A Closer Look At Beaming The Columns In The Charcot Diabetic Foot
- Volume 27 - Issue 3 - March 2014
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Advanced glycation end products crosslink within and around collagen fibers, and compromise their functionality.10 Type 1 collagen’s main function is to resist tension and accounts for the for rigidity in bone. Its primary locations are skin, tendon, bone and dentin.6 Collagen crosslinking within bone is known to affect bone stiffness and Young’s modulus independent of the bones’ mineralization and microarchitecture. This leads to weakening of bone strength without evidence of demineralization.11
Advanced glycation end product accumulation recruits the increased formation of the pattern recognition receptor for AGE, known as RAGE, which expresses constitutively and causes increased downstream activation of RANKL when bound. According to Macaione and colleagues, increased RANKL activation causes osteoclastogenesis.12 The soluble receptor (sRAGE) competes with RAGE to bind RANKL. The sRAGE also inhibits RAGE by binding to RAGE.13
Witzke and colleagues assessed the loss of RAGE defense as a cause of Charcot neuroarthropathy by focusing on three groups of patients.6 The three groups included healthy control patients, patients with type 2 diabetes and patients with diabetic Charcot neuroarthropathy. Researchers recorded circulating levels of sRAGE and bone stiffness for each group. The study authors noted an 86 percent decrease in sRAGE values for patients with Charcot neuroarthropathy in comparison to the healthy control population. Bone stiffness was markedly reduced in the Charcot group. The study authors concluded that RAGE did in fact increase RANKL activation and RANKL is responsible for increased osteoclastic activity. Additionally, a reduction in bone stiffness with a concomitant increase in bone density may suggest a pathologic proliferation of cross-linked collagen.
Another potentially deleterious effect of reduction in circulating sRAGE is AGE-induced osteoblast apoptosis, which has been implicated in alterations to bone repair in the face of elevated osteocalcin.13 This may explain why Charcot fusion sites remain weak even after consolidation.
For the foot and ankle surgeon, the most important part of these biochemical studies is the finding that bone stiffness was markedly reduced in patients with Charcot neuroarthropathy.6 These findings correlate directly with studies that demonstrate decreased Young’s modulus of elasticity and tensile strength in the Achilles tendon in patients with Charcot neuroarthropathy.14
Carboxymethyl lysine of type I collagen is a major constituent of bone, tendon and the ligaments that holds bones together. There is a combination of biochemical evidence and laboratory testing evidence that shows that AGE radically alters bone and tendon.14 The best clinical treatment solution for this process would be a reversal of AGEs or a replacement of sRAGE, but these options are not feasible at this time.
Why Beaming May Be Effective In Charcot
The alternative for surgeons is to design methods of reconstruction that deal directly with the decrease in tissue strength. This demands an approach different from traditional fixation with plates and/or screws that count on a normal healthy arthrodesis to be the arbiter of load bearing. In fact with Charcot neuroarthropathy, even if arthrodesis occurs, there is compelling evidence to believe that the healed bones are abnormal and at risk of re-fracture.15
The concept of beaming is such a solution. In the field of engineering, beams accept loads of tension and compression. These are exactly the same types of loads that the foot experiences during weightbearing and propulsion. In the case of Charcot neuroarthropathy, beaming provides the appropriate load sharing for pathologic bone and ligament.15