A Closer Look At Beaming The Columns In The Charcot Diabetic Foot

Start Page: 52
William P. Grant, DPM, FACFAS, Bryan Barbato, BS, and Lisa M. Grant-McDonald, BS

In the unstable Charcot foot, the concept of beaming may help patients with diabetes attain stability and greater weightbearing. These authors discuss the pathway of Charcot neuroarthropathy and offer essential surgical pearls.

Charcot neuroarthropathy is a disease that arises secondarily in patients with diabetes mellitus and peripheral neuropathy although there are cases of Charcot in which patients may or may not have diabetes or neuropathy.1 Due to fast food diets and eating-on-the-go lifestyles, diabetes has become an epidemic across the globe.2 Charcot neuroarthropathy results in structural deformities and most commonly occurs in the foot and ankle. Bony deformities of the foot can result in the development of ulcerations in areas of high pressure. Diabetic foot ulcers are a frequent cause of foot amputations.2

   Charcot neuroarthropathy disease is characterized by increased local bone resorption by osteoclasts in small weightbearing joints, particularly in the foot. Osteoclasts are among the three main cells present in bone and they resorb bone tissue.3 The elevated bone resorptive process that occurs in Charcot neuroarthropathy is a product of more than just one cellular pathway. The receptor activator of nuclear factor-kB ligand (RANKL) is an integral component in the regulation of osteoclast differentiation and activation. The RANKL activates the osteoclast membrane protein known as RANK.4

   Advanced glycation end products (AGEs) regulate RANKL activation. The AGEs modify type 1 collagen and these end products are a normal result of aging but can form prematurely.5 The receptor for advanced glycation end products (RAGE) expresses continually and increases RANKL activation. The soluble receptor for AGE (sRAGE) down-regulates RANKL activation.6

Current Insights On Pathways For Charcot Neuroarthropathy

Researchers have yet to determine the cellular process primarily responsible for Charcot neuroarthropathy but there are multiple pathways to consider.

   Receptor activator of nuclear factor-kB ligand induces the activation and differentiation of osteoclasts by binding to the osteoclasts’ RANK.7 Both RANK and RANKL are expressed constitutively. The RANKL overproduction is a characteristic of Charcot but it is not limited to Charcot. It also occurs in many bone diseases such as psoriatic arthritis, rheumatoid arthritis and osteoporosis.1

   In a study involving three patient groups, Mabilleau and colleagues compared monocyte formation into osteoclasts and osteoclastic activity in vitro with and without the addition of RANKL.8 The groups included patients with diabetic Charcot neuroarthropathy, healthy patients and patients with diabetes. Without the addition of RANKL, researchers noted a significant increase in osteoclast formation in the Charcot group in comparison with the healthy and control groups. There was also increased osteoclastic activity in the Charcot group in comparison with the others.

   With the presence of RANKL, the study authors noted an increase in osteoclastic activity in all three of the groups.8 However, osteoclastic activity was considerably more aggressive in the Charcot neuroarthropathy group and was four times greater than the osteoclastic activity in the healthy group. Osteoclasts in patients with Charcot neuroarthropathy differentiate to become highly active.5

   The formation of AGEs is a common consequence of aging. Increased AGE production occurs in patients with prolonged elevated blood glucose levels, frequently termed hyperglycemia. Advanced glycation end products modify N-carboxymethyl lysine of type I collagen (CML collagen).9 The post-translational modification of the CML collagen occurs by non-enzymatic glycosylation, termed glycation. This primarily occurs in tissues with a slow turnover rate, exposing collagen proteins to the extracellular environment where non-enzymatic glycosylation takes place.5

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