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The Thomson Newsroom have released this from the Diabetic Foot:
Ten years of Charcot: what have we learned?
By: Edmonds, Mike, Petrova, Nina
Quote:
Over the last decade, advances have been made in the understanding and management of Charcot osteoarthopathy with new observations on pathogenesis, presentation, diagnosis and treatment.
Pathogenesis
The receptor activator of nuclear factor KB ligand (RANKL) has been identified as an essential cytokine for the formation and activation of osteoclasts and may play a role in the pathogenesis of Charcot osteoarthropathy (Jeffcoate, 2004). RANKL activates the receptor RANK which is expressed on osteoclasts, thus promoting osteoclastogenesis. RANKL is expressed on bone-forming osteoblasts and thus bone resorption and bone formation are coupled through RANKL. The effects of RANKL are physiologically counterbalanced by the glycoprotein osteoprotegerin (OPG), which acts as a decoy receptor for RANKL. The balance between RANKL and OPG determines osteoclast functions. Alterations of the RANKL:OPG ratio are critical in the pathogenesis of bone diseases that result from increased bone resorption and thus may be important in the pathogenesis of Charcot osteoarthropathy.
Furthermore, in Charcot osteoarthropathy there is an excessive inflammatory response to minor trauma in which pro-inflammatory cytokines may play a role (Jeffcoate et al, 2005). A recent immunohistochemical analysis of surgical specimens from patients with Charcot osteoarthropathy has shown excessive osteoclastic activity in the environment of cytokine mediators of bone resorption (IL-1, IL-6 and TNFa; Baumhauer, 2006). Although the local inflammatory response may be excessive, systemic features are often limited. A recent study has shown that C-reactive protein was within the normal range in almost 50% of individuals presenting with acute Charcot osteoarthropathy and only moderately elevated in the remainder (Petrova et al, 2007).
Predisposition
Previous studies have suggested that reduced bone mineral density (BMD) in people with diabetes predisposes them to fracture, which in turn can lead to Charcot osteoarthropathy (Young et al, 1995). Recently, reduced stiffness has been demonstrated in the calcaneum in the Charcot and non-Charcot foot compared with controls (Jirkovska et al, 2001). However, at the onset of Charcot osteoarthropathy, there is pre-existing osteopenia in type 1 diabetes but not in type 2 diabetes (Petrova et al, 2005). One study has shown that people with diabetes and Charcot osteoarthropathy who presented with fractures had a lower BMD compared with people who presented with a dislocation pattern of osteoarthropathy (Herbst et al, 2004).....
i have a patient 57yo F with 4 month hx of diffuse dorsal midfoot pain. She thought her new brooks shoes were too aggressive. I recommended she get a more cushioning shoe (rigid painful foot on ROM testing). and sent her for xrays. She is obese but no history of diabetes etc.
Xrays came back today.... Right foot: weightbearing pes planus. Advanced midfoot degeneration with hypertrophic new bone formation particularly around intercuneiform joints. There is subarticular cyst formation and advanced joint space reduction at tarsometatarsal joints, especially 2 and 3.
Hallux MTP joint degeneration with subarticular cyst formation and mild HAV.
Left: Normal joint alignment. mod-severe mid foot joint degeneration although less than R. preserved medial longitudinal arch on wb. there is a degree of naviculocuneiform degeneration. Increased sclerosis with loss of joint space 2nd/3rd ray TMT joints. NO HAV but significant MTP joint degeneration.
This sounds and looks like charcot neuroarthropathy to me, but she doesnt have diabetes. Can you have Charcot without diabetes?
Yes you can. But I beleive there has to be some form of peripheral neuropathy present.
Is she alcohol dependant? Has she had bone density tests taken recently i.e. osteoporosis? How are her vascular and neurological tests? Was there anything there, particularly neurologically wise, which would be more indicative of the pt having a Charcot foot?
It is extremely important to have a high index of suspicion for Charcot neuro-osteoarthropathy (CN) and to encourage early presentation of the patient. This should be followed by a rapid diagnosis and early intervention, and with such a modern approach many CN can now be healed and deformity prevented. CN can be divided into two phases: acute active phase and chronic stable phase.The acute active phase includes those patients presenting early with normal X-ray and those presenting later with deformity and radiological changes of CN. The acute phase is characterized by unilateral erythema and oedema. The foot is at least 2 degrees C hotter than the contralateral foot.Patients should have initially an X-ray examination which, at this time, may be normal. We then proceed to two investigations: initially a technetium diphosphonate bone scan, which will detect early evidence of bone damage and also locate the site of this damage. If the result of the bone scan is positive, we would proceed to magnetic resonance imaging (MRI) examination, which would describe in more detail the nature of the bony damage.The aim of treatment is immobilization in a plaster cast until there is no longer evidence on X-ray of continuing bone destruction, and the foot temperature is within 2 degrees C of the contralateral foot. An alternative treatment is a prefabricated walking cast, such as the Aircast. A randomized controlled study of a single 90 mg pamidronate infusion has shown a significant reduction of the markers of bone turnover and skin temperature in treated, compared with control subjects although the fall in skin temperature was similar in both groups. There was a similar finding in a recent study with alendronate. Calcitonin has also been used in the acute stage and there was a more rapid transition to the stable chronic phase in the treated group compared with controls.In the chronic stable phase, the foot is no longer warm and red. There may still be oedema but the difference in skin temperature between the feet is usually less than 2 degrees C. The X-ray shows fracture healing, sclerosis and bone remodelling. The patient must now be rehabilitated and gradually moved from cast treatment to suitable footwear. The patient needs close observation to detect any relapse, which will be evident from further swelling and heat in the foot. Careful rehabilitation is always necessary after a long period in a cast.
Magnetic resonance imaging in early stage charcot arthropathy - correlation of imaging findings and clinical symptoms.
Schlossbauer T, Mioc T, Sommerey S, Kessler SB, Reiser MF, Pfeifer KJ. Eur J Med Res. 2008 Sep 22;13(9):409-14
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Objective: To report on qualitative and quantitative MRI findings in early stage of diabetic osteoarthropathy (CA) and correlation with clinical symptoms. -
Materials and Methods: Clinical data of 13 patients (mean age = 61.2 years) with Charcot arthropathy (CA, Eichenholtz 0) were compared with findings in native and contrast-enhanced MRI. 12 patients had diabetes mellitus (7 type 2, 5 type 1), one had idiopathic polyneuropathy. Evaluation was performed at acute stage of CA and at a 4 months follow-up. After baseline assessment, patients were treated with pressure-relieving means. Mean values of signal-intensity in short T1 inversion recovery (STIR) images of bones of the foot and ankle and corresponding contrast-enhancement were evaluated. Additional MRI-findings (soft tissue edema, varicosis, tenovaginitis, joint effusion) were analyzed. A correlation with symptoms (reddening, swelling, hyperthermia, pain) was performed. -
Results: Bone marrow edema in affected bones significantly decreased (p<0.001). Soft tissue edema and pain showed a significant correlation with intensity of bone marrow edema (p<0.05). The presence of bone marrow edema in the STIR sequence was strongly associated with a corresponding contrast enhancement (p<0.0001, kappa-coefficients 0.976 at baseline and 0.953 at follow-up). -
Conclusion: MRI in early stage of CA provides valuable diagnostic information on the activity of the disease. A significant correlation of intensity of bone marrow edema in MRI and some clinical parameters (soft tissue edema and pain) was found. Paramagnetic contrast-agent did not provide additional information. This is the first report on quantitative assessment of signal alterations in stage 0 CA before and after treatment.
Purpose
To examine the association of obesity, peripheral neuropathy, and other risk factors with the Charcot arthropathy incidence rate in a large diabetic population.
Methods
The Department of Veterans Affairs inpatient and outpatient administrative datasets were used to identify persons with diabetes in 2003. Logistic regressions were used to model the likelihood of a person developing Charcot arthropathy as a function of individual characteristics, obesity, peripheral neuropathy, diabetic control, and comorbidities.
Results
Of Veterans Affairs users with diabetes, 652 (0.12%) were newly diagnosed with Charcot arthropathy in 2003. Compared with persons without obesity or peripheral neuropathy, those with obesity alone were approximately 59% more likely, those with neuropathy alone were 14 times more likely, and those with both obesity and neuropathy were 21 times more likely to develop Charcot arthropathy. Ages 55 to 64 years, diabetes duration 6 years or more, hemoglobin-A1c 7% or more, renal failure, arthritis, and deficiency anemia also were associated with an increased incidence of Charcot arthropathy.
Conclusion
Obesity is significantly associated with an increased incidence of Charcot arthropathy independently of other risk factors. When obesity is combined with neuropathy, the Charcot arthropathy incidence rate increases multiplicatively. Prevention and detection of Charcot arthropathy should take the interaction between obesity and neuropathy into consideration
Marked loss of sympathetic nerve fibers in chronic Charcot foot of diabetic origin compared to ankle joint osteoarthritis.
Koeck FX, Bobrik V, Fassold A, Grifka J, Kessler S, Straub RH. J Orthop Res. 2008 Nov 21. [Epub ahead of print]
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The pathogenesis of Charcot foot is based on three disputed factors: (1) loss of neurotrophic influence, (2) microtraumatic lesions, and (3) neurovascular disturbances. These etiological causes were uncovered by clinicophysiological tests. However, no results of quantitative nerve density studies of sympathetic and sensory substance P-positive (SP+) nerve fibers are available. We studied the density of sympathetic and SP+ nerve fibers in three distinct areas of the tarsus. Fifteen patients with ankle osteoarthritis (OA) and 15 patients with diabetic Charcot foot were included. Patients with OA did not differ from those with Charcot foot in SP+ sensory nerve fiber density. However, at all three areas, the density of sympathetic nerve fibers was significantly lower in patients with Charcot foot compared to OA (p = 0.006). In addition, we found that the sympathetic nerve repellent factor semaphorin 3C was highly expressed in inflamed tissue in Charcot patients. In Charcot foot of diabetic origin a severe loss of sympathetic nerve fibers was observed. These findings in chronically inflamed Charcot foot lend support to the neurovascular theory in the late chronic phase, which probably depends on the inflammatory upregulation of nerve repellent factors.
Charcot neuroarthropathy triggered by osteomyelitis and/or surgery.
Ndip A, Jude EB, Whitehouse R, Prescott M, Boulton AJ. Diabet Med. 2008 Dec;25(12):1469-72.
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Introduction: Charcot neuroarthropathy (CN) is a rare but devastating complication of diabetic neuropathy. Osteomyelitis is also a complication of the diabetic foot and it may be difficult to differentiate from CN.
Patients and methods: A patient with Type 1 diabetes and peripheral neuropathy developed a foot ulcer complicated by osteomyelitis of the first proximal phalanx. He was successfully treated with antibiotics and surgical excision of the infected bone. Six months later, he developed a hot, swollen, red foot and X-ray showed destruction of the second and third metatarsal heads. At the second presentation, it was difficult to determine whether this was a recurrence of osteomyelitis or a new onset of CN. Thus, to obtain a definitive diagnosis, recourse was made to more sophisticated imaging techniques.
Results: (99m)Tc methylenediphosphonate (MDP) bone scans and magnetic resonance imaging proved inconclusive to differentiate between osteomyelitis and CN. Subsequently, an indium-labelled white cell scan confirmed the absence of osteomyelitis and the patient was successfully treated for CN.
Discussion: Infection and/or surgery may be predisposing factors in the development of diabetic CN but the combination of the two could accelerate the onset of the Charcot process in people with diabetes and neuropathy.
Charcot arthropathy risk elevation in the obese diabetic population.
Stuck RM, Sohn MW, Budiman-Mak E, Lee TA, Weiss KB. Am J Med. 2008 Nov;121(11):1008-14.
Quote:
PURPOSE: To examine the association of obesity, peripheral neuropathy, and other risk factors with the Charcot arthropathy incidence rate in a large diabetic population.
METHODS: The Department of Veterans Affairs inpatient and outpatient administrative datasets were used to identify persons with diabetes in 2003. Logistic regressions were used to model the likelihood of a person developing Charcot arthropathy as a function of individual characteristics, obesity, peripheral neuropathy, diabetic control, and comorbidities.
RESULTS: Of Veterans Affairs users with diabetes, 652 (0.12%) were newly diagnosed with Charcot arthropathy in 2003. Compared with persons without obesity or peripheral neuropathy, those with obesity alone were approximately 59% more likely, those with neuropathy alone were 14 times more likely, and those with both obesity and neuropathy were 21 times more likely to develop Charcot arthropathy. Ages 55 to 64 years, diabetes duration 6 years or more, hemoglobin-A1c 7% or more, renal failure, arthritis, and deficiency anemia also were associated with an increased incidence of Charcot arthropathy.
CONCLUSION: Obesity is significantly associated with an increased incidence of Charcot arthropathy independently of other risk factors. When obesity is combined with neuropathy, the Charcot arthropathy incidence rate increases multiplicatively. Prevention and detection of Charcot arthropathy should take the interaction between obesity and neuropathy into consideration.
Use of platelet-rich concentrate and bone marrow aspirate in high-risk patients with charcot arthropathy of the foot.
Pinzur MS. Foot Ankle Int. 2009 Feb;30(2):124-7.
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BACKGROUND: Diabetic patients with Charcot arthropathy of the foot are at high risk for nonunion when undergoing arthrodesis. There is increasing evidence that cytokines identified in platelet rich concentrate and bone marrow aspirate may show equivalence to autologous bone graft in supporting arthrodesis.
MATERIALS AND METHODS: Prospectively, 44 high-risk diabetic patients with Charcot foot arthropathy underwent surgical correction of 46 feet through a limited surgical approach. The average age of the patients was 54.9 +/- 10.4 years. Their mean BMI was 38.0 +/- 9.7. Twenty-four were male and 20 were female. Twenty-eight had open wounds with chronic draining osteomyelitis. Surgical correction was maintained postoperatively with static circular ring fixation. At the time of wound closure, all of the patients had injection of autologous platelet rich concentrate and bone marrow aspirate.
RESULTS: Forty-two of the 46 feet had radiographic evidence of bony union at 26.2 +/- 12.2 months following surgery. One patient died of unrelated causes. Two underwent amputation for persistent infection. Six had recurrent ulcers which resolved with local treatment. One patient required a fifth ray resection for gangrene following surgery. There were three tibial stress fractures, with two requiring intramedullary nailing to achieve union.
CONCLUSIONS: Platelet-rich concentrate, when combined with a small amount of autologous bone marrow aspirate, may well be as effective as autologous bone grafting when performing arthrodesis of high risk diabetic patients with Charcot foot arthropathy
Objective: To compare risks of lower-extremity amputation between patients with Charcot arthropathy and those with diabetic foot ulcers.
Research Design and Methods: A retrospective cohort of patients with incident Charcot arthropathy or diabetic foot ulcers in 2003 was followed for five years for any major and minor amputations in the lower extremities.
Results: After a mean follow-up of 37+/-20 and 43+/-18 months, the Charcot and ulcer groups had 4.1 and 4.7 amputations per 100 person-years, respectively. Among patients < 65 years old at the end of follow-up, amputation risk relative to patients with Charcot alone was seven times higher for patients with ulcer alone and twelve times higher for patients with Charcot and ulcer.
Conclusions: Charcot arthropathy by itself does not pose a serious amputation risk, but ulcer complication multiplicatively increased the risk. Early surgical intervention for Charcot patients in the absence of deformity or ulceration may not be advisable.
Pro-inflammatory modulation of the surface and cytokine phenotype of monocytes in patients with acute Charcot foot.
Uccioli L, Sinistro A, Almerighi C, Ciaprini C, Cavazza A, Giurato L, Ruotolo V, Spasaro F, Vainieri E, Rocchi G, Bergamini A. Diabetes Care. 2009 Oct 30. [Epub ahead of print]
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Objective: Despite increased information on the importance of an inappropriate inflammatory response in the acute Charcot process, there has been no previous attempt to define the specific pathways that mediate its pathogenesis. Here, the role played by monocytes was analyzed.
Research design and methods The immune phenotype of peripheral monocytes was studied by FACS analysis comparing patients with acute Charcot (n=10), in both the active and recovered phase, diabetic patients with neuropathy, with or without osteomyelitis and normal controls.
Results As compared to diabetic controls and healthy subjects, monocytes from acute Charcot patients showed a proinflammatory immune phenotype characterized by increased production of proinflammatory cytokines, reduced secretion of antiinflammatory cytokines, increased expression of surface costimulatory molecules, and increased resistance to serum withdrawal-induced apoptosis. In addition, the pattern of circulating cytokines confirmed activation of proinflammatory cytokines. No modulation of the monocyte phenotype was documented in diabetic controls and healthy subjects, thus indicating that the proinflammatory alterations of monocytes are specific and causative of acute Charcot.
Conclusions Together, these data provide evidence for the role of proinflammatory changes in the immune phenotype of monocytes in the pathogenesis of acute Charcot. These alterations may explain the abnormally intense and prolonged inflammatory response that characterizes this disorder and may represent a potential therapeutic target for specific pharmacological interventions.
The Role of Quantitative Bone Scanning in the Assessment of Bone Turnover in Patients with Charcot Foot.
Bem R, Jirkovská A, Dubsky M, Fejfarová V, Buncová M, Skibová J, Jude EB. Diabetes Care. 2009 Nov 23. [Epub ahead of print]
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Objective: To assess the new quantitative bone scan parameters as markers of Charcot neuroosteoarthropathy (CNO) activity.
Reasearch Design And Methods: Forty-two patients with acute (n=21) and non-acute (n=21) CNO underwent quantitative bone scanning. Patients with acute CNO were followed for 3-12 months and bone scans were repeated after treatment. New quantitative parameters were assessed and compared with markers of bone turnover and with skin temperature difference (STD).
Results: Significant correlations between quantitative bone scan parameters and bone turnover markers were observed (all p<0.05). These parameters decreased after treatment of CNO and its reduction to the baseline value correlated with differences of bone turnover markers and STD (all p<0.05).
Conclusions: Our study suggests that bone scanning can be used not only for diagnosis of CNO, but also for monitoring disease activity by quantitative bone scan parameters.
Bone mineral density in diabetes mellitus patients with and without a Charcot foot.
Christensen TM, Bülow J, Simonsen L, Holstein PE, Svendsen OL. Clin Physiol Funct Imaging. 2010 Jan 18.
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Summary Objective: To measure bone mineral density in patients with diabetes mellitus and the complication Charcot osteoarthropathy (CA). Research design and methods: A total of 49 patients with diabetes were investigated. The population consisted of patients with an acute CA (n = 17) or chronic CA (n = 7). Control groups consisted of diabetes patients with (n = 9) and without neuropathy (n = 11) and who had an amputation of the first toe (n = 5). Values measured were bone mineral density (BMD) in lumbar spine, hip and calcaneus, using lunar DEXA scanner. The bone turnover markers CTX-1 and N-MID were measured. Results: There were no differences in BMD measured in the spine and hip. There was an increase in the markers of bone turnover in the patients with acute CA. The BMD of the calcaneus was statistically lower in the affected foot in patients with chronic Charcot (P < 0.01), than in the unaffected foot, but there were no statistically significant differences between the BMD of the calcaneus in the feet in the other groups. Conclusions: From this study, we can conclude that there were no differences in BMD values in the spine and hip between groups. There were no differences between BMD of the calcaneus between groups, except that patients with chronic Charcot had a significantly lower calcaneal BMD in the affected foot than in the healthy foot. Furthermore, there was an increased bone turnover in the group with acute CA, which was not found in the other patients groups. This suggests that the Charcot foot is a rather local phenomenon, with little effect on the skeleton in general.
Role of Quantitative Bone Scanning in the Assessment of Bone Turnover in Patients With Charcot Foot
Robert Bem, Alexandra Jirkovská, Michal Dubský, Vladimira Fejfarová, Marie Buncová, Jelena Skibová, and Edward B. Jude Diabetes Care February 2010 vol. 33 no. 2 348-349
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OBJECTIVE To assess the new quantitative bone scan parameters as markers of Charcot neuroosteoarthropathy (CNO) activity.
RESEARCH DESIGN AND METHODS Forty-two patients with acute (n = 21) and nonacute (n = 21) CNO underwent quantitative bone scanning. Patients with acute CNO were followed for 3–12 months and bone scans were repeated after treatment. New quantitative parameters were assessed and compared with markers of bone turnover and with skin temperature difference (STD).
RESULTS Significant correlations between quantitative bone scan parameters and bone turnover markers were observed (all P < 0.05). These parameters decreased after treatment of CNO, and its reduction to the baseline value correlated with differences of bone turnover markers and STD (all P < 0.05).
CONCLUSIONS Our study suggests that bone scanning can be used not only for diagnosis of CNO but also for monitoring disease activity by quantitative bone scan parameters.
Ten years of Charcot: what have we learned?
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