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Orthopaedic Proceedings
Vol. 96-B, Issue SUPP_17 | Pages 32 - 32
1 Nov 2014
Ball T Readman H Kendal A Rogers M Sharp R Lavis G Cooke P
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Introduction:. Vitamin D plays an important role in bone turnover. Deficiency (including borderline deficiency, or insufficiency) has a known association with fractures and has been linked to delayed or nonunion of fractures. We therefore routinely test vitamin D in cases of nonunion. Noting a high rate of vitamin D deficiency in this group, we instituted a policy to routinely screen for and treat vitamin D deficiency in both post-operative and pre-operative patients. We hypothesised that, in the post-operative patients, levels would correlate with rates of union. Methods:. We sent serum vitamin D levels on consecutive post-operative patients seen in clinics between January and May 2014. They included those with an arthrodesis of the ankle, triple joint or first MTPJ. Union was deemed to have occurred when the patient was comfortable full weight bearing and radiographs showed trabeculae crossing the fusion site. Nonunions were all confirmed with computed tomography. Results:. Ten patients were treated for nonunion, and had a mean serum vitamin D of 58nmol/L. Fourteen patients (collected over a shorter time period) had confirmed union, with a mean vitamin D of 90nmol/L. This was statistically significant on a one tailed Student's t test (p=0.038). Vitamin D was deficient in five (50%) of nonunions and in three (21%) of unions, giving an odds ratio of 3.67. Conclusions:. Our early results show a significant association of serum vitamin D levels with likelihood of nonunion, and we continue to collect data. There is a high prevalence of vitamin D deficiency in our patient population. This is of concern both for the outcome of their surgery and for their lifetime fracture risk. We recommend either screening for or presumptively treating vitamin D deficiency


Bone & Joint Research
Vol. 7, Issue 5 | Pages 373 - 378
1 May 2018
Johnson-Lynn SE McCaskie AW Coll AP Robinson AHN

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.


The Bone & Joint Journal
Vol. 98-B, Issue 9 | Pages 1155 - 1159
1 Sep 2016
Trieb K

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.


The Bone & Joint Journal
Vol. 97-B, Issue 6 | Pages 809 - 813
1 Jun 2015
Butt DA Hester T Bilal A Edmonds M Kavarthapu V

Charcot neuro-osteoarthropathy (CN) of the midfoot presents a major reconstructive challenge for the foot and ankle surgeon. The Synthes 6 mm Midfoot Fusion Bolt is both designed and recommended for patients who have a deformity of the medial column of the foot due to CN. We present the results from the first nine patients (ten feet) on which we attempted to perform fusion of the medial column using this bolt. Six feet had concurrent hindfoot fusion using a retrograde nail. Satisfactory correction of deformity of the medial column was achieved in all patients. The mean correction of calcaneal pitch was from 6° (-15° to +18°) pre-operatively to 16° (7° to 23°) post-operatively; the mean Meary angle from 26° (3° to 46°) to 1° (1° to 2°); and the mean talometatarsal angle on dorsoplantar radiographs from 27° (1° to 48°) to 1° (1° to 3°).

However, in all but two feet, at least one joint failed to fuse. The bolt migrated in six feet, all of which showed progressive radiographic osteolysis, which was considered to indicate loosening. Four of these feet have undergone a revision procedure, with good radiological evidence of fusion. The medial column bolt provided satisfactory correction of the deformity but failed to provide adequate fixation for fusion in CN deformities in the foot.

In its present form, we cannot recommend the routine use of this bolt.

Cite this article: Bone Joint J 2015; 97-B:809–13


The Bone & Joint Journal
Vol. 95-B, Issue 8 | Pages 1083 - 1087
1 Aug 2013
Shaikh N Vaughan P Varty K Coll AP Robinson AHN

Limited forefoot amputation in diabetic patients with osteomyelitis is frequently required. We retrospectively reviewed diabetic patients with osteomyelitis, an unhealed ulcer and blood pressure in the toe of > 45 mmHg who underwent limited amputation of the foot with primary wound closure. Between 2006 and 2012, 74 consecutive patients with a mean age of 67 years (29 to 93), and a median follow-up of 31 months, were included. All the wounds healed primarily at a median of 37 days (13 to 210; mean 48). At a median of 6 months (1.5 to 18; mean 353 days), 23 patients (31%) suffered a further ulceration. Of these, 12 patients (16% of the total) required a further amputation.

We conclude that primary wound closure following limited amputation of the foot in patients with diabetes is a safe and effective technique when associated with appropriate antibiotic treatment.

Cite this article: Bone Joint J 2013;95-B:1083–7.