Diabetes Complication Strikes Three Joints in Seven Years in Rare Case Report

A single medical case has drawn attention to one of the most feared and least understood complications of diabetes: Charcot neuro-osteoarthropathy, a condition in which the bones and joints of a numb limb quietly disintegrate. In a report published in BMC Endocrine Disorders, physician Dured Dardari of Centre Hospitalier Sud Francilien in Corbeil-Essonnes, France, describes a young woman with childhood-onset type 1 diabetes who experienced three separate, anatomically distinct episodes of active Charcot disease over the course of seven years, affecting her right foot, her left knee, and finally her left foot and ankle. The case is striking not only for its rarity but also for the unusual sequence of triggers that appeared to accompany each flare, offering clinicians a rare longitudinal view of how this destructive disorder can unfold in a single patient.

Charcot neuro-osteoarthropathy, often abbreviated CNO, is an inflammatory and destructive disorder of bones, joints, and soft tissues that occurs in the setting of peripheral neuropathy. When nerve damage dulls sensation, ordinary mechanical stresses go unnoticed, and the protective pain reflexes that normally force us to rest an injured limb are lost. The result can be a cascade of microfractures, joint collapse, and progressive deformity that many patients initially mistake for a simple sprain. Diabetes mellitus is the leading cause of CNO in most contemporary case series, but the condition is not exclusive to diabetes and can arise in other neuropathic disorders, including leprosy. Recurrent disease is uncommon enough, and multifocal disease involving joints beyond the foot is rarer still, which is precisely what makes this new report noteworthy.

The patient at the center of the report was diagnosed with type 1 diabetes at the age of five and carried a long history of unstable blood glucose control. In 2017, at twenty-five years old and during pregnancy, her glycated haemoglobin, or HbA1c, fell dramatically from 12.0 percent to 7.2 percent over just six weeks. At twenty-four weeks of gestation, after what was described as a minor injury to her right ankle and foot, she developed persistent swelling of the right foot and ankle. Radiographs taken at the time, together with magnetic resonance imaging performed after delivery, revealed active destructive Charcot disease of the right midfoot, most consistent with Sanders-Frykberg zone III involvement and Eichenholtz stage 1, the earliest and most inflammatory phase of the classical staging system.

The clinical response to that first episode illustrates how easily management can falter. Offloading, the cornerstone of Charcot treatment, was prescribed, but the patient’s adherence was suboptimal. Without consistent removal of weight-bearing forces from a skeleton that is actively fragmenting, deformity can progress rapidly and irreversibly. In this case, progressive deformity ultimately required a right transtibial amputation two years after the initial diagnosis. The trajectory underscores a central paradox of Charcot management: the treatments are conceptually simple, yet they demand months of disciplined immobilization from patients who, by definition, cannot feel the harm of walking on a collapsing foot.

What happened next is perhaps the most remarkable part of the story. Just two weeks after delivery, while the first episode was still active and long before the amputation, the patient presented with a painless, warm, swollen left knee. Computed tomography demonstrated severe fragmentation and collapse of the tibial plateau, the upper surface of the shin bone that forms the lower half of the knee joint, consistent with active Charcot arthropathy of the knee. Charcot disease of the knee is decidedly uncommon; the overwhelming majority of cases involve the foot and ankle. Total knee arthroplasty was performed two months later, followed by three months of rehabilitation and the recovery of a satisfactory gait, a genuinely successful outcome in an otherwise grim sequence.

The report’s authors suggest several plausible, overlapping mechanisms for this second, contralateral episode. With the right foot destroyed and painful, the patient’s weight-bearing pattern would have shifted dramatically onto the left leg, loading a knee that neuropathy had rendered unable to complain. Postpartum biomechanical factors, including ligamentous laxity and altered gait, may have compounded the stress. Some researchers have also proposed that abrupt improvement in glycaemia, as occurred during this patient’s pregnancy, could paradoxically provoke inflammatory flares, a hypothesis that has been debated in the diabetes literature and that a single case cannot confirm or refute. The authors are careful to note that no single case can establish causality for any of these candidate triggers.

The third act arrived in 2024, after the patient had progressed to end-stage kidney disease, spent two years on haemodialysis, and undergone a living-donor kidney transplantation. Her immunosuppressive regimen included belatacept, a costimulation blocker used to prevent organ rejection, along with a short prednisone taper running from 60 milligrams per day for three days, to 40 milligrams for three days, to 20 milligrams for three days. Shortly afterward, she developed a new episode involving the left foot and ankle. Magnetic resonance imaging supported a diagnosis of active Charcot disease of the medial midfoot and hindfoot, and treatment with a non-removable cast was initiated. Kidney failure and transplantation introduce yet another layer of bone biology, since chronic kidney disease disrupts mineral metabolism through the syndrome known as CKD-MBD, and immunosuppressive drugs, particularly glucocorticoids, can accelerate bone loss.

Underlying all of these episodes is a biology that remains incompletely mapped. The leading model implicates dysregulated inflammation driven by the RANKL and osteoprotegerin pathway, which governs the balance between bone-resorbing osteoclasts and bone-forming osteoblasts, together with neuropeptides such as calcitonin gene-related peptide that link the nervous system to skeletal remodeling. When neuropathy removes both sensory feedback and normal autonomic regulation of blood flow, the bones of the affected limb may become targets of unchecked osteoclastic activity, turning routine mechanical loads into a destructive positive feedback loop. The International Working Group on the Diabetic Foot recognizes active Charcot as a medical emergency in the diabetic foot, because early offloading during the active phase is the single most effective intervention to prevent permanent deformity.

The clinical lessons of this case are sobering but actionable. Active Charcot disease can strike at a young age in people with childhood-onset type 1 diabetes, and it can recur sequentially at multiple sites, including joints as unexpected as the knee. The report emphasizes early recognition, prompt offloading, careful functional rehabilitation, and lifelong surveillance in high-risk patients. It also argues that long-term prevention should include sustained achievement of individualised glycaemic targets to reduce neuropathic and microvascular risk, with a caution attached: in people with marked chronic hyperglycaemia, correction of blood glucose should be carefully planned and monitored rather than abrupt, given the theoretical concern that rapid normalization may itself provoke flares. For a condition that can silently dismantle a joint in weeks, the difference between vigilance and delay can be the difference between walking and amputation, a truth this patient’s seven-year odyssey makes painfully concrete.

Subject of Research: Recurrent multifocal Charcot neuro-osteoarthropathy in a young woman with childhood-onset type 1 diabetes

Article Title: Recurrent multifocal active Charcot neuro-osteoarthropathy in a young woman with childhood-onset type 1 diabetes mellitus: a case report

Article References: Recurrent multifocal active Charcot neuro-osteoarthropathy in a young woman with childhood-onset type 1 diabetes mellitus: a case report. (n.d.). https://doi.org/10.1186/s12902-026-02528-z

Image Credits: AI Generated

DOI: 10.1186/s12902-026-02528-z

Keywords: Charcot neuro-osteoarthropathy, type 1 diabetes, peripheral neuropathy, multifocal Charcot, Charcot knee, kidney transplantation, pregnancy, rapid glycaemic control, offloading, bone destruction, case report, diabetic foot