Abstract
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Charcot neuroarthropathy is the most severe complication of the diabetic foot. Its diagnosis is difficult and often overlooked, delaying management, with sometimes disastrous consequences. Its incidence is increasing due to the rapid global rise in the number of people with diabetes.
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Its pathophysiology remains unclear, although the activation of the RANK/RANK-L system appears to be involved, triggered either by neurotraumatic or neurovascular mechanisms, leading to the differentiation of monocytes into osteoclasts.
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Diagnosis relies on clinical and radiological arguments, particularly MRI.
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There are different types of Charcot foot depending on the evolution, according to Eichenholtz’s classification and based on location according to Sanders and Brodsky’s classifications.
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Treatment involves a multidisciplinary approach with diabetes management and addressing other general complications. Medical treatment is indicated as the first line, with offloading and immobilisation using a ‘total contact cast’. In case of failure of this method, or if there is immediate deformity, surgical intervention is indicated, and techniques are evolving rapidly. Depending on the deformity, minimally invasive or arthroscopic procedures may be performed. In cases of significant deformity, foot reconstruction may be proposed, using the so-called ‘super construct’ technique if necessary. Infection will be treated concurrently or initially, depending on severity.
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Many complications are reported, but increasingly early and aggressive surgery improves patients’ quality of life and reduces amputation rates.
Introduction
According to the International Diabetes Federation, the number of diabetic patients worldwide is expected to increase by 46% by 2045, reaching approximately 783 million people. Consequently, the incidence of Charcot neuroarthropathy is expected to follow the same increase (1). It is the ultimate complication of the diabetic foot, occurring after an average duration of diabetes exceeding 10 years, with an incidence of 6.4–9.5 per 10,000 (2). First described by Jean-Martin Charcot in 1868, it was in 1936 that William Riely Jordan linked Charcot neuroarthropathy to diabetes, which is currently its main cause (3). The pathophysiology is currently poorly understood, but it appears that the activation of the RANK/RANK-L axis, leading to the differentiation of monocytes into osteoclasts, is the primary aetiology of Charcot foot (4). Diagnosis is also challenging, leading to delayed management in 25% of cases (5), with major foot deformities potentially resulting in wounds and osteoarticular infections. In the early stage, medical treatment involving offloading and immobilisation is indicated, and no pharmacological treatment has proven effective in reducing the inflammatory phase. In more advanced stages, or in cases of unfavourable evolution of early medical treatment, surgical treatment may be proposed based on the anatomical location of Charcot foot. Techniques are evolving rapidly (6). This will involve stabilising the foot, correcting morphostatic disorders and managing osteoarticular infections if necessary (7). Various techniques have been described, but mixed osteosynthesis (internal and external) seems to yield the best results, even though the complication rate is significant, potentially leading to amputation (8).
Epidemiology
The incidence of Charcot foot ranges from 0.3 to 0.85% in the type 2 diabetic population (9, 10). Type 1 diabetic patients are affected earlier, around their third or fourth decade, while type 2 patients are more commonly affected in their sixth or seventh decade (11). The mortality rate is 30% at 5 years, with an average reduction in life expectancy of 14 years compared to the general population. Charcot neuroarthropathy increases the risk of foot ulcers by up to 30%, and the risk of amputation is multiplied by 7–12, affecting approximately 25% of patients. Charcot foot decreases quality of life due to foot deformity, loss of mobility and thus autonomy, as well as frequent hospitalisations (9).
Pathophysiology
The causes of Charcot neuroarthropathy and its sequelae are multifactorial. There is no Charcot foot without neuropathy. Numerous risk factors have been identified: duration of diabetes, presence of retinopathy, microalbuminuria and macroalbuminuria, elevated HbA1C levels and the presence of atherosclerosis (2). Currently, two hypotheses stand out: the neurovascular theory and the neurotraumatic theory. Regarding the former, it involves a hyperaemic state secondary to damage to the sympathetic nervous system, leading to venous hypertension that causes suffering of the soft tissues of the foot. This suffering prevents the maintenance of the foot’s architecture. This hyperaemia is also responsible for the activation of the RANK/RANK-L system, which would cause an imbalance by activating bone resorption through the differentiation of monocytes into osteoclasts (12). As for the neurotraumatic theory, it is attributed to repeated microtraumas to the lower limb, where the loss of proprioception triggers a pro-inflammatory process that activates osteoclastogenesis through the same enzyme system. The loading of the foot on these inflammatory processes leads to failure of the muscles supporting the foot, and fractures responsible for instability, leading to its collapse.
Diagnosis
The clinical diagnosis of acute Charcot foot is challenging. According to the recommendations of the International Working Group on Diabetic Foot (IWGDF), the clinical diagnosis is based on the association, in a diabetic patient with neuropathy and without skin lesions, of local temperature elevation with oedema and redness of the foot compared to the contralateral foot (13). Temperature should be measured using an infrared thermometer at the ankle and foot at the same location on each side (14). The paraclinical assessment relies on a weight-bearing, bilateral and comparative radiographic evaluation (15). In the case of normal radiographic findings, MRI is recommended to confirm or rule out the diagnosis and quantify its activity if necessary. If MRI is contraindicated, CT, scintigraphy or PET scans may be performed (16). It is not recommended to conduct blood tests such as C-reactive protein (CRP) or erythrocyte sedimentation rate (ESR), as no biological marker allows for early diagnosis (17).
Classification
Several classifications facilitate the analysis of Charcot foot. Eichenholtz’s classification evaluates the temporal evolution of the disease, while Sanders’ and, more recently, Brodsky’s classifications analyse the anatomical location (18). The modified Eichenholtz classification is summarised in Table 1 (19). This historical classification is now supplanted by the MRI classification into four stages as well (Table 2) (15), although Eichenholtz’s classification remains widely used. Regarding the anatomical level of Charcot neuroarthropathy involvement, Sanders’ classification (Fig. 1), historically simple, and more recently Brodsky’s classification (Fig. 2) are utilised (20). These classifications are based on the most frequently affected anatomical regions. Brodsky’s classification has the advantage of considering hindfoot dislocations. The midfoot and hindfoot are the most commonly affected locations.
Eichenholtz classification.
| Stage | Radiographic findings | Clinical findings | Treatment |
|---|---|---|---|
| 0 (prodromal) | Normal radiographs | Swelling, erythema, warmth | Patient education, serial radiographs to monitor progression, protected weight-bearing |
| I (development) | Osteopenia, fragmentation, joint subluxation or dislocation | Swelling, erythema, warmth, ligamentous laxity | Protected weight-bearing with total contact casting or prefabricated pneumatic brace. Cast or brace should be used until radiographic resolution of fragmentation and presence of normal skin temperature (usually needed for 2–4 months) |
| II (coalescence) | Absorption of debris, sclerosis, fusion of larger fragments | Decreased warmth, decreased swelling, decreased erythema | Total contact casting, prefabricated pneumatic brace, Charcot restraint, orthotic walker or clamshell ankle-foot orthosis |
| III (reconstruction) | Consolidation of deformity, joint arthrosis, fibrous ankyloses, rounding and smoothing of bone fragments | Absence of warmth, absence of swelling, absence of erythema, stable joint ± fixed deformity | Plantigrade foot: custom inlay shoes with rigid shank and rocker bottom sole |
| Nonplantigrade foot or ulceration: debridement, exostectomy, deformity correction or fusion with internal fixation |
Clinicopathological and CT/MRI features of the proposed categories of the Charcot foot.
| Category | Clinical symptoms | CT and MRI features | Histopathology |
|---|---|---|---|
| Active stage, grade 0 | Mild inflammation (swelling, warmth, pain (?), increased by unprotected walking); no gross deformity | Obligatory: diffuse BMO and STO (Kiuru Grade I–III), no cortical disruption | Lamellar bone with active surface. Remodelling of trabeculae associated with microfractures. Marrow space replaced by loose spindles |
| Facultative: subchondral trabecular microfractures (bone bruise); ligament damage | |||
| Active stage, grade 1 | Severe inflammation (swelling, warmth, pain (?), increased by unprotected walking); gross deformity, increased by unprotected walking | Obligatory: fracture(s) with cortical disruption, BMO and STO (Kiuru Grade IV) | Increased vascularity of the marrow space, active remodelling of woven bone. Compatible with response to (impaction) fracture. Osteonecrosis. Thickened synovium, fragmented cartilage and subchondral bone, invasion of inflammatory cells and vascular elements |
| Facultative: osteoarthritis, cysts, cartilage damage, osteochondrosis, joint effusion, fluid collection, bone erosion/necrosis, bone lysis, debris, bone destruction, bone luxation/subluxation, ligament damage, tenosynovitis, bone dislocation | |||
| Inactive stage, grade 0 | No inflammation, no gross deformity | No abnormal imaging or minimal residue BMO; subchondral sclerosis, bone cysts, osteoarthrosis, ligament damage | Sclerosis of bone characterised by broad lamellar trabeculae with collagenous replacement and a low vascularity of the marrow space |
| Inactive stage, grade 1 | No inflammation, persistent gross deformity, ankylosis | Residual BMO, cortical callus (Kiuru Grade IV); joint effusion, subchondral cysts, joint destruction, joint dislocation, fibrosis, osteophyte formation, bone remodelling, cartilage damage, ligament damage, bone sclerosis, ankyloses, pseudoarthrosis | Woven bone, immature and structurally disorganised, fibrosis |
BMO, bone marrow oedema; STO, soft tissue oedema.
Medical treatment
Management should be multidisciplinary around the patient (21). Medical treatment, aside from managing diabetes itself with glycaemic control, involves offloading the lower limb and complete immobilisation of the affected foot using a non-removable total contact cast (22). This is indicated regardless of the location of neuroarthropathy. It has not been proven that offloading with immobilisation is more effective than immobilisation with weight-bearing. The latter would allow for more patient autonomy (23). It is essential to monitor and protect the contralateral foot to prevent bilateral Charcot foot (24, 25). Medical treatment may last 4–6 months, until the clinical or radiological signs disappear (26). Regarding specific pharmacological treatments for Charcot foot, although many molecules have been tested and studied, none have truly proven effective. This includes bone resorption inhibitors such as calcitonin and bisphosphonates. Only immunotherapy with denosumab currently shows effects on bone resorption, but without impact on the duration of remission of the inflammatory phase (27). Bone stimulators such as parathyroid hormone and anti-inflammatory medications such as cortisone have not demonstrated any efficacy (28).
Surgical treatment
The surgical approach will depend on the anatomical location of Charcot foot.
Before any orthopaedic surgery, a comprehensive arterial assessment (Doppler, CT angiography or contrast-enhanced MRI) should be performed. If vascular intervention is necessary, it must be carried out before any orthopaedic treatment.
Numerous surgical techniques have been described, including percutaneous and arthroscopic approaches, as well as open surgery (29). Similarly, various osteosynthesis methods are used, whether internal (30), external or mixed (31). In percutaneous surgery, procedures such as Achilles tendon lengthening, exostectomies and deformity corrections have been described (32). Arthroscopy is reserved for the ankle and hindfoot. Open surgery is performed for all locations of Charcot foot (33).
Achilles tendon lengthening is primarily indicated to reduce pressure on the forefoot and midfoot, but in peri-talar or even talocrural dislocations, its lengthening is often necessary (34). This may even slow the progression (35) of Charcot foot and reduce the recurrence of ulcers (36). Exostectomies are performed for plantar conflicts, often at a late stage (Eichenholtz stage 3), in the midfoot and hindfoot, for minor deformities. They are currently gaining traction, but the risk remains foot destabilisation. Percutaneous deformity correction is under development and evaluation (37), but early results seem promising (38). There are few studies on arthroscopy in Charcot foot (39). One study, involving arthrodesis with external fixation, reported fewer complications than open surgery but no difference in terms of consolidation and deformity correction.
Regarding open surgery, it addresses static disorders. The literature describes two major approaches:
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The Charcot foot reconstruction technique, which corrects static disorders while preserving foot bones through various options. This is the most commonly used method with the best outcomes (40) (Fig. 3).
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The ‘super construct’ technique, which immobilises the affected anatomical region as well as adjacent regions, with bone resection if necessary to relieve skin tension while shortening the limb (41) (Fig. 4).
Surgical treatment also includes the debridement of infectious lesions and collection of bacterial samples (42). When Charcot foot is complicated by sepsis, the risk of major lower limb amputation is increased twelvefold. Furthermore, the risk of generalised sepsis is significant, as is the risk of foot destruction. Infection must therefore be managed urgently. Radical debridement should be performed using the ‘Red-Amber-Green’ technique (43), which involves single-stage debridement of all inflamed and infected tissues. As with any osteoarticular infection, broad-spectrum antibiotic therapy should be administered postoperatively according to hospital protocols. Iterative surgical debridements are often required (44). Antibiotic therapy should then be adjusted based on bacterial cultures. In cases of significant tissue loss, negative pressure therapy may sometimes be necessary, although it has not been proven superior to directed healing (45, 46). The management of foot static disorders in such cases will be undertaken at a later stage.
Amputation surgery is also an integral part of Charcot foot treatment, whether as a first-line option or in cases of failed medical or surgical treatment (47). Most cases involve major amputations, defined as above-ankle amputations, which incur the highest costs (48).
Regardless of the surgical treatment, the goal is to achieve a plantigrade, shoe-able foot and to prevent ulcers.
Indications
Charcot involvement of the ankle and hindfoot corresponds to Sanders’ stages 3 and 4 and Brodsky’s types 2 and 3, representing 10–20% of cases. This is the most common location after the midfoot (49).
When diagnosed early, medical treatment with offloading and non-removable immobilisation has proven effective in reducing the 1-year amputation rate and achieving Charcot remission (normalisation of foot temperature) (50). If, despite well-conducted medical treatment, or if the foot is already deformed at diagnosis, surgery is indicated. Early management of deformities in Eichenholtz stages 0–2, before the appearance of wounds or even deformities, has shown better outcomes (51). At stage 3, surgery is indicated for feet that are minimally or not deformed but remain painful.
For this location, the most commonly used surgical techniques are ankle arthrodesis and tibio-talo-calcaneal arthrodesis (49). Intramedullary nailing, internal osteosynthesis (large-diameter screws, plates) and external fixation (peri-articular fixator) are employed, sometimes in combination. Intramedullary nailing offers the advantage of allowing earlier weight-bearing and stabilising axial and rotational stresses more effectively than external fixation (52). The surgical techniques remain the same regardless of the Eichenholtz stage.
The surgical correction of Charcot foot is combined with osteoarticular infection treatment (53). A single-stage surgical approach is performed in cases of chronic sepsis. In cases of acute sepsis, such as ‘diabetic foot attack’ (54), treatment is carried out in two stages: an initial debridement to stabilise the foot (Figs 5 and 6), followed by a second-stage correction of morphostatic disorders (Fig. 7) (55).
Diabetic foot attack after debridement.
Citation: EFORT Open Reviews 10, 6; 10.1530/EOR-2025-0057
Second stage with morphostatic correction.
Citation: EFORT Open Reviews 10, 6; 10.1530/EOR-2025-0057
Complications
Regardless of the surgical technique used for Charcot foot treatment in the hindfoot and ankle, complications are frequent (8, 56).
The most common complications of internal osteosynthesis are uncontrolled infection, hardware failure and non-union (57). The use of local bone grafting may reduce the incidence of non-union (58). For external fixation, pin-site infections are the most common complication (59).
A systematic review by Cossins et al. on tibio-calcaneal arthrodesis reported an overall complication rate of 69.8% (60). External fixators exhibited the highest complication rates, followed by internal osteosynthesis with screws/plates, and finally, intramedullary nailing, which required no surgical revision. However, external fixation is mainly used in cases of skin ulceration.
In Ha et al.’s study, the overall complication rate was 36%, regardless of location. The mixed fixation method had the highest complication rate at 70%. In this study, the amputation rate with foot reconstruction was 5%, but the follow-up period was short.
Despite the high complication rate, surgical management improves patients’ quality of life (61, 62, 63) and reduces mortality rates (64, 65, 66).
Conclusion
Charcot foot management is evolving rapidly, with an increasing volume of the surgical literature in recent years, although most studies have a low level of evidence.
Management must be multidisciplinary, and diagnosis should be made as early as possible for optimal treatment.
Surgical treatment for hindfoot and ankle Charcot is becoming more common to improve patient quality of life and reduce mortality. Early intervention is increasingly performed as soon as foot deformity occurs, regardless of Eichenholtz stage.
Moreover, surgery is becoming more aggressive, particularly with the ‘super construct’ technique, which appears to yield the best results. Mixed osteosynthesis, combining intramedullary nailing of the hindfoot and peri-articular fixation for overall foot stabilisation, seems to be the best approach despite its high complication rate.
In cases of severe infection, a two-stage surgical approach should be undertaken.
ICMJE Statement of Interest
The author declares that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research reported.
Funding Statement
This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector.
References
- 1↑
Jude EB , Siafarikas C , Rastogi A , et al. Demographic and clinical characteristics of patients with Charcot neuro-osteoarthropathy in people with diabetes mellitus in six countries: a multicenter observational study from 1996 to 2022. J Diabetes Res 2025 2025 4275741. (https://doi.org/10.1155/jdr/4275741)
- 2↑
Tsatsaris G . Risk factors for Charcot foot development in individuals with diabetes mellitus. Diabetologia 2024 67 2702–2710. (https://doi.org/10.1007/s00125-024-06271-9)
- 3↑
Jordan WR . Neuritic manifestations in diabetes mellitus. Arch Intern Med 1936 57 307–366. (https://doi.org/10.1001/archinte.1936.00170060069004)
- 4↑
Kloska A , Korzon-Burakowska A , Malinowska M , et al. The role of genetic factors and monocyte-to-osteoclast differentiation in the pathogenesis of Charcot neuroarthropathy. Diabetes Res Clin Pract 2020 166 108337. (https://doi.org/10.1016/j.diabres.2020.108337)
- 5↑
Myerson MS , Henderson MR , Saxby T , et al. Management of midfoot diabetic neuroarthropathy. Foot Ankle Int 1994 15 233–241. (https://doi.org/10.1177/107110079401500502)
- 6↑
Khan O , Kavarthapu M , Edmonds M , et al. Surgical management of Charcot foot – the advancements over the past decade. J Clin Orthop Trauma 2023 47 102317. (https://doi.org/10.1016/j.jcot.2023.102317)
- 7↑
Schneekloth BJ , Lowery NJ & Wukich DK . Charcot neuroarthropathy in patients with diabetes: an updated systematic review of surgical management. J Foot Ankle Surg 2016 55 586–590. (https://doi.org/10.1053/j.jfas.2015.12.001)
- 8↑
Regauer M , Grasegger V , Fürmetz J , et al. High rate of complications after corrective midfoot/subtalar arthrodesis and Achilles tendon lengthening in Charcot arthropathy type Sanders 2 and 3. Int Orthop 2023 47 141–150. (https://doi.org/10.1007/s00264-022-05567-y)
- 9↑
Argyropoulos M , Wynell-Mayow W , Johnson O , et al. Charcot neuro-osteoarthropathy: a review of key concepts and an evidence-based surgical management algorithm. Front Clin Diabetes Healthc 2024 5 1344359. (https://doi.org/10.3389/fcdhc.2024.1344359)
- 10↑
Wukich DK , Frykberg RG & Kavarthapu V . Charcot neuroarthropathy in persons with diabetes: it’s time for a paradigm shift in our thinking. Diabetes Metab Res Rev 2024 40 e3754. (https://doi.org/10.1002/dmrr.3754)
- 11↑
Armstrong DG , Swerdlow MA , Armstrong AA , et al. Five year mortality and direct costs of care for people with diabetic foot complications are comparable to cancer. J Foot Ankle Res 2020 13 16. (https://doi.org/10.1186/s13047-020-00383-2)
- 12↑
Greco T , Mascio A , Comisi C , et al. RANKL-RANK-OPG pathway in Charcot diabetic foot: pathophysiology and clinical-therapeutic implications. Int J Mol Sci 2023 24 3014. (https://doi.org/10.3390/ijms24033014)
- 13↑
Wukich DK , Schaper NC , Gooday C , et al. Guidelines on the diagnosis and treatment of active Charcot neuro-osteoarthropathy in persons with diabetes mellitus (IWGDF 2023). Diabetes Metab Res Rev 2024 40 e3646. (https://doi.org/10.1002/dmrr.3646)
- 14↑
Mascio A , Comisi C , Cinelli V , et al. Radiological assessment of Charcot neuro-osteoarthropathy in diabetic foot: a narrative review. Diagnostics 2025 15 767. (https://doi.org/10.3390/diagnostics15060767)
- 15↑
Chantelau E & Grützner G . Is the Eichenholtz classification still valid for the diabetic Charcot foot? Swiss Med Wkly 2014 144 1718. (https://smw.ch/index.php/smw/article/view/1862)
- 16↑
Cecchini S , Gatti C , Fornarelli D , et al. Magnetic resonance imaging and 99Tc WBC-SPECT/CT scanning in differential diagnosis between osteomyelitis and Charcot neuroarthropathy: a case series. Tomography 2024 10 1312–1319. (https://doi.org/10.3390/tomography10080098)
- 17↑
Blathra E , Anastasiou IA , Eleftheriadou I , et al. Charcot osteoarthropathy: a comprehensive analysis of recent research on novel biomarkers for early detection. Int J Low Extrem Wounds 2025 [In press]. (https://doi.org/10.1177/15347346251328436)
- 18↑
Wukich DK , Raspovic K , Liu GT , et al. Are the Sanders-Frykberg and Brodsky-Trepman classifications reliable in diabetic Charcot neuroarthropathy? J Foot Ankle Surg 2021 60 432–435. (https://doi.org/10.1053/j.jfas.2020.03.003)
- 19↑
Shibata T , Tada K & Hashizume C . The results of arthrodesis of the ankle for leprotic neuroarthropathy. J Bone Joint Surg Am 1990 72 749–756. (https://doi.org/10.2106/00004623-199072050-00016)
- 20↑
E Galhoum A . Charcot ankle neuroarthropathy pathology, diagnosis and management: a review of literature. MOJ Orthop Rheumatol 2016 6 00218. (https://medcraveonline.com/MOJOR/charcot-ankle-neuroarthropathy-pathology-diagnosis-and-management-a-review-of-literature.html)
- 21↑
Sellés Dechent R , Rueda Alcárcel C , Primo Romaguera V , et al. Role of the general surgeon in the early diagnosis and treatment of Charcot’ foot. Cir Esp 2015 93 320–325. (https://doi.org/10.1016/j.cireng.2013.04.016)
- 22↑
Berhane T , Jeyaraman K , Hamilton M , et al. Offloading interventions for the management of Charcot neuroarthropathy in diabetes. Foot Ankle Orthop 2025 10 24730114251315670. (https://doi.org/10.1177/24730114251315670)
- 23↑
Prem R , Vignaraja V , Lewis T , et al. Weight bearing versus non-weight bearing total contact cast in the management of active Charcot foot: a systematic review. SAGE Open Med 2024 12 20503121241306957. (https://doi.org/10.1177/20503121241306957)
- 24↑
Cheong KY , Bergin SM , Munteanu SE , et al. Factors associated with the development of recurrent and contralateral Charcot neuroarthropathy in individuals with diabetes mellitus: a scoping review. J Foot Ankle Res 2024 17 e70016. (https://doi.org/10.1002/jfa2.70016)
- 25↑
Hurst M & Shin L . Charcot neuroarthropathy: surgical and conservative treatment approaches. Semin Vasc Surg 2025 38 74–84. (https://doi.org/10.1053/j.semvascsurg.2025.01.004)
- 26↑
Gooday C , Gray K , Game F , et al. Systematic review of techniques to monitor remission of acute Charcot neuroarthropathy in people with diabetes. Diabetes Metab Res Rev 2020 36 e3328. (https://doi.org/10.1002/dmrr.3328)
- 27↑
Lasschuit JWJ , Center JR , Greenfield JR , et al. Effect of denosumab on inflammation and bone health in active Charcot foot: a phase II randomised controlled trial. J Diabetes Complications 2024 38 108718. (https://doi.org/10.1016/j.jdiacomp.2024.108718)
- 28↑
Bell DSH & Jerkins T . Diabetic Charcot neuroarthropathy: a threat to both limb and life. Diabetes Obes Metab 2025 27 35–39. (https://doi.org/10.1111/dom.15994)
- 29↑
Pattisapu N , Skinner WC , Rogero RG , et al. Operative management of Charcot neuropathy of the foot and ankle: a retrospective cohort study of long-term outcomes. J Foot Ankle Surg 2025 64 166–170. (https://doi.org/10.1053/j.jfas.2024.09.012)
- 30↑
Caravaggi C , Cimmino M , Caruso S , et al. Intramedullary compressive nail fixation for the treatment of severe Charcot deformity of the ankle and rear foot. J Foot Ankle Surg 2006 45 20–24. (https://doi.org/10.1053/j.jfas.2005.10.003)
- 31↑
Zgonis T , Roukis TS , Polyzois V , et al. Surgical management of the unstable diabetic Charcot deformity using the taylor spatial frame. Oper Tech Orthop 2006 16 10–17. (https://doi.org/10.1053/j.oto.2006.01.004)
- 32↑
Lamm BM , Gottlieb HD & Paley D . A two-stage percutaneous approach to Charcot diabetic foot reconstruction. J Foot Ankle Surg 2010 49 517–522. (https://doi.org/10.1053/j.jfas.2010.07.014)
- 33↑
Aikawa T , Watanabe K , Matsubara H , et al. Tibiocalcaneal fusion for Charcot ankle with severe talar body loss: case report and a review of the surgical literature. J Foot Ankle Surg 2016 55 247–251. (https://doi.org/10.1053/j.jfas.2014.06.003)
- 34↑
Richter M , Mittlmeier T , Rammelt S , et al. Intramedullary fixation in severe Charcot osteo-neuroarthropathy with foot deformity results in adequate correction without loss of correction – results from a multi-centre study. Foot Ankle Surg 2015 21 269–276. (https://doi.org/10.1016/j.fas.2015.02.003)
- 35↑
Tiruveedhula M , Graham A , Thapar A , et al. Outcomes of Tendo-Achilles lengthening and weight-bearing total contact cast for management of early midfoot Charcot neuroarthropathy. J Clin Orthop Trauma 2021 17 128–138. (https://doi.org/10.1016/j.jcot.2021.03.001)
- 36↑
Dallimore SM & Kaminski MR . Tendon lengthening and fascia release for healing and preventing diabetic foot ulcers: a systematic review and meta-analysis. J Foot Ankle Res 2015 8 33. (https://doi.org/10.1186/s13047-015-0085-6)
- 37↑
Pate J , Jagiella-Lodise O , Dunson J , et al. Minimally invasive exostectomy for Charcot neuroarthropathy. Foot Ankle Orthop 2024 9 24730114241232977. (https://doi.org/10.1177/24730114241232977)
- 38↑
Greenblatt M , Mateen S & Siddiqui NA . Where minimal incision surgery can have maximum results with Charcot reconstruction. Clin Podiatr Med Surg 2025 42 167–176. (https://doi.org/10.1016/j.cpm.2024.06.002)
- 39↑
Gutteck N . Comparative results of arthroscopic ankle arthrodesis vs. open arthrodesis in patients with diabetes-associated Charcot Neuro-Arthropathy. Eur J Orthop Surg Traumatol 2023 33 3577–3584. (https://doi.org/10.1007/s00590-023-03592-0)
- 40↑
Ha J , Hester T , Foley R , et al. Charcot foot reconstruction outcomes: a systematic review. J Clin Orthop Trauma 2020 11 357–368. (https://doi.org/10.1016/j.jcot.2020.03.025)
- 41↑
Sammarco VJ & Chevillet J . The role of internal fixation in surgery of the Charcot foot and the evolution of “super-construct” techniques. Curr Orthop Pract 2010 21 233–239. (https://journals.lww.com/c-orthopaedicpractice/fulltext/2010/05000/the_role_of_internal_fixation_in_surgery_of_the.4.aspx)
- 42↑
Roberts RHR , Davies-Jones GR , Brock J , et al. Surgical management of the diabetic foot: the current evidence. World J Orthop 2024 15 404–417. (https://doi.org/10.5312/wjo.v15.i5.404)
- 43↑
Ahluwalia R , Vainieri E , Tam J , et al. Surgical diabetic foot debridement: improving training and practice utilizing the traffic light principle. Int J Low Extrem Wounds 2019 18 279–286. (https://doi.org/10.1177/1534734619853657)
- 44↑
Vas PRJ , Edmonds M , Kavarthapu V , et al. The diabetic foot attack: ‘tis too late to retreat!’. Int J Low Extrem Wounds 2018 17 7–13. (https://doi.org/10.1177/1534734618755582)
- 45↑
Kavitha KV , Tiwari S , Purandare VB , et al. Choice of wound care in diabetic foot ulcer: a practical approach. World J Diabetes 2014 5 546–556. (https://doi.org/10.4239/wjd.v5.i4.546)
- 46↑
Liu Z , Dumville JC , Hinchliffe RJ , et al. Negative pressure wound therapy for treating foot wounds in people with diabetes mellitus. Cochrane Database Syst Rev 2018 10 CD010318. (https://doi.org/10.1002/14651858.cd010318.pub3)
- 47↑
López Capdevilla L , Santamaría Fumas A , Sales Pérez JM , et al. Amputation versus circular external fixation in the treatment of diabetic foot with osteomyelitis: a cost and quality-of-life analysis. Ther Adv Endocrinol Metab 2024 15 20420188241271795. (https://doi.org/10.1177/20420188241271795)
- 48↑
Shehaj A , Dopke KM , Paracha AW , et al. Cost-effective modeling for management options in Charcot neuroarthropathy. Int J Low Extrem Wounds 2025 [In press]. (https://doi.org/10.1177/15347346251313652)
- 49↑
Bajuri MY , Ong SL , Das S , et al. Charcot neuroarthropathy: current surgical management and update. A systematic review. Front Surg 2022 9 820826. (https://doi.org/10.3389/fsurg.2022.820826)
- 50↑
Bittante C , Cerasari V , Bellizzi E , et al. Early treatment of acute stage 0/1 diabetic Charcot foot can avoid major amputations at one year. J Clin Med 2024 13 1633. (https://doi.org/10.3390/jcm13061633)
- 51↑
Lowery NJ , Woods JB , Armstrong DG , et al. Surgical management of Charcot neuroarthropathy of the foot and ankle: a systematic review. Foot Ankle Int 2012 33 113–121. (https://doi.org/10.3113/fai.2012.0113)
- 52↑
Hasenboehler E , Smith WR , Laudicina L , et al. Fatigue behavior of Ilizarov frame versus tibial interlocking nail in a comminuted tibial fracture model: a biomechanical study. J Orthop Surg 2006 1 16. (https://josr-online.biomedcentral.com/articles/10.1186/1749-799X-1-16)
- 53↑
Balakrishnan KR , Selva Raj DR , Ghosh S , et al. Diabetic foot attack: managing severe sepsis in the diabetic patient. World J Crit Care Med 2025 14 98419. (https://doi.org/10.5492/wjccm.v14.i1.98419)
- 54↑
Bonanni FR , Meloni M , Salvi M , et al. Characteristics and outcomes of patients admitted for diabetic foot attack. Int J Low Extrem Wounds 2025 28 15347346251328724. (https://doi.org/10.1177/15347346251328724)
- 55↑
Vas PRJ , Edmonds M , Kavarthapu V , et al. The diabetic foot attack: ‘tis too late to retreat!’. Int J Low Extrem Wounds 2018 17 7–13. (https://doi.org/10.1177/1534734618755582)
- 56↑
Tsikopoulos K , Sidiropoulos K , Meroni G , et al. Deap-seated infection and nonunion following internal fixation for Charcot foot deformity correction. A proportional meta-analysis of level 4 evidence. J Orthop Sci 2025 30 119–125. (https://doi.org/10.1016/j.jos.2024.03.004)
- 57↑
Hanada M , Hotta K & Matsuyama Y . Difficulty in bone union after arthrodesis to treat Charcot arthropathy of the foot and ankle. J Orthop 2025 62 13–16. (https://doi.org/10.1016/j.jor.2024.10.018)
- 58↑
Osman AE , El-Adly W , Haroun KM , et al. Locally obtained autologous bone grafts are effective for achieving arthrodesis while managing foot and ankle Charcot’s neuroarthropathy: short to mid-term results from a specialized north African foot and ankle surgery unit. J Orthop Surg Res 2024 19 570. (https://doi.org/10.1186/s13018-024-05036-9)
- 59↑
Dayton P , Feilmeier M , Thompson M , et al. Comparison of complications for internal and external fixation for Charcot reconstruction: a systematic review. J Foot Ankle Surg 2015 54 1072–1075. (https://doi.org/10.1053/j.jfas.2015.06.003)
- 60↑
Cossins C , George B , Talia AJ , et al. The outcomes of isolated tibiocalcaneal arthrodesis: a systematic review. Foot Ankle Orthop 2024 9 24730114241247547. (https://doi.org/10.1177/24730114241247547)
- 61↑
McGregor PC , Lyons MM , Pinzur MS . Quality of life improvement following reconstruction of midtarsal Charcot foot deformity: a five year follow-up. Iowa Orthop J 2022 42 109–112.
- 62↑
Bajuri MY , Manas AM & Zamri KS . Functional outcomes of tibiotalocalcaneal arthrodesis using a hindfoot arthrodesis nail in treating Charcot’s arthropathy deformity. Front Surg 2023 9 862133. (https://doi.org/10.3389/fsurg.2022.862133)
- 63↑
Cho E , Pinzur MS , Schiff AP , et al. Outcomes following surgical correction of talocalcalcaneal joint dislocation in diabetes associated Charcot foot arthropathy. Foot Ankle Int 2024 45 972–978. (https://doi.org/10.1177/10711007241255373)
- 64↑
Sabaghi J . Association between the procedure of tibiotalocalcaneal arthrodesis by hindfoot nailing and quality of life in Charcot’s joint. J Orthop Surg Res 2024 19 332. (https://doi.org/10.1186/s13018-024-04787-9)
- 65↑
Grant WP , Garcia-Lavin SE , Sabo RT , et al. A retrospective analysis of 50 consecutive Charcot diabetic salvage reconstructions. J Foot Ankle Surg 2009 48 30–38. (https://doi.org/10.1053/j.jfas.2008.10.004)
- 66↑
Skinner WC , Pattisapu N , Yeoh J , et al. Surgical outcomes in Charcot arthropathy. Orthop Clin North Am 2024 55 393–401. (https://doi.org/10.1016/j.ocl.2023.11.001)
