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Neuropathic osteoarthropathy is characterised by relatively painless swelling together with extensive damage in bones and joints, predominantly in the feet and ankles. The uncontrolled natural course of the condition leads to gross foot deformity, skin pressure ulceration, spreading infections, and sometimes amputation. Jean-Martin Charcot in 1883 described "Charcot foot" named after him in patients with tabes dorsalis insensitivity. Charcot believed that intrinsic bone weakness was the underlying condition, and was caused by neurogenic deficiencies in bone nutrition. His followers believed such dystrophy to be mediated by sympathetic denervation of the bone vasculature (neurotrophic, or neurovascular theory). Attempts to prove this theory were futile. A neurogenic circulatory disorder potentially relevant to bone nutrition could not be identified. Nowadays, Charcot foot is mostly seen in diabetic neuropathy, which has replaced syphilis as a frequent cause of peripheral nerve dysfunction. Recent studies in the diabetic Charcot foot and bone turnover indicate that the neurotrophic theory is a myth. The assumption of bone resorption due to sympathetic denervation proved to be false - sympathetic activity increases osteoclastic activity and thereby bone loss (sympathomimetic bone resorption). Except for the transient, inflammatory stage of the diabetic Charcot foot, there is no evidence of relevant osteoporosis or demineralisation of the foot skeleton in diabetes.
In order to treat Charcot neuroarthropathy effectively, one must have a strong understanding of the etiology and potential contributing factors to the disease process. Accordingly, this author offers a thorough review of the literature in an attempt to find answers and a more defined standard of care.
The purpose of the study was to investigate the relationship between the intensity of unrestrained weight bearing after a non-fracture injury (e.g. sprain), and the development of osteoarthropathic deformities of the foot (Charcot foot) in patients with diabetic neuropathy.
METHODS: 34 diabetic patients (14 Type 1, 20 Type 2) with foot bone injuries were studied in retrospect. At onset of injury symptoms (e.g. foot swelling), 32 of 34 feet displayed unremarkable X-ray, but pathologic MR imaging (e.g. bone marrow edema along the Lisfranc and/or the Chopart joint). Cumulative load forces after the onset of symptoms until treatment by total contact cast (TCC) were estimated using the product of body weight and number of weeks of ambulation (kgxweek) as a surrogate. Feet were classified in 3 groups according to the degree of foot deformities found at the start of treatment with TCC: Feet without deformities (group A, n=16), feet with minor deformities (partially reduced plantar arch (group B, n=6) and feet with major deformities (collapsed plantar arch, group C, n=12)
RESULTS: Feet in group A had been exposed to 262 (95% CI 135-390) kgxweek, compared to 974 (95% CI 342-1606) in group B, and to 2348 (95% CI 1265-3430) kgxweek in group C (p<0.05 between groups), indicative of a dose-response relationship between weight-bearing and progressive foot deformities. Destruction along the Lisfranc joint was observed in 2/16 feet in group A, versus 18/18 feet in group B and C combined (p<0.001). In group A, the undeformed feet were healed without major deformities (except for 2 non-compliant patients), whereas in group B and C feet remained as deformed as they were at TCC application.
CONCLUSION: Unrestrained weight-bearing of injured foot bones and joints of more than 400 kgxweek (equivalent to 8 weeks of normal walking by a person of 50 kg body weight) prompts Charcot deformities, with disintegration of the Lisfranc joint. Early off-loading by TCC treatment allows healing without deformities.
Re: Charcot's: farewell to the neurotrophic theory.
Microvascular and C-Fiber Function in Diabetic Charcot Neuroarthropathy and Diabetic Peripheral Neuropathy
Neil Baker, Alistair Green, Singhan Krishnan, Gerry Rayman Diabetes Care 30:3077-3079, 2007
Quote:
OBJECTIVE—Sympathetic denervation and hyperemia are implicated in the pathogenesis of Charcot neuroarthropathy (CN) but are also features of diabetic peripheral neuropathy (DPN). Differences in these physiological parameters were sought by determining C-fiber function (laser Doppler imager [LDI]flare technique) and maximum microvascular hyperemia (MMH) in 13 subjects with diabetic CN (DCN), 10 subjects with DPN, and 10 healthy control subjects. Additionally, unaffected limbs of the nine DCN subjects with unilateral CN (UCN) were studied to determine whether any observed differences precede CN.
RESULTS—LDIflare area was reduced in DPN (mean ± SD 1.41 ± 0.51 cm2) and DCN (1.42 ± 0.37) groups compared with the healthy control group (5.24 ± 1.33; P < 0.0001). MMH was higher in DCN (432 ± 88 PU [perfusion units]) than in DPN (262 ± 71; P = 0.001) subjects but lower than in the control group (564 ± 112; P < 0.01). LDIflare area and MMH were similar in the UCN and DCN groups.
CONCLUSIONS—C-fiber function is equally impaired in neuropathic patients with and without CN; however, a higher MMH distinguishes those with CN. Unaffected and affected limbs of those with unilateral CN have the same neurovascular abnormalities, suggesting that these abnormalities precede CN and are not a result of CN.
The classical neurotraumatic and neurotrophic theories for the pathogenesis of the acute Charcot neuro-osteoarthropathy (CN) in diabetes, do not address certain key features of the disease. These features include the facts that the condition usually affects just one side, that it is self-limiting, and that it is also very uncommon. Similarly, it is not known to what extent the condition may depend, as suggested by Jean-Martin Charcot, on pre-morbid osteopenia. Recent advances in understanding the mechanisms underlying the pathogenesis of osteopenia and osteoporosis and the central role of the RANKL/OPG signalling system have, however, suggested the possible involvement of other factors in the evolution of the disease. Specifically, it has been suggested that acute CN may be triggered in a susceptible individual by any event that leads to localized inflammation in the affected foot. This local inflammation leads to a vicious cycle in which there is increasing inflammation, increasing expression of RANKL, and increasing bone breakdown. The likely central role for the RANKL/OPG pathway suggests new possibilities for future treatments.
Re: Charcot's: farewell to the neurotrophic theory.
Inflammatory Osteolysis in Diabetic Neuropathic (Charcot) Arthropathies of the Foot.
Sinacore DR, Hastings MK, Bohnert KL, Fielder FA, Villareal DT, Blair VP 3rd, Johnson JE. Phys Ther. 2008 Sep 18. [Epub ahead of print]
Quote:
Objective Osteolysis and low bone mineral density (BMD) are underappreciated consequences of several chronic diseases that may elevate the risk for fracture. The purpose of this study was to assess tarsal BMD associated with acute inflammation (ie, inflammatory osteolysis) in individuals with chronic diabetes mellitus (DM), peripheral neuropathy (PN), and recent-onset neuropathic (Charcot) arthropathy (NCA) of the foot.
Research Design and METHODS: This was a case-control study of 32 people (11 men, 21 women) with DM, PN, and NCA of the foot or ankle. The subjects with DM, PN, and NCA were compared with 64 age-, sex-, and race-matched control subjects (24 men, 40 women) without DM, PN or NCA. Within the first 3 weeks of cast immobilization, BMD was estimated in both calcanei using quantitative ultrasonometry. Acute inflammation was confirmed by comparing skin temperature differences between the feet of the subjects with DM, PN, and NCA and the feet of the control subjects.
RESULTS: Skin temperature differences averaged 6.7 degrees F (SD=4.0 degrees F) (involved foot minus noninvolved foot) in the feet of the subjects with DM, PN, and NCA compared with 0.0 degrees F (SD=1.3 degrees F) in the feet of the control subjects. Calcaneal BMD averaged 384 mg/cm(2) (SD=110) in the involved feet and 467 mg/cm(2) (SD=123) in the noninvolved feet of the subjects with DM, PN, and NCA and 545 mg/cm(2) (SD=121) in combined right and left feet of the control subjects.
CONCLUSIONS: Inflammation in individuals with DM, PN, and NCA may contribute to or exacerbate a rapid loss of BMD. Inflammatory osteolysis may be a prominent factor responsible for both the spontaneous onset of neuropathic fracture and the insidious and progressive foot deformity that is the hallmark of the chronic Charcot foot.
Charcot's: farewell to the neurotrophic theory.
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