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Pathogenesis and Potential Relative Risk Factors of Diabetic Neuropathic Zhao et al. Journal of Orthopaedic Surgery and Research (2017) 12:142 DOI 10.1186/s13018-017-0634-8 REVIEW Open Access Pathogenesis and potential relative risk factors of diabetic neuropathic osteoarthropathy Hong-Mou Zhao1, Jia-Yu Diao2, Xiao-Jun Liang1, Feng Zhang3* and Ding-Jun Hao4* Abstract Diabetic neuropathic osteoarthropathy (DNOAP) is an uncommon, but with considerable morbidity and mortality rates, complication of diabetes. The real pathogenesis is still unclear. The two popular theories are the neuro-vascular theory and neuro-traumatic theory. Most theories and pathways focused on the uncontrolled inflammations that resulted in the final common pathway, receptor activator of nuclear factor κβ ligand (RANKL)/osteoprotegerin (OPG) axis, for the decreased bone density in DNOAP with an osteoclast and osteoblast imbalance. However, the RANKL/OPG pathway does not explain all the changes, other pathways and factors also play roles. A lot of DNOAP potential relative risk factors were evaluated and reported in the literature, including age, gender, weight, duration and type of diabetes, bone mineral density, peripheral neuropathy and arterial disease, trauma history, and some others. However, most of them are still in debates. Future studies focus on the pathogenesis of DNOAP are still needed, especially for the genetic factors. And, the relationship between DNOAP and those potential relative risk factors are still need to further clarify. Keywords: Charcot foot, Diabetic neuropathic osteoarthropathy, Pathogenesis, Risk factor, Receptor activator of nuclear factor κβ ligand (RANKL) Background DNOAP is a devastating complication for diabetes, Musgrave firstly reported neuropathic joint changes as a culminating in bone destruction and involving joints and complication of venereal disease in 1703 [1]. And neuro- articular cartilage with high inflammatory environment pathic arthropathy is named after the French neurologist and potentially leading to osteolysis and low bone min- Jean-Martin Charcot (1825 to 1893), who firstly eral density, dislocations, fractures, and deformities described the condition in 1868 as a complication of pa- (Fig. 1). The prevalence of DNOAP was reported from tients with tabes dorsalis [2]. However, the neuropathic 0.08 to 13.0% in all patients with diabetes mellitus [5, 6], inflammatory osteoarthropathy associated with the foot and the prevalence rise up to 29.0% in high-risk patients was firstly reported in 1881 by an English surgeon, [7]. It was well established that DNOAP and relative Herbert William Page [3]. In 1936, Jordan was the first complications severely reduces the overall quality of life to describe Charcot in diabetes [4]. In more recent and dramatically increases the morbidity and mortality times, diabetes has become the most common etiology of patients [8]. for the development of neuropathic arthropathy. Hence, The etiology of DNOAP is supposed to be multifactor- the term diabetic neuropathic osteoarthropathy ial. Two main theories concerning the origin of the con- (DNOAP) has been used to describe such changes in the dition are neuro-vascular theory and neuro-traumatic feet and ankles of patients with diabetes. theory. However, classical etiological theories assessed the pivotal role of diabetic peripheral neuropathy (DPN), * Correspondence: [email protected]; [email protected] but clinical differences between DNOAP and DPN sug- 3School of Public Health, Health Science Center Xi’an Jiaotong University, No. gest that DPN is necessary but insufficient in explaining 76 Yan Ta West Road, Xi’an 710061, People’s Republic of China 4Spine Surgery Department, Honghui Hospital of Xi’an Jiaotong University the pathogenesis of DNOAP [9]. Till now, the exact College of Medicine, No. 76 Nanguo Road, Xi’an 710054, People’s Republic of nature of DNOAP remains unknown. Many studies fo- China cused on the pathogenesis of DNOAP were published in Full list of author information is available at the end of the article © The Author(s). 2017 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. Zhao et al. Journal of Orthopaedic Surgery and Research (2017) 12:142 Page 2 of 8 Fig. 1 The radiographic characters of DNOAP. The fracture type (a) and the dislocation type (b) recent two decades, and a lot of pathways were reported cytokines, tumor necrosis factor-α (TNF-α), interleukin- correlated with the development of DNOAP. A better 1β (IL-1β), and IL-6 [19]. And the cytokines upregulate understanding of the interplay between these complex the receptor activator of nuclear factor κβ ligand pathways and common genetic polymorphisms among (RANKL) system. Study reported that after minor joint those affected by DNOAP is required to fully understand trauma, the progress of DNOAP might develop rapidly its pathogenesis [10–12]. A lot of DNOAP potential rela- in weeks [20]. However, the neuropathic theory does not tive risk factors were reported in the literature; however, explain all the changes as only a small proportion of most of them are still in debates. In the current study, patients with neuropathy develop a Charcot foot [2, 18]. we give comprehensive review of the current updates of There is evidence that the nervous system and neuro- pathogenesis and those potential relative risk factors of peptides effect bone metabolism [21]. DNOAP showed DNOAP. higher degree of sympathetic and parasympathetic dysfunction than diabetic patients and normal control Pathogenesis [22]. Sensory fibers contribute to the maintenance of tra- Neuro-vascular theories becular bone integrity through mechanisms mediated by The neuro-vascular theory, first described by Charcot, calcitonin gene-related peptide (CGRP) and/or substance predicates a state of hyperemia generated from over- P; in addition, ablation of CGRP results in osteopenia active vaso-autonomic neuropathy [13]. The increased due to reduced osteoblastic bone formation [23, 24]. blood flow increases venous pressure and enhances fluid filtration through capillary leakage [8]. This in turn leads Pro-inflammatory state to increased compartmental pressure and deep tissue is- The pro-inflammatory state in diabetes is attributed to chemia. The increased pressure and ischemia compro- elevated concentrations of pro-inflammatory cytokines mises tendons and ligaments in the foot and ankle which are derived from increased protein kinase C leading to joint instability [14]. Additionally, the (PKC) activity and advanced glycation end products increased blood flow may directly cause increased bone (AGE)/receptor of AGE (RAGE) interactions accompan- resorption by increasing the delivery of osteoclasts and ied by suppressed phosphatidylinositol 3 (PI3) kinase ac- monocytes resulting in greater osteoclastic activity in tivity [25]. Also, repetitive or unrecognized trauma can this area [15]. This is consistent with the finding that trigger a cascade of inflammatory events. Munson et al. patients with a Charcot foot show increased blood flow [26] concluded that identified novel associations with to the area whereas patients with peripheral arterial DNOAP in the context of pathogenesis models that in- disease and diabetes are relatively protected from devel- clude neurotrophic, neurovascular, and microtraumatic oping the arthropathy [16, 17]. factors mediated through inflammatory cytokines. The main pro-inflammatory cytokines, TNF-α, IL-1β, Neuro-traumatic theory and IL-6, play a pivotal role in the inception of DNOAP Volkmann and Virchow proposed a neuro-traumatic via amplified RANKL expression and cause localized theory for the pathogenesis of neuro-arthropathy [18]. osteolysis that jeopardizes bone integrity making the This theory hypothesizes trauma (acute, subacute, or re- high-risk diabetic foot vulnerable to ulceration, deform- petitive) as the causative factor in the setting of absent ity, and fractures [27]. Meanwhile, there is a decrease in protective sensation. The bone and soft tissues respond anti-inflammatory cytokines, IL-4 and IL-10, and osteo- with an acute-phase release of pro-inflammatory protegerin (OPG) [19, 27–29]. Mabilleau et al. [19] Zhao et al. Journal of Orthopaedic Surgery and Research (2017) 12:142 Page 3 of 8 found that the percentage of cluster of differentiation of osteoclasts from osteoclast precursor cells [28, 37]. A (CD) nomenclature 14 positive cells in acute DNOAP repetitive trauma with the loss of pain sensation results in was significantly increased compared with diabetic and continual production of pro-inflammatory cytokines, healthy controls, with a strong positive correlation to RANKL, NF-κβ, and osteoclasts, which in turn leads to the TNF-α level. continuing local osteolysis [33]. Under inflammatory conditions, both B and T cells Oxidative stress can be considerable sources of RANKL and may con- In DNOAP, an essential pathogenic pathway is consid- tribute to pathological bone resorption [38, 39]. How- ered to be a local dysregulation of immunoinflammatory ever, in acute DNOAP, the local inflammatory response processes, in
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