling. Int J Mol Sci. 2019; 20 (22): 5525. https://doi.org/10.3390/ijms20225525.
16. Deng H., Liu H., Yang Z., et al. Progress of selenium deficiency in the pathogenesis of arthropathies and selenium supplement for their treatment. Biol Trace Elem Res. 2021; Nov. 15. https://doi.org/10.1007/s12011-021-03022-4.
17. Hong S.W., Kang J.H. Bone mineral density, bone microstructure, and bone turnover markers in females with temporomandibular joint osteoarthritis. Clin Oral Investig. 2021; 25 (11): 6435–48. https://doi.org/10.1007/s00784-021-03946-0.
18. Lin Z., Miao J., Zhang T., et al. d-Mannose suppresses osteoarthritis development in vivo and delays IL-1β-induced degeneration in vitro by enhancing autophagy activated via the AMPK pathway. Biomed Pharmacother. 2021; 135: 111199. https://doi.org/10.1016/j.biopha.2020.111199.
19. Monasterio G., Castillo F., Rojas L., et al. Th1/Th17/Th22 immune response and their association with joint pain, imagenological bone loss, RANKL expression and osteoclast activity in temporomandibular joint osteoarthritis: a preliminary report. J Oral Rehabil. 2018; 45 (8): 589–97. https://doi.org/10.1111/joor.12649.
20. Berardi S., Corrado A., Maruotti N., et al. Osteoblast role in the pathogenesis of rheumatoid arthritis. Mol Biol Rep. 2021; 48 (3): 2843–52. https://doi.org/10.1007/s11033-021-06288-y.
21. Ragipoglu D., Dudeck A., Haffner-Luntzer M., et al. The role of mast cells in bone metabolism and bone disorders. Front Immunol. 2020; 11: 163. https://doi.org/10.3389/fimmu.2020.00163.
22. Kamiya N., Kuroyanagi G., Aruwajoye O., Kim H.K.W. IL6 receptor blockade preserves articular cartilage and increases bone volume following ischemic osteonecrosis in immature mice. Osteoarthritis Cartilage. 2019; 27 (2): 326–35. https://doi.org/10.1016/j.joca.2018.10.010.
23. Ren Y., Deng Z., Gokani V., et al. Anti-interleukin-6 therapy decreases hip synovitis and bone resorption and increases bone formation following ischemic osteonecrosis of the femoral head. J Bone Miner Res. 2021; 36 (2): 357–68. https://doi.org/10.1002/jbmr.4191.
24. Takeuchi T., Sugimoto A., Imazato N., et al. Glucosamine suppresses osteoclast differentiation through the modulation of glycosylation including O-GlcNAcylation. Biol Pharm Bull. 2017; 40 (3): 352–6. https://doi.org/10.1248/bpb.b16-00877.
25. Nagaoka I., Igarashi M., Sakamoto K. Biological activities of glucosamine and its related substances. Adv Food Nutr Res. 2012; 65: 337–52. https://doi.org/10.1016/B978-0-12-416003-3.00022-6.
26. Ivanovska N., Dimitrova P. Bone resorption and remodeling in murine collagenaseinduced osteoarthritis after administration of glucosamine. Arthritis Res Ther. 2011; 13 (2): R44. https://doi.org/10.1186/ar3283.
27. Zolotovskaya I.A., Davydkin I.L. Antiresorptive-cytokine effects of the chondroprotective therapy in patients with lower back pain. S.S. Korsakov Journal of Neurology and Psychiatry. 2020; 120 (4): 65–71 (in Russ.). https://doi.org/10.17116/jnevro202012004165.
28. Veronese N., Koyanagi A., Stubbs B., et al. Mediterranean diet and knee osteoarthritis outcomes: a longitudinal cohort study. Clin Nutr. 2019; 38 (6): 2735–9. https://doi.org/10.1016/j.clnu.2018.11.032.
29. Bahrambeigi S., Yousefi B., Rahimi M., Shafiei-Irannejad V. Metformin; an old antidiabetic drug with new potentials in bone disorders. Biomed Pharmacother. 2019; 109: 1593–601. https://doi.org/10.1016/j.biopha.2018.11.032.
30. Zheng H.X., Chen J., Zu Y.X., et al. Chondroitin sulfate prevents STZ induced diabetic osteoporosis through decreasing blood glucose, antioxidative stress, anti-inflammation and OPG/RANKL expression regulation. Int J Mol Sci. 2020; 21 (15): 5303. https://doi.org/10.3390/ijms21155303.
31. Fan R., Hao Y., Liu X., et al. Undenatured type II collagen relieves bone impairment through improving inflammation and oxidative stress in ageing db/db mice. Molecules. 2021; 26 (16): 4942. https://doi.org/10.3390/molecules26164942.
32. Veronese N., Cooper C., Reginster J.Y., et al. Type 2 diabetes mellitus and osteoarthritis. Semin Arthritis Rheum. 2019; 49 (1): 9–19. https://doi.org/10.1016/j.semarthrit.2019.01.005.
33. Gromova O.A., Torshin I.Yu., Zaychik B.T., et al. Differences in the standardization of medicinal products based on extracts of chondroitin sulfate. FARMAKOEKONOMIKA. Sovremennaya farmakoekonomika i farmakoepidemiologiya / FARMAKOEKONOMIKA. Modern Pharmacoeconomics and Pharmacoepidemiology. 2021; 14 (1): 40–52 (in Russ.). https://doi.org/10.17749/2070-4909/farmakoekonomika.2021.083.
34. Wu Y., Kadota-Watanabe C., Ogawa T., Moriyama K. Combination of estrogen deficiency and excessive mechanical stress aggravates temporomandibular joint osteoarthritis in vivo. Arch Oral Biol. 2019; 102: 39–46. https://doi.org/10.1016/j.archoralbio.2019.03.012.
35. Asai H., Nakatani S., Kato T., et al. Glucosamines attenuate bone loss due to menopause by regulating osteoclast function in ovariectomized mice. Biol Pharm Bull. 2016; 39 (6): 1035–41. https://doi.org/10.1248/bpb.b16-00066.
36. Jiang Z., Li Z., Zhang W., et al. Dietary natural N-acetyl-D-glucosamine prevents bone loss in ovariectomized rat model of postmenopausal osteoporosis. Molecules. 2018; 23 (9): 2302. https://doi.org/10.3390/molecules23092302.
37. Miyazaki T., Miyauchi S., Anada T., et al. Chondroitin sulfate-E binds to both osteoactivin and integrin αVβ3 and inhibits osteoclast differentiation. J Cell Biochem. 2015; 116 (10): 2247–57. https://doi.org/10.1002/jcb.25175.
38. Koike T., Mikami T., Shida M., et al. Chondroitin sulfate-E mediates estrogeninduced osteoanabolism. Sci Rep. 2015; 5: 8994. https://doi.org/10.1038/srep08994.
39. Yoo T.K., Kim S.K., Kim D.W., et al. Osteoporosis risk prediction for bone mineral density assessment of postmenopausal women using machine learning. Yonsei Med J. 2013; 54 (6): 1321–30. https://doi.org/10.3349/ymj.2013.54.6.1321.
40. Kiyomoto K., Iba K., Hanaka M., et al. High bone turnover state under osteoporotic changes induces pain-like behaviors in mild osteoarthritis model mice. J Bone Miner Metab. 2020; 38 (6): 806–18. https://doi.org/10.1007/s00774-020-01124-y.
41. Sun Q., Zhen G., Li T.P., et al. Parathyroid hormone attenuates osteoarthritis pain by remodeling subchondral bone in mice. Elife. 2021; 10: e66532. https://doi.org/10.7554/eLife.66532.
42. Nwosu L.N., Allen M., Wyatt L., et al. Pain prediction by serum biomarkers of bone turnover in people with knee osteoarthritis: an observational study of TRAcP5b and cathepsin K in OA. Osteoarthritis Cartilage. 2017; 25 (6): 858–65. https://doi.org/10.1016/j.joca.2017.01.002.
43. Nakamura Y., Uchiyama S., Kamimura M., et al. Bone alterations are associated with ankle osteoarthritis joint pain. Sci Rep. 2016; 6: 18717. https://doi.org/10.1038/srep18717.
44. Torshin I.Yu., Lila A.M., Naumov A.V., et al. Meta-analysis of clinical trials of osteoarthritis treatment effectiveness with Chondroguard. FARMAKOEKONOMIKA. Sovremennaya farmakoekonomika i farmakoepidemiologiya / FARMAKOEKONOMIKA. Modern Pharmacoeconomics and Pharmacoepidemiology. 2020; 13 (4): 18–29 (in Russ.). https://doi.org/10.17749/2070-4909/farmakoekonomika.2020.066.
45. Salbach-Hirsch J., Ziegler N., Thiele S., et al. Sulfated glycosaminoglycans support osteoblast functions and concurrently suppress osteoclasts. J Cell Biochem. 2014; 115 (6): 1101–11. https://doi.org/10.1002/jcb.24750.
46. Salbach J., Kliemt S., Rauner M., et al. The effect of the degree of sulfation of glycosaminoglycans on osteoclast function and signaling pathways. Biomaterials. 2012; 33 (33): 8418–29. https://doi.org/10.1016/j.biomaterials.2012.08.028.
47. Trabszo C., Ramms B., Chopra P., et al. Arylsulfatase K inactivation causes mucopolysaccharidosis due to deficient glucuronate desulfation of heparan and chondroitin sulfate. Biochem J. 2020; 477 (17): 3433–51. https://doi.org/10.1042/BCJ20200546.
48. Peck S.H., Tobias J.W., Shore E.M., et al. Molecular profiling of failed endochondral ossification in mucopolysaccharidosis VII. Bone. 2019; 128: 115042. https://doi.org/10.1016/j.bone.2019.115042.
49. Lila A.M., Gromova O.A., Torshin I.Yu., et al. Molecular effects of chondroguard in osteoarthritis and herniated discs. Neurology, Neuropsychiatry, Psychosomatics. 2017; 9 (3): 88–97 (in Russ.). https://doi.org/10.14412/2074-2711-2017-3-88-97.
50. Noonan K.J., Stevens J.W., Tammi R., et al. Spatial distribution of CD44 and hyaluronan in the proximal tibia of the growing rat. J Orthop Res. 1996; 14 (4): 573–81. https://doi.org/10.1002/jor.1100140411.
51. Martins J.M.S., Dos Santos Neto L.D., Noleto-Mendonça R.A., et al. Dietary supplementation with glycosaminoglycans reduces locomotor problems in broiler chickens. Poult Sci. 2020; 99 (12): 6974–82. https://doi.org/10.1016/j.psj.2020.09.061.
52. Lambertini E., Penolazzi L., Pandolfi A., et al. Human osteoclasts/osteoblasts 3D dynamic co-culture system to study the beneficial effects of glucosamine on bone microenvironment. Int J Mol Med. 2021; 47 (4): 57. https://doi.org/10.3892/ijmm.2021.4890.
53. Lv C., Wang L., Zhu X., et al. Glucosamine promotes osteoblast proliferation by modulating autophagy via the mammalian target of rapamycin pathway. Biomed Pharmacother. 2018; 99: 271–7. https://doi.org/10.1016/j.biopha.2018.01.066.
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Gromova О.А., Lila А.М., Torshin I.Yu., Reier I.А. Application of chondroprotective agents to inhibit osteodestructive processes in the subchondral bone in patients with osteoarthritis. FARMAKOEKONOMIKA. Modern Pharmacoeconomics and Pharmacoepidemiology. 2022;15(1):107-118. https://doi.org/10.17749/2070-4909/farmakoekonomika.2022.126
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