Emerging Concepts In The Etiology Of Charcot Joints

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Author(s): 
John D. Miller, BS, Jonathan Shih, BS, Michelle Zhubrak, DPM, Nicholas A. Giovinco, DPM, and David G. Armstrong DPM, MD, PhD

With new developments in the research on Charcot neuroarthropathy, these authors examine emerging research findings on osteoclastic activity, the RAGE pathway and cytokine recruitment, and share insights on current imaging tools and treatment modalities.

While the treatment modalities and physiological understanding of Charcot neuroarthropathy may be much different today than in 1827, the presentation has remained relatively the same.1 Classically, Charcot neuroarthropathy presents as a unilateral redness and swelling of a lower extremity. Typically, this increase in warmth precipitates bony changes visible on X-rays and bone scans.

   Due to coexisting peripheral neuropathy, only around 30 percent of patients will notice pain or discomfort prior to these changes.2 In our experience, acute trauma is often a common trigger for a Charcot “flare-up.” However, researchers report this in only 22 to 53 percent of patients.3 Currently, Charcot neuroarthropathy is one of the most devastating conditions secondary to diabetes, affecting up to 13 percent of high-risk patients with diabetes mellitus.4

   Modern treatment modalities for Charcot foot center on immobilization and offloading either by total contact casts or removable controlled ankle motion (CAM) boot walkers.5 These attempts at preventing further deformity minimize the chance of ulceration leading to amputation. Surgical debridement and episodic reconstructions are also common, despite their high cost and unlikeliness to resolve the causative underlying physiologic mechanisms. These limitations typically keep these treatments from being functionally first-line treatment efforts.

   We commonly prescribe adjunctive therapies such as biguanides and bisphosphonates in the acute Charcot osteoarthropathy although current evidence is inconclusive.6,7 Larger clinical trials are still needed to establish the efficacy of pharmaceutical intervention.

Where The Previous Theories On Charcot Etiology Fall Short

Understanding the biomechanical alterations present in Charcot neuroarthropathy is important for understanding its development. Commonly, neuropathic loss of sensation conjoins with metabolic compromise. This tandem sequelae leads to the musculoskeletal breakdown of pedal architecture. Often, this leads to subluxation of the forefoot and rearfoot at one of many possible locations. The distortion of muscular balance and functional vectors of tendon leverage further exacerbate this progression.

   There have been two main competing theories behind the etiology of Charcot development. Classically, the neurovascular theory holds that vascular damage to the autonomic nervous system causes a reflex hyperemia and an increase in blood flow to the limbs via arteriovenous shunts.7 The second theory holds that mechanical microtrauma initiates an inflammatory cascade that self-perpetuates into gross bony breakdown.7 However, it is more likely that both of these theories function together as autonomic dysfunction inhibits the perception of repetitive stress amid the accumulation of circulating inflammatory cytokines.

   However, neither theory explains why Charcot episodes typically develop unilaterally and occur in only a small percentage of patients with diabetic neuropathy. Also, Charcot can develop secondary to vascular disease, skirting many of the aforementioned pathways.8 Foot and ankle specialists often relate the incidence of inflammation (itself a possible initiator of Charcot episodes) with gross bony changes. At times, this may appear secondary to infection and can be misleading to unfamiliar diagnosticians, such as clinicians at urgent care facilities.

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