Charcot neuroarthropathy is a rare but serious complication of diabetes, causing progressive destruction of the bones and joints of the foot leading to deformity, altered biomechanics and an increased risk of ulceration. Management is complicated by a lack of consensus on diagnostic criteria and an incomplete understanding of the pathogenesis. In this review, we consider recent insights into the development of Charcot neuroarthropathy. It is likely to be dependent on several interrelated factors which may include a genetic pre-disposition in combination with diabetic neuropathy. This leads to decreased neuropeptides (nitric oxide and calcitonin gene-related peptide), which may affect the normal coupling of bone formation and resorption, and increased levels of Receptor activator of nuclear factor kappa-B ligand, potentiating osteoclastogenesis. Repetitive unrecognized trauma due to neuropathy increases levels of pro-inflammatory cytokines (interleukin-1β, interleukin-6, tumour necrosis factor α) which could also contribute to increased bone resorption, in combination with a pre-inflammatory state, with increased autoimmune reactivity and a profile of monocytes primed to transform into osteoclasts - cluster of differentiation 14 (CD14). Increased blood glucose and loss of circulating Receptor for Advanced Glycation End-Products (AGLEPs), leading to increased non-enzymatic glycation of collagen and accumulation of AGLEPs in the tissues of the foot, may also contribute to the pathological process. An understanding of the relative contributions of each of these mechanisms and a final common pathway for the development of Charcot neuroarthropathy are still lacking. Cite this article: S. E. Johnson-Lynn, A. W. McCaskie, A. P. Coll, A. H. N. Robinson. Neuroarthropathy in diabetes: pathogenesis of Charcot arthropathy. Bone Joint Res 2018;7:373–378. DOI: 10.1302/2046-3758.75.BJR-2017-0334.R1

Aims. The Chopart joint complex is a joint between the midfoot and hindfoot. The static and dynamic support system of the joint is critical for maintaining the medial longitudinal arch of the foot. Any dysfunction leads to progressive collapsing flatfoot deformity (PCFD). Often, the tibialis posterior is the primary cause; however, contrary views have also been expressed. The present investigation intends to explore the comprehensive anatomy of the support system of the Chopart joint complex to gain insight into the cause of PCFD. Methods. The study was conducted on 40 adult embalmed cadaveric lower limbs. Chopart joint complexes were dissected, and the structures supporting the joint inferiorly were observed and noted. Results. The articulating bones exhibit features like a cuboid shelf and navicular beak, which appear to offer inferior support to the joint. The expanse of the spring ligament complex is more medial than inferior, while the superomedial part is more extensive than the intermediate and inferoplantar parts. The spring ligament is reinforced by the tendons in the superomedial part (the main tendon of tibialis posterior), the inferomedial part (the plantar slip of tibialis posterior), and the master knot of Henry positioned just inferior to the gap between the inferomedial and inferoplantar bundles. Conclusion. This study highlights that the medial aspect of the talonavicular articulation has more extensive reinforcement in the form of superomedial part of spring ligament and tibialis posterior tendon. The findings are expected to prompt further research in weightbearing settings on the pathogenesis of flatfoot. Cite this article: Bone Jt Open 2024;5(4):335–342

Aims. The pathogenesis of intraneural ganglion cysts is controversial. Recent reports in the literature described medial plantar intraneural ganglion cysts (mIGC) with articular branches to subtalar joints. The aim of the current study was to provide further support for the principles underlying the articular theory, and to explain the successes and failures of treatment of mICGs. Patients and Methods. Between 2006 and 2017, five patients with five mICGs were retrospectively reviewed. There were five men with a mean age of 50.2 years (33 to 68) and a mean follow-up of 3.8 years (0.8 to 6). Case history, physical examination, imaging, and intraoperative findings were reviewed. The outcomes of interest were ultrasound and/or MRI features of mICG, as well as the clinical outcomes. Results. The five intraneural cysts followed the principles of the unifying articular theory. Connection to the posterior subtalar joint (pSTJ) was identified or suspected in four patients. Re-evaluation of preoperative MRI demonstrated a degenerative pSTJ and denervation changes in the abductor hallucis in all patients. Cyst excision with resection of the articular branch (four), cyst incision and drainage (one), and percutaneous aspiration/steroid injection (two) were performed. Removing the connection to the pSTJ prevented recurrence of mIGC, whereas medial plantar nerves remained cystic and symptomatic when resection of the communicating articular branch was not performed. Conclusion. Our findings support a standardized treatment algorithm for mIGC in the presence of degenerative disease at the pSTJ. By understanding the pathoanatomic mechanism for every cyst, we can improve treatment that must address the articular branch to avoid the recurrence of intraneural ganglion cysts, as well as the degenerative pSTJ to avoid extraneural cyst formation or recurrence. Cite this article: Bone Joint J 2018;100-B:183–9

Neuropathic changes in the foot are common with a prevalence of approximately 1%. The diagnosis of neuropathic arthropathy is often delayed in diabetic patients with harmful consequences including amputation. The appropriate diagnosis and treatment can avoid an extensive programme of treatment with significant morbidity for the patient, high costs and delayed surgery. The pathogenesis of a Charcot foot involves repetitive micro-trauma in a foot with impaired sensation and neurovascular changes caused by pathological innervation of the blood vessels. In most cases, changes are due to a combination of both pathophysiological factors. The Charcot foot is triggered by a combination of mechanical, vascular and biological factors which can lead to late diagnosis and incorrect treatment and eventually to destruction of the foot.

This review aims to raise awareness of the diagnosis of the Charcot foot (diabetic neuropathic osteoarthropathy and the differential diagnosis, erysipelas, peripheral arterial occlusive disease) and describe the ways in which the diagnosis may be made. The clinical diagnostic pathways based on different classifications are presented.

Cite this article: Bone Joint J 2016;98-B:1155–9.

Pigmented villonodular synovitis (PVNS) is a rare benign disease of the synovium of joints and tendon sheaths, which may be locally aggressive. We present 18 patients with diffuse-type PVNS of the foot and ankle followed for a mean of 5.1 years (2 to 11.8). There were seven men and 11 women, with a mean age of 42 years (18 to 73). A total of 13 patients underwent open or arthroscopic synovectomy, without post-operative radiotherapy. One had surgery at the referring unit before presentation with residual tibiotalar PVNS. The four patients who were managed non-operatively remain symptomatically controlled and under clinical and radiological surveillance. At final follow-up the mean Musculoskeletal Tumour Society score was 93.8% (95% confidence interval (CI) 85 to 100), the mean Toronto Extremity Salvage Score was 92 (95% CI 82 to 100) and the mean American Academy of Orthopaedic Surgeons foot and ankle score was 89 (95% CI 79 to 100). The lesion in the patient with residual PVNS resolved radiologically without further intervention six years after surgery. Targeted synovectomy without adjuvant radiotherapy can result in excellent outcomes, without recurrence. Asymptomatic patients can be successfully managed non-operatively. This is the first series to report clinical outcome scores for patients with diffuse-type PVNS of the foot and ankle.

Cite this article: Bone Joint J 2013;95-B:384–90.

Charcot osteoarthropathy of the foot is a chronic and progressive disease of bone and joint associated with a risk of amputation. The main problems encountered in this process are osteopenia, fragmentation of the bones of the foot and ankle, joint subluxation or even dislocation, ulceration of the skin and the development of deep sepsis. We report our experience of a series of 20 patients with Charcot osteoarthropathy of the foot and ankle treated with an Ilizarov external fixator. The mean age of the group was 30 years (21 to 50). Diabetes mellitus was the underlying cause in 18 patients. Five had chronic ulcers involving the foot and ankle. Each patient had an open lengthening of the tendo Achillis with excision of all necrotic and loose bone from the ankle, subtalar and midtarsal joints when needed. The resulting defect was packed with corticocancellous bone graft harvested from the iliac crest and an Ilizarov external fixator was applied. Arthrodesis was achieved after a mean of 18 weeks (15 to 20), with healing of the skin ulcers. Pin track infection was not uncommon, but no frame had to be removed before the arthrodesis was sound.

Every patient was able to resume wearing regular shoes after a mean of 26.5 weeks (20 to 45).

Between 2002 and 2008, 130 consecutive ankles were replaced with an hydroxyapatite (HA) and titanium-HA-coated Ankle Evolutive System total ankle prosthesis. Plain radiographs were analysed by two independent observers. Osteolytic lesions were classified by their size and location, with cavities > 10 mm in diameter considered to be ‘marked’. CT scanning was undertaken in all patients with marked osteolysis seen on the plain radiographs.

Osteolytic lesions were seen on the plain films in 48 (37%) and marked lesions in 27 (21%) ankles. The risk for osteolysis was found to be 3.1 (95% confidence interval 1.6 to 5.9) times higher with implants with Ti-HA porous coating.

Care should be taken with ankle arthroplasty until more is known about the reasons for these severe osteolyses.