Выход
Вход/Login
 
E-mail
Пароль/Password
Забыли пароль?
Введите E-mail и жмите тут. Пароль будет выслан на указанный адрес
Войти (LogIn)

 

Если вы первый раз здесь, то зарегистрируйтесь

Регистрация/Sign Up
Полное имя (Ф И О)/Full name
E-mail
Повторите E-mail
Телефон/Phone
Зарегистрироваться,
на ваш E-mail будет выслан временный пароль

Нажимая кнопку Зарегистрироваться, вы соглашаетесь с Правилами сайта и Политикой Конфиденциальности http://vidar.ru/rules.asp

 

Медицинская литература. Новинки


 

 

 

 

 

 
вce журналы << Эндокринная хирургия << 2014 год << №4 <<
стр.5
отметить
статью

Патогенез остеоартропатии Шарко: роль периферической нервной системы

Галстян Г. Р., Каминарская Ю. А.
Вы можете загрузить полный текст статьи в формате pdf
Галстян Гагик Радикович - доктор мед. наук, профессор, заведующий отделением диабетической стопы ФГБУ, ФГБУ ''''Эндокринологический научный центр'''' Минздрава России, Каминарская Юлия Андреевна - клинический ординатор, ФГБУ ''''Эндокринологический научный центр'''' Минздрава России, 117036 Москва. ул.Дм.Ульянова. д.11,

Нейроостеоартропатия является редким, но тяжелым осложнением периферической нейропатии. Это состояние характеризуется прогрессирующей деструкцией костей и суставов стопы и приводит к необратимой инвалидизации пациентов. На сегодняшний день безусловно лидирующей причиной нейроостеоартропатии является сахарный диабет, преимущественно с поражением стопы и голеностопного сустава. Патогенез до сих остается предметом дискуссий. Последние исследования указывают на ведущую роль системы RANK/RANKL/OPG в развитии данного осложнения. На настоящий момент отсутствуют фармакологические методы терапии с доказанной эффективностью. Со времен Жан-Мартена Шарко был достигнут лишь небольшой прогресс в лечении. Общепризнанным стандартом лечения на сегодняшний день является полная разгрузка конечности при помощи иммобилизирующей повязки из полимерных материалов. Целью этой обзорной статьи является анализ исследований, проведенных в области патогенеза остеоартропатии Шарко (ОШ), обсуждение возможного дальнейшего развития представления о природе данного состояния. Особое внимание уделено современной концепции, рассматривающей поражение нервной системы в качестве ведущего звена в развитии костной патологии. Выявление новых аспектов патогенеза ОШ способно привести к появлению фармакологических методов лечения этой группы пациентов.

Ключевые слова:
сахарныйдиабет, стопа Шарко, нервные волокна, нейропептиды, патофизиология, diabetes mellitus, Charcot joint, nerve fibres, neuropeptides, physiopathology

Литература:
1.Petrova N.L., Edmonds M.E. Charcot neuro-osteoarthropathy-current standards. // Diabetes Metab Res Rev. 2008;24(S1): S58-S61. doi: 10.1002/dmrr.846
2.Jones K.B., Mollano A.V., Morcuende J.A., et al. Bone and brain: a review of neural, hormonal, and musculoskeletal connections. // Iowa Orthop J. 2004;24:123-32.
3.Rostom S., Bahiri R., Mahfoud-Filali S., et al. Neurogenic osteoarthropathy in leprosy. // Clin Rheumatol. 2007;26(12): 2153-2155. doi: 10.1007/s10067-007-0629-
4.Mabilleau G., Edmonds M.E. Role of neuropathy on fracture healing in Charcot neuro-osteoarthropathy. // J Musculoskelet Neuronal Interact. 2010;10:84-91.
5.Larson Sa.M., Burns P.R. The pathogenesis of charcot neuro-arthropathy: Current concepts. // Diabetic Foot & Ankle. 2012;3(0). doi: 10.3402/dfa.v3i0.12236
6.Chisholm K.A., Gilchrist J.M. The charcot joint: A modern neurologic perspective. // Journal of Clinical Neuromuscular Disease. 2011;13(1):1-13.doi: 10.1097/CND.0b013e3181c6f55b
7.Slater R.A., Ramot Y., Buchs A., et al.The diabetic charcot foot. // Isr Med Assoc J 2004;6:280-3
8.Wukich D.K., Sung W. Charcot arthropathy of the foot and ankle: Modern concepts and management review. // J Diabetes Complications. 2009;23(6):409-426. doi: 10.1016/j.jdiacomp.2008.09.004
9.Van Baal J., Hubbard R., Game F., et al. Mortality associated with acute charcot foot and neuropathic foot ulceration. // Diabetes Care. 2010;33(5):1086-1089. doi: 10.2337/dc09-1428
10.Armstrong D.G., Lavery L.A. Elevated peak plantar pressures in patients who have Charcot arthropathy. // J Bone Jt Surg-Ser A 1998;80:365-369.
11.Бреговский В.Б., Цветкова Т.П., Лебедев В.В., и др. Особенности биомеханики стопы при диабетической артропатии Шарко. // Сахарный диабет. - 2005. -№ 1 - С.38-40. doi: 10.14341/2072-0351-5440
12.Edmonds M.E., Clarke M.B., Newton S., et al. Increased uptake of bone radiopharmaceutical in diabetic neuropathy. // Q J Med. 1985;57:843-855.
13.Chantelau E., Onvlee G. Charcot foot in diabetes: Farewell to the neurotrophic theory. // Hormone and Metabolic Research. 2006;38(6):361-367. doi: 10.1055/s-2006-944525
14.Jeffcoate W.J., Game F., Cavanagh P.R. The role of proinflammatory cytokines in the cause of neuropathic osteoarthropathy (acute charcot foot) in diabetes. // The Lancet. 2005; 366(9502): 2058-2061. doi: 10.1016/s0140-6736(05)67029-8
15.Baumhauer J.F., OKeefe R.J., Schon L.C., et al. Cytokine-induced osteoclastic bone resorption in charcot arthropathy: An immunohistochemical study. // Foot Ankle Int. 2006; 27(10):797-800
16.Uccioli L., Sinistro A., Almerighi C., et al. Proinflammatory modulation of the surface and cytokine phenotype of monocytes in patients with acute charcot foot. // Diabetes Care. 2009;33(2):350-355. doi: 10.2337/dc09-1141
17.Petrova N.L., Moniz C., Elias D.A., et al. Is there a systemic inflammatory response in the acute charcot foot? // Diabetes Care. 2007;30(4):997-998. doi: 10.2337/dc06-2168
18.Jeffcoate W. Vascular calcification and osteolysis in diabetic neuropathy? Is rank-l the missing link? // Diabetologia. 2004;47(9):1488-1492. doi: 10.1007/s00125-004-1477-5
19.Hofbauer L.C. The role of receptor activator of nuclear factor-b ligand and osteoprotegerin in the pathogenesis and treatment of metabolic bone diseases. // Journal of Clinical Endocrinology & Metabolism. 2000;85(7):2355-2363. doi: 10.1210/jc.85.7.2355
20.Ярославцева М.В., Ульянова И.Н., Галстян Г.Р., и др. Состояние системы остеопротегерин (OPG)-лиганд рецептора-активатора ядерного фактора каппа-В (RANKL) у пациентов с диабетической остеоартропатией и медиакальцинозом артерий нижних конечностей. // Остеопороз и Остеопатии. - 2008. - №1 - С.9-13
21.Ndip A., Williams A., Jude E.B., et al. The RANKL/RANK/OPG signaling pathway mediates medial arterial calcification in diabetic Charcot neuroarthropathy. // Diabetes. 2011;60: 2187-2196. doi:10.2337/db10-1220
22.Mabilleau G., Petrova N.L., Edmonds M.E., et al. Increased osteoclastic activity in acute Charcot''s osteoarthropathy: the role of receptor activator of nuclear factor-kappaB ligand. // Diabetologia. 2008;51:1035-1040. doi:10.1007/s00125-008-0992-1.
23.Boyle W.J., Simonet W.S., Lacey D.L. Osteoclast differentiation and activation. // Nature. 2003;423:337-342. doi:10.1038/nature01658.
24.Jeffcoate W.J., Rasmussen L.M., Hofbauer L.C., et al. Medial arterial calcification in diabetes and its relationship to neuropathy. // Diabetologia. 2009;52:2478-2488. doi:10.1007/s00125-009-1521-6.
25.Sinha S., Munichoodappa C.S., Kozak G.P. Neuro-arthropathy (charcot joints) in diabetes mellitus. // Medicine (Baltimore). 1972; 51(3):191-210. doi: 10.1097/00005792-197205000-00006
26.Salo P. The role of joint innervation in the pathogenesis of arthritis. // Can J Surg. 1999;42:91-100.
27.Craig A.D., Heppelmann B., Schaible H.G. The projection of the medial and posterior articular nerves of the cat''s knee to the spinal cord. // J Comp Neurol. 1988;276:279-88.
28.Schaible H.G., Schmidt R.F. Activation of groups III and IV sensory units in medial articular nerve by local mechanical stimulation of knee joint. // J Neurophysiol. 1983;49:35-44.
29.Schenk I., Spaethe A., Halata Z. The structure of sensory nerve endings in the knee joint capsule of the dog. // Ann Anat. 1996;178:515-21.
30.Li J., Kreicbergs A., Bergstrom J., et al. Site-specific CGRP innervation coincides with bone formation during fracture healing and modeling: A study in rat angulated tibia. // J Orthop Res. 2007;25:1204-12. doi:10.1002/jor.20406.
31.Hukkanen M., Konttinen Y.T., Santavirta S., et al. Rapid proliferation of calcitonin gene-related peptide-immunoreactive nerves during healing of rat tibial fracture suggests neural involvement in bone growth and remodelling. // Neuroscience. 1993;54:969-79.
32.Santavirta S., Konttinen Y.T., Nordstrom D., et al. Immunologic studies of nonunited fractures. // Acta Orthop. 1992;63(6): 579-586. doi: 10.1080/17453679209169713
33.Bjurholm A., Kreicbergs A., Brodin E., et al. Substance p- and cgrp-immunoreactive nerves in bone. // Peptides. 1988;9(1): 165-171. doi: 10.1016/0196-9781(88)90023-x
34.Hill E.L., Elde R. Distribution of cgrp-, vip-, dpH-, sp-, and npy-immunoreactive nerves in the periosteum of the rat. // Cell Tissue Res. 1991;264(3):469-480. doi: 10.1007/bf00319037
35.Salo P.T., Theriault E. Number, distribution and neuropeptide content of rat knee joint afferents. // J Anat. 1997;190:515-22. doi:10.1017/S0021878296001902.
36.Offley S.C., Guo T-Z., Wei T., et al. Capsaicin-sensitive sensory neurons contribute to the maintenance of trabecular bone integrity. // J Bone Miner Res. 2005;20:257-267. doi:10.1359/JBMR.041108.
37.Uzan B., de Vernejoul M-C., Cressent M. RAMPs and CRLR expressions in osteoblastic cells after dexamethasone treatment. // Biochem Biophys Res Commun. 2004;321:802-808. doi:10.1016/j.bbrc.2004.07.037.
38.Schinke T., Liese S., Priemel M., et al. Decreased bone formation and osteopenia in mice lacking alpha-calcitonin gene-related peptide. // J Bone Miner Res. 2004;19:2049-2056. doi:10.1359/JBMR.040915.
39.Kawase T., Okuda K., Burns D.M. Immature human osteoblastic MG63 cells predominantly express a subtype 1-like CGRP receptor that inactivates extracellular signal response kinase by a cAMP-dependent mechanism. // Eur J Pharmacol. 2003;470:125-137. doi:10.1016/S0014-2999(03)01763-1.
40.Vignery A., McCarthy T.L. The neuropeptide calcitonin gene-related peptide stimulates insulin-like growth factor I production by primary fetal rat osteoblasts. // Bone. 1996;18:331-335. doi:10.1016/8756-3282(96)00017-8.
41.Ballica R., Valentijn K., Khachatryan A., et al. Targeted expression of calcitonin gene-related peptide to osteoblasts increases bone density in mice. // J Bone Miner Res. 1999; 14:1067-1074. doi:10.1359/jbmr.1999.14.7.1067.
42.Huebner A.K., Schinke T., Priemel M., et al. Calcitonin deficiency in mice progressively results in high bone turnover. // J Bone Miner Res. 2006;21:1924-1934. doi:10.1359/jbmr.060820.
43.Wang L., Shi X., Zhao R., et al. Calcitonin-gene-related peptide stimulates stromal cell osteogenic differentiation and inhibits RANKL induced NF-kappaB activation, osteoclastogenesis and bone resorption. // Bone. 2010;46:1369-1379. doi:10.1016/j.bone.2009.11.029.
44.Imai S., Matsusue Y. Neuronal regulation of bone metabolism and anabolism: calcitonin gene-related peptide-, substance P-, and tyrosine hydroxylase-containing nerves and the bone. // Microsc Res Tech. 2002;58:61-69. doi:10.1002/jemt.10119.
45.Goto T., Nakao K., Gunjigake K.K., et al. Substance P stimulates late-stage rat osteoblastic bone formation through neuroki-nin-1 receptors. // Neuropeptides. 2007;41:25-31. doi:10.1016/j.npep.2006.11.002.
46.Wang L., Zhao R., Shi X., et al. Substance P stimulates bone marrow stromal cell osteogenic activity, osteoclast differentiation, and resorption activity in vitro. // Bone. 2009;45:309-320. doi:10.1016/j.bone.2009.04.203
47.Sherman B., Chole R. A mechanism for sympathectomy-induced bone resorption in the middle ear. // Otolaryngology-Head and Neck Surgery. 1995;113(5):569-581. doi: 10.1016/s0194-5998(95)70048-x
48.Matayoshi T., Goto T., Fukuhara E., et al. Neuropeptide substance P stimulates the formation of osteoclasts via synovial fibroblastic cells. // Biochem Biophys Res Commun. 2005; 327:756-764. doi:10.1016/j.bbrc.2004.12.055.
49.Rusanen M., Korkala O., Gronblad M., et al. Evolution of substance P immunofluorescent nerves in callus tissue during fracture healing. // J Trauma. 1987;27:1340-1343.
50.Hukkanen M., Konttinen Y.T., Rees R.G., et al. Distribution of nerve endings and sensory neuropeptides in rat synovium, meniscus and bone. // Int J Tissue React. 1992;14:1-10.
51.Mukohyama H., Ransjo M., Taniguchi H., et al. The inhibitory effects of vasoactive intestinal peptide and pituitary adenyl-ate cyclase-activating polypeptide on osteoclast formation are associated with upregulation of osteoprotegerin and downregulation of RANKL and RANK. // Biochem Biophys Res Commun. 2000;271:158-163. doi:10.1006/bbrc.2000.2599.
52.Delgado M., Abad C., Martinez C., et al. Vasoactive intestinal peptide prevents experimental arthritis by downregulating both autoimmune and inflammatory components of the disease. // Nat Med. 2001;7:563-568. doi:10.1038/87887.
53.Pittenger G., Vinik A. Nerve growth factor and diabetic neuropathy. // Experimental Diabesity Research. 2003;4(4):271-285. doi: 10.1155/edr.2003.271
54.Donaghy M., Hakin R.N., Bamford J.M., et al. Hereditary sensory neuropathy with neurotrophic keratitis. // Brain. 1987;110(3): 563-583. doi: 10.1093/brain/110.3.563
55.Lindberger M., Schroder H.D., Schultzberg M., et al. Nerve fibre studies in skin biopsies in peripheral neuropathies. I. Immunohistochemical analysis of neuropeptides in diabetes mellitus. // J Neurol Sci. 1989;93(2-3):289-296. doi: 10.1016/0022-510x(89)90198-6.
56.Koeck F-X., Bobrik V., Fassold A., et al. Marked loss of sympathetic nerve fibers in chronic Charcot foot of diabetic origin compared to ankle joint osteoarthritis. // J Orthop Res. 2009;27: 736-741. doi:10.1002/jor.20807
57.Shakoor N., Agrawal A., Block J.A. Reduced lower extremity vibratory perception in osteoarthritis of the knee. // Arthritis & Rheumatism. 2008;59(1):117-121. doi: 10.1002/art.23241
58.La Fontaine J., Harkless L.B., Sylvia V.L., et al. Levels of endothelial nitric oxide synthase and calcitonin gene-related peptide in the Charcot foot: a pilot study. // J Foot Ankle Surg. 2008; 47:424-429. doi:10.1053/j.jfas.2008.05.009.
59.Tracey K.J., Borovikova L.V., Ivanova S., et al. Vagus nerve stimulation attenuates the systemic inflammatory response to endotoxin. // Nature. 2000;405(6785):458-462. doi: 10.1038/35013070
60.Van Maanen M.A., Lebre M.C., van der Poll T., et al. Stimulation of nicotinic acetylcholine receptors attenuates collagen-induced arthritis in mice. // Arthritis Rheum. 2009;60:114-122. doi:10.1002/art.24177.
61.Elefteriou F., Ahn J.D., Takeda S., et al. Leptin regulation of bone resorption by the sympathetic nervous system and CART. // Nature. 2005;434:514-520. doi:10.1038/nature03398.
62.Ishizuka K., Hirukawa K., Nakamura H., et al. Inhibitory effect of CGRP on osteoclast formation by mouse bone marrow cells treated with isoproterenol. // Neurosci Lett. 2005;379:47-51. doi:10.1016/j.neulet.2004.12.046.
63.Amano S., Arai M., Goto S., et al. Inhibitory effect of NPY on isoprenaline-induced osteoclastogenesis in mouse bone marrow cells. // Biochim Biophys Acta. 2007;1770:966-973. doi:10.1016/j.bbagen.2007.02.009.
64.Aro H., Eerola E., Aho A.J. Development of nonunions in the rat fibula after removal of periosteal neural mechanoreceptors. // Clin Orthop Relat Res. 1985;199:292-299.
65.Dysart P.S., Harkness E.M., Herbison G.P. Growth of the humerus after denervation. An experimental study in the rat. // J Anat. 1989;167:147-159.
66.Dietz F.R. Effect of peripheral nerve on limb development. // Journal of Orthopaedic Research. 1987;5(4):576-585. doi: 10.1002/jor. 1100050413
67.Singer M. The influence of the nerve in regeneration of the amphibian extremity. // The Quarterly Review of Biology. 1952;27(2):169. doi: 10.1086/398873
68.Aro H. Effect of nerve injury on fracture healing: Callus formation studied in the rat. // Acta Orthop. 1985;56(3):233-237. doi: 10.3109/17453678508993002
69.Glenn J.N., Miner M.E., Peltier L.F. The treatment of fractures of the femur in patients with head injuries. // The Journal of Trauma: Injury, Infection, and Critical Care. 1973;13(11):958-961. doi: 10.1097/00005373-197311000-00004
70.McMaster W.C., Stauffer E.S. The management of long bone fracture in the spinal cord injured patient. // Clin Orthop Relat Res. 1975;112:44-52.
71.Irie K., Hara-Irie F., Ozawa H., et al. Calcitonin gene-related peptide (CGRP)-containing nerve fibers in bone tissue and their involvement in bone remodeling. // Microsc Res Tech. 2002;58:85-90. doi:10.1002/jemt.10122.
72.Richard J-L., Almasri M., Schuldiner S. Treatment of acute Charcot foot with bisphosphonates: a systematic review of the literature. // Diabetologia. 2012;55:1258-1264. doi:10.1007/s00125-012-2507-3.
73.Zhang Y-B., Wang L., Jia S., et al. Local injection of substance p increases bony formation during mandibular distraction osteogenesis in rats. // British Journal of Oral and Maxillofacial Surgery. 2014;52(8):697-702. doi: 10.1016/j.bjoms.2014.07.002
74.Ma L., Xiang L., Yao Y., et al. CGRP-alpha application: a potential treatment to improve osseoperception of endosseous dental implants. // Med Hypotheses 2013;81:297-299. doi:10.1016/j.mehy.2013.04.025.

The pathogenesis of Charcot osteoarthropathy: the role of the peripheral nervous system

Galstyan G.R., Kaminarskaya Yu.A.

Neuroosteoarthropathy is a rare, but devastating complication affecting patients with peripheral neuropathy. It is a progressive, destructive condition that is characterised by progressive bone and joint deterioration of the foot leading to permanent incapacity. Nowadays, diabetes mellitus is by far the most common etiology of CNO (Charcot neuro-osteoarthropathy), especially if it affects the foot or ankle. The cause of the condition is still controversial among experts. In particular, new data have emerged on the central role of RANK/ RANKL/OPG in the pathogenesis of this complication, also known as Charcot foot. No pharmacological methods of therapy have proven effective to date. Very little progress has been made in treating this condition since the days of Jean-Martin Charcot. Today, the universally accepted treatment involves completely relieving pressure from the limb using a polymer retaining bandage. The aim of this review is to analyze research into the pathogenesis of CNO and our potential to better understand the nature of this condition. Particular attention is paid to modern concept of neuroosteopathology, according to which neuropathy is crucial to developing acute osseous pathology. Revealing new aspects of CNO pathogenesis can help extend therapeutic resources for treating this patient group.

Keywords:
сахарныйдиабет, стопа Шарко, нервные волокна, нейропептиды, патофизиология, diabetes mellitus, Charcot joint, nerve fibres, neuropeptides, physiopathology

Новости   Магазин   Журналы   Контакты   Правила   Доставка   О компании  
ООО Издательский дом ВИДАР-М, 2024