Application of Burow's solution for cement foreign body in the external auditory canal.

INTRODUCTION: Only two reports in English literature have described cement foreign bodies in the external auditory canal. CASE SUMMARY: We present the case of a 37 year-old man with cement foreign body in the right external auditory canal. Removal of the foreign body was difficult because of severe adhesion to the external auditory canal and tympanic membrane. We therefore used acidic Burow's solution to dissolve the alkaline cement deposition. Application of Burow's solution immediately caused the deposition to take on a paste-like consistency that was easily removed. DISCUSSION: Burow's solution seems useful for removing cement foreign bodies in the external auditory canal.

Cochlear implantation is a therapeutic option for superficial siderosis patients with sensorineural hearing loss.

BACKGROUND: Superficial siderosis is a rare disease that results from chronic bleeding in the subarachnoid space. Haemosiderin deposits throughout the subpial layers of the brain and spinal cord lead to progressive sensorineural hearing loss, which is seen in 95 per cent of patients with superficial siderosis. The impact of cochlear implantation on the quality of life of superficial siderosis patients is under debate. CASE REPORT: A 38-year-old male with superficial siderosis presented with bilateral progressive sensorineural hearing loss. The patient underwent cochlear implantation and his quality of life was improved as evaluated by the Abbreviated Profile of Hearing Aid Benefit inventory. CONCLUSION: The remarkable improvement in Abbreviated Profile of Hearing Aid Benefit scores shown in this study indicates that cochlear implantation leads to a better quality of life in superficial siderosis patients.

REPEATED INTRANODAL LYMPHANGIOGRAPHY FOR THE TREATMENT OF LYMPHATIC LEAKAGE.

Treatment of patients with chylous or non-chylous lymphatic leakage can be difficult. An approach using therapeutic lymphangiography can reduce the lymphatic leakage, but it seldom stops the leakage immediately and subsequent conservative treatment is necessary. We report three cases in which intranodal lymphangiography was performed multiple times to inhibit lymphatic leakage. In each case, the lymph node was punctured under ultrasound guidance using a 23-gauge needle and lipiodol was injected manually at a rate of 1 ml/3 min. The procedure was repeated twice in two cases of gastrointestinal carcinoma and four times in one case of lymphoma. In all three cases, the postoperative lymphatic leakage stopped after the repeated intranodal lymphangiography.

Role of macrophage migration inhibitory factor in age-related hearing loss.

Hearing loss related to aging is the most common sensory disorder among elderly individuals. Macrophage migration inhibitory factor (MIF) is a multi-functional molecule. The aim of this study was to identify the role of MIF in the inner ear. MIF-deficient mice (MIF(-/-) mice) of BALB/c background and wild-type BALB/c mice were used in this study. Expression of MIF protein in the inner ear was examined by immunohistochemistry in wild-type mice (WT). The hearing function was assessed by the click-evoked auditory brainstem response in both MIF(-/-) mice and WT at 1, 3, 6, 9, 12, and 18months of age. Morphological examination of the cochlea was also performed using scanning electron microscopy and light microscopy. MIF was observed in the spiral ligament, stria vascularis, Reissner's membrane, spiral ganglion cells (SGCs), saccular macula, and membranous labyrinth. The MIF(-/-) mice had a significant hearing loss as compared with the WT at 9, 12, and 18months of age. In the MIF(-/-) mice, scanning electron microscopy showed that the outer cochlear hair cells were affected, but that the inner cochlear hair cells were relatively well preserved. The number of SGCs was lower in the MIF(-/-) mice. MIF was strongly expressed in the mouse inner ear. Older MIF(-/-) mice showed accelerated age-related hearing loss and morphological inner ear abnormalities. These findings suggest that MIF plays an important role in the inner ear of mice.

Pulmonary function in patients with chronic rhinosinusitis and allergic rhinitis.

BACKGROUND: A close relationship between upper and lower respiratory tract diseases has been reported. However, little is known about pulmonary function in patients with upper respiratory tract diseases. METHODS: Pulmonary function was measured in: 68 patients with chronic rhinosinusitis without nasal polyps, 135 patients with chronic rhinosinusitis with nasal polyps, 89 patients with allergic rhinitis and 100 normal control subjects. The relationships between pulmonary function and clinical parameters were assessed. These parameters included radiographic severity of chronic rhinosinusitis, serum total immunoglobulin E levels, concentrations of cytokines in nasal secretions and exhaled nitric oxide levels. RESULTS: The pulmonary function of patients with chronic rhinosinusitis was significantly affected. The level of interleukin-5 in nasal secretions was significantly correlated with pulmonary function in patients with chronic rhinosinusitis. CONCLUSION: The findings indicated latent obstructive lung function changes in chronic rhinosinusitis patients. The cytokines in nasal secretions might be related to obstructive lung function changes in chronic rhinosinusitis.

CO2 microbubble contrast enhancement in x-ray angiography.

AIM: To demonstrate that carbon dioxide (CO2) microbubble contrast enhancement depicts blood vessels when used for x-ray examinations. MATERIALS AND METHODS: Microbubbles were generated by cavitation of physiological saline to which CO2 gas had been added using an ejector-type microbubble generator. The input pressure values for CO2 gas and physiological saline that produced a large quantity of CO2 microbubbles were obtained in a phantom. In an animal study, angiography was performed in three swine using three types of contrast: CO2 microbubbles, conventional CO2 gas, and iodinated contrast medium. For CO2 microbubble contrast enhancement, physiological saline, and CO2 gas were supplied at the input pressures calculated in the phantom experiment. Regions of interest were set in the abdominal aorta, external iliac arteries, and background. The difference in digital values between each artery and the background was calculated. RESULTS: The input pressures obtained in the phantom experiment were 0.16 MPa for physiological saline and 0.5 MPa for CO2 gas, with physiological saline input volume being 8.1 ml/s. Three interventional radiologists all evaluated the depictions of all arteries as "present" in the CO2 microbubble contrast enhancement, conventional CO2 contrast enhancement, and iodinated contrast enhancement performed in three swine. Digital values for all vessels with microbubble CO2 contrast enhancement were higher than background values. CONCLUSIONS: In x-ray angiography, blood vessels can be depicted by CO2 microbubble contrast enhancement, in which a large quantity of CO2 microbubbles is generated within blood vessels.

COX/PGE(2) axis critically regulates effects of LPS on eosinophilia-associated cytokine production in nasal polyps.

BACKGROUND: Lipopolysaccharide (LPS) has shown heterogeneous effects on eosinophilic inflammation in airways. However, little is known about how LPS regulates pathogenesis of chronic rhinosinusitis with nasal polyps, a major form of eosinophilic inflammation in the upper airway. OBJECTIVE: We sought to investigate the effect of LPS on cytokine production by dispersed nasal polyp cells (DNPCs). METHODS: Either diclofenac-treated or untreated DNPCs were cultured with or without staphylococcal enterotoxin B (SEB) in the presence or absence of LPS, after which the levels of IL-5, IL-13, IL-17A and IFN-γ within the supernatant were measured. The effects of PGE(2) on LPS-induced responses by diclofenac-treated DNPCs were also examined. LPS-induced PGE(2) production and mRNA expression of COX-1, COX-2 and microsomal PGE(2) synthase-1 (m-PGES-1) were measured. RESULTS: Staphylococcal enterotoxin B induced IL-5, IL-13, IL-17A and IFN-γ production by DNPCs. Pre-treatment with LPS prior to SEB stimulation inhibited production of these cytokines. After stimulation with LPS, PGE(2) production and expression of COX-2 and m-PGES-1 mRNA by DNPCs increased significantly. In the presence of diclofenac, the suppressive effects of LPS were eliminated. LPS pre-treatment enhanced SEB-induced IL-5, IL-13 and IL-17A production in diclofenac-treated DNPCs, while addition of PGE(2) inhibited IL-5, IL-13 and IFN-γ production. LPS alone induced IL-5, IL-13 and IFN- γ production by diclofenac-treated DNPCs, while the addition of EP2 and EP4 receptor-selective agonists, as well as PGE(2) itself, inhibited IL-5 and IL-13 production. CONCLUSIONS AND CLINICAL RELEVANCE: These results suggest that the regulatory effects of LPS on eosinophilic airway inflammation are controlled via the COX-2/PGE(2) axis. For clinical implications, indiscreet use of non-steroidal anti-inflammatory drugs should be avoided in patients with chronic rhinosinusitis with nasal polyps.

Transcatheter arterial embolisation for paediatric inflammatory pseudotumour of the maxillary sinus.

BACKGROUND: Inflammatory pseudotumours are mostly seen in the lung, and occasionally in the head and neck region including the sinonasal area. Reported treatment modalities comprise corticosteroid treatment, surgical excision and radiotherapy. The latter option is required because wide surgical resection may be difficult for head and neck lesions, especially in children. However, clinicians should be aware of the risk of late-onset side effects of radiotherapy in children. CASE REPORT: We present a two-year-old girl with a massive inflammatory pseudotumour of the maxillary sinus. Transcatheter arterial embolisation was performed, and the lesion was successfully managed without additional therapy. There was no evidence of recurrence over the next five years. CONCLUSION: This is the first report presenting the utility of arterial embolisation for inflammatory pseudotumour.

Lipopolysaccharide induces proinflammatory cytokines and chemokines in experimental otitis media through the prostaglandin D2 receptor (DP)-dependent pathway.

Otitis media is one of the most common and intractable ear diseases, and is the major cause of hearing loss, especially in children. Multiple factors affect the onset or development of otitis media. Prostaglandin D2 is the major prostanoid involved in infection and allergy. However, the role of prostaglandin D2 and prostaglandin D2 receptors on the pathogenesis of otitis media remains to be determined. Recent studies show that D prostanoid receptor (DP) and chemoattractant receptor-homologous molecule expressed on T helper type 2 (Th2) cells (CRTH2) are major prostaglandin D2 receptors. In this study, homozygous DP single gene-deficient (DP⁻(/)⁻) mice, CRTH2 single gene-deficient (CRTH2⁻(/)⁻) mice and DP/CRTH2 double gene-deficient (DP⁻(/)⁻ CRTH2⁻(/)⁻) mice were used to investigate the role of prostaglandin D2 and its receptors in otitis media. We demonstrate that prostaglandin D2 is induced by lipopolysaccharide (LPS), a major component of Gram-negative bacteria, and that transtympanic injection of prostaglandin D2 up-regulates macrophage inflammatory protein 2 (MIP-2), interleukin (IL)-1ß and IL-6 in the middle ear. We also show that middle ear inflammatory reactions, including infiltration of inflammatory cells and expression of MIP-2, IL-1ß and IL-6 induced by LPS, are reduced significantly in DP⁻(/)⁻ mice and DP⁻(/)⁻ CRTH2⁻(/)⁻ mice. CRTH2⁻(/)⁻ mice display inflammatory reactions similar to wild-type mice. These findings indicate that prostaglandin D2 may play significant roles in LPS-induced experimental otitis media via DP.

Role of fungal antigens in eosinophilia-associated cellular responses in nasal polyps: a comparison with enterotoxin.

BACKGROUND: Fungi and/or Staphylococcus aureus enterotoxins (SEs) may participate in the pathogenesis of eosinophilic inflammation in cases of chronic rhinosinusitis with nasal polyps (CRSwNP). Objective We sought to determine the effects of fungal antigens on eosinophilia-associated cellular responses in nasal polyps. METHODS: Dispersed nasal polyp cells (DNPCs) were prepared from 13 patients with CRSwNP. DNPCs were cultured with fungal extracts (Aspergillus, Alternaria and Candida) or SEB for 72 h, after which the levels of IL-5, IL-13 and RANTES were measured within the supernatant. Responses to ß-d-glucan, mannan and chitin were also examined. RESULTS: 38.5%, 69.2% and 30.8% of DNPCs produced IL-5, IL-13 and RANTES, respectively, in response to 200 µg/mL of Aspergillus. 53.8%, 53.8% and 7.7% of DNPCs produced IL-5, IL-13 and RANTES, respectively, in response to 200 µg/mL of Alternaria. 53.8%, 38.5% and 15.4% of DNPCs produced IL-5, IL-13 and RANTES, respectively, in response to 200 µg/mL of Candida. All DNPCs produced these cytokines in response to 0.1 µg/mL of SEB. SEB induced significantly greater cytokine levels than the fungal extracts. No correlation between cytokine production following exposure to each of the fungal extracts or SEB and various clinical features, including nasal polyp eosinophilia and radiological severity of sinusitis was observed. Neither sensitization to fungus nor comorbidity with bronchial asthma was correlated with the fungal extract-induced cytokine production by DNPCs. ß-d-glucan, mannan and chitin did not induce significant cytokine production. CONCLUSIONS: These results suggest that, although DNPCs produce IL-5, IL-13 and RANTES in response to fungal extracts, fungal antigens including major carbohydrates are less capable of inducing eosinophilia-associated cellular responses in nasal polyps than SEB.

Composite material stent comprising metallic wire and polylactic acid fibers, and its mechanical strength and retrievability.

BACKGROUND: Although metallic stents are characterized by strong expanse of force, thin walls, and easy stent deployment, their removal from the body is usually difficult or impossible due to the difficulty of unraveling their mesh structure. A stent built of a composite material comprising a metallic wire and a polylactic acid (PLA) fiber, in which the metallic wire component could be unraveled after PLA fiber degradation in the body, should allow easy stent removal. PURPOSE: To evaluate the mechanical strength and retrievability of a composite material stent comprising a metallic wire and a PLA fiber. MATERIAL AND METHODS: We produced a composite material stent comprising a metallic wire and a biodegradable fiber (hybrid stent). As the metallic wire is not cross-linked with itself, but with the PLA fibers only, the hybrid stent can be easily unraveled after PLA fiber degradation. This stent was built with a 0.2-mm stainless-steel wire and a 0.23-mm PLA fiber knitted in the same textile as an Ultraflex stent. For comparison, an identical stent was built using PLA fiber only (PLA stent). The mechanical strength of these stents was tested by the radial expansive force response against circumferential shrinkage stress load. Change in radial force due to PLA fiber degradation was estimated by adding an artificial PLA degeneration process, by immersing each stent in a water bath at 80 degrees C for 48 hours. Retrievability of the hybrid stent after PLA degeneration was examined by hooking and pulling out the residual stainless-steel wire from a silicon tube. RESULTS: The hybrid stent exhibited a linear response in radial expansive force within the range of 15% diameter reduction. The PLA stent did not exhibit linear response at over 15% diameter reduction. Decrease of radial expansive force after PLA degradation was within 5% of the original force in the hybrid stent, but the PLA stent did not create effective radial expansive force. Hybrid stents, even after PLA degradation, exhibited a linear response in radial expansive force, within the range of 15% diameter reduction. The metallic component of the heat-processed hybrid stent was easily unraveled by pulling out the wire. CONCLUSION: The hybrid stent comprising a stainless-steel wire and a PLA fiber appears to provide effective radial expansive force and retrievability.

Transcatheter coil embolization for steal syndrome in patients with hemodialysis access.

BACKGROUND: Drainage of large amounts of shunt blood into deep veins via collaterals reduces resistance to venous outflow and decreases blood flow to the artery distal to the arterial anastomotic site, potentially resulting in steal syndrome. PURPOSE: To evaluate the effectiveness of transcatheter coil embolization for collateral veins of hemodialysis access in the treatment of steal syndrome. MATERIALS AND METHODS: Five hemodialysis patients (four male, one female; mean age 58.8 years, range 40-71 years) with symptomatic steal syndrome were treated. Steal syndrome was diagnosed based on decreased or absent distal pulse, coolness, pain, abnormal skin color, ischemic ulceration of digits, numbness, sensory impairment, or motor impairment. Coil embolization was performed to block collaterals communicating with deep veins, with conscious sedation and local anesthesia. Fistulography was performed before, immediately after, and 1 month after embolization. Ultrasonography was performed 2 days after embolization. Symptoms and signs were assessed 2 days after embolization. Clinical findings related to steal syndrome and access failure were observed at each hemodialysis. RESULTS: Blood flow in the collaterals was successfully blocked by coil embolization in all patients. Distal pulse, coolness, pain, and skin color improved in all patients. Numbness, sensory impairment, and motor impairment were unimproved in two patients. In all patients, hemodialysis following embolization was performed normally. The mean observation period after embolization was 33 months (range 9-75 months). CONCLUSION: Coil embolization of collaterals that drain shunt blood into deep veins is effective for steal syndrome for hemodialysis access originating in the brachial artery.

Cerebral microembolisation during radiofrequency ablation of lung tumours: detection by carotid duplex ultrasound.

The aim of this study was to investigate the appearance of microbubbles during radiofrequency ablation (RFA) of lung tumours. Eight consecutive patients (mean age, 73.1 years; 3 men and 5 women; 10 malignant lesions; mean lesion size, 24.8 mm) who underwent RFA of lung tumours using internally cooled single electrodes were enrolled. During the RFA procedure, the right internal carotid artery was continuously monitored by duplex ultrasound. High-intensity transient signals (HITS) that occurred in the Doppler blood flow waveform were taken to indicate microbubbles. 21 RFA applications were performed for the 10 lesions. HITS were observed in 19 of 21 RFA applications; the mean frequency in a single application was 10+/-13.3. A statistical correlation was seen between the duration of energy deposition and the number of HITS, and between tumour size and the number of HITS. Microbubbles were detected in all patients in the late phase of the first session of RFA.

Allergen-specific immunotherapy alters the expression of B and T lymphocyte attenuator, a co-inhibitory molecule, in allergic rhinitis.

BACKGROUND: B7/CD28 family co-signalling molecules play a key role in regulating T cell activation and tolerance. Allergen-specific immunotherapy (SIT) alters allergen-specific T cell responses. However, the effect of SIT on the expression of various co-signalling molecules has not been clarified. OBJECTIVE: We sought to determine whether SIT might affect the expression of three co-inhibitory molecules, programmed death (PD)-1, B7-H1 and B and T lymphocyte attenuator (BTLA), in Japanese cedar pollinosis (JCP). METHODS: Peripheral blood mononuclear cells (PBMCs) were isolated from JCP patients who had or had not received SIT. PBMC were cultured in the presence or absence of Cry j 1, after which the cell surface expression of PD-1, B7-H1 and BTLA, as well as IL-5 production, were determined. In addition, the effect of BTLA cross-linking on IL-5 production was examined. RESULTS: After Cry j 1 stimulation, no significant differences in PD-1 and B7-H1 expression were observed between SIT-treated and SIT-untreated patients. BTLA expression was down-regulated in untreated patients after Cry j 1 stimulation and up-regulated in SIT-treated patients. Up-regulation of BTLA in SIT-treated patients was particularly apparent in a CD4(+) T cell subset. IL-5 production was clearly reduced among SIT-treated patients, and the observed changes in BTLA expression correlated negatively with IL-5 production. Moreover, immobilization of BTLA suppressed IL-5 production in JCP patients. CONCLUSION: These results suggest that both IL-5 production and down-regulation of BTLA in response to allergen are inhibited in SIT-treated patients with JCP. BTLA-mediated co-inhibition of IL-5 production may contribute to the regulation of allergen-specific T cell responses in patients receiving immunotherapy.

Expression of inflammatory mediators in the otitis media induced by Helicobacter pylori antigen in mice.

Helicobacter pylori is a Gram-negative bacterium that is recognized as one of the key factors in gastric diseases such as gastritis, peptic ulcer and gastric cancer. Recent studies have shown relationships between H. pylori and extra-digestive diseases, and the presence of H. pylori in the middle ear and upper respiratory tract has been reported. However, the role of H. pylori in middle ear disease remains unclear. The present study demonstrated that H. pylori whole-cell protein directly induces macrophage migration inhibitory factor, macrophage inflammatory protein 2, interleukin 1 beta and tumor necrosis factor alpha in middle ear epithelium in mice, and severe proliferation of inflammatory cells was observed in middle ear cavity inoculated with H. pylori whole-cell protein. In addition, trans-tympanic injection of macrophage migration inhibitory factor up-regulated expression of macrophage inflammatory protein 2 in the middle ear. These findings indicate that H. pylori infection causes immunological inflammation in middle ear epithelium, and H. pylori may play a significant role in otitis media.

Improvement in respiratory function by percutaneous vertebroplasty.

BACKGROUND: Percutaneous vertebroplasty (PVP) improves back pain and corrects spinal misalignment to some extent, and thus may improve respiratory function. PURPOSE: To retrospectively investigate changes in respiratory function after PVP. MATERIAL AND METHODS: 41 patients (mean age 72.0 years, range 59-86 years; 39 women, two men) who had undergone PVP for vertebral compression fractures (37 thoracic vertebral bodies [Th6-Th12] and 50 lumbar vertebral bodies [L1-L5]) caused by osteoporosis visited our hospital for follow-up consultation between January and June 2005. At this follow-up consultation, respiratory function testing, including percent forced vital capacity (FVC%) and percent forced expiratory volume in 1 s (FEV(1)%), was performed. We retrospectively compared these values with those taken before PVP using a Wilcoxon signed-rank test. RESULTS: FVC% was 85.2+/-30.3% before PVP and 91.5+/-16.8% at follow-up (mean 10 months after PVP), which represented a significant difference (P<0.003). No significant difference in FEV(1)% was detected. Regarding the number of treatment levels, that is, single vertebroplasty versus multiple vertebroplasty, no significant difference in improvement of FVC% was confirmed (P=0.1). FVC% was abnormally low (

Diffusion-weighted imaging for predicting new compression fractures following percutaneous vertebroplasty.

BACKGROUND: Percutaneous vertebroplasty (PVP) is a technique that structurally stabilizes a fractured vertebral body. However, some patients return to the hospital due to recurrent back pain following PVP, and such pain is sometimes caused by new compression fractures. PURPOSE: To investigate whether the apparent diffusion coefficient (ADC) of adjacent vertebral bodies as assessed by diffusion-weighted imaging before PVP could predict the onset of new compression fractures following PVP. MATERIAL AND METHODS: 25 patients with osteoporotic compression fractures who underwent PVP were enrolled in this study. ADC was measured for 49 vertebral bodies immediately above and below each vertebral body injected with bone cement before and after PVP. By measuring ADC for each adjacent vertebral body, ADC was compared between vertebral bodies with a new compression fracture within 1 month and those without new compression fractures. In addition, the mean ADC of adjacent vertebral bodies per patient was calculated. RESULTS: Mean preoperative ADC for the six adjacent vertebral bodies with new compression fractures was 0.55 x 10(-3) mm(2)/s (range 0.36-1.01 x 10(-3) mm(2)/s), and for the 43 adjacent vertebral bodies without new compression fractures 0.20 x 10(-3) mm(2)/s (range 0-0.98 x 10(-3) mm(2)/s) (P < 0.001). Mean preoperative ADC for the six patients with new compression fractures was 0.55 x 10(-3) mm(2)/s (range 0.21-1.01 x 10(-3) mm(2)/s), and that for the 19 patients without new compression fractures 0.17 x 10(-3) mm(2)/s (range 0.01-0.43 x 10(-3) mm(2)/s) (P < 0.001). CONCLUSION: The ADC of adjacent vertebral bodies as assessed by diffusion-weighted imaging before PVP might be one of the predictors for new compression fractures following PVP.

Inner-ear obliteration in ulcerative colitis patients with sensorineural hearing loss.

OBJECTIVE: Systemic autoimmune diseases, including ulcerative colitis, may involve the inner ear. Several ulcerative colitis cases presenting with sensorineural hearing loss have been reported. We report the T2-weighted, three-dimensional, inner-ear magnetic resonance imaging findings in the inner ears of two such patients. METHODS: Case reports and a review of the literature concerning autoimmune disease and sensorineural hearing loss are presented. RESULTS: We describe two cases of ulcerative colitis with sensorineural hearing loss in which three-dimensional magnetic resonance imaging revealed obliteration of the inner ear. Those inner ears with obliteration had severe hearing loss, and responded poorly to steroid therapy. CONCLUSION: To our knowledge, there has been no previous published report of the T2-weighted, inner-ear magnetic resonance imaging findings of cases of ulcerative colitis with sensorineural hearing loss. This paper represents the first published report in the world literature of inner-ear obliteration in such patients. Three-dimensional magnetic resonance imaging is beneficial in elucidating the pathophysiology of the inner-ear involvement seen in ulcerative colitis.

Lower limb ischaemia caused by fractured osteochondroma of the femur.

Osteochondroma is the most common benign bone tumour and can arise in any bone. They frequently develop around the knee in the distal femur and the proximal tibia. These are usually asymptomatic, but can occasionally impinge on the surrounding vessels and cause various clinical manifestations. We have encountered a patient with multiple hereditary exostoses, in whom the osteochondroma located in the distal portion of the femur fractured as a result of an injury from a traffic accident. The migrated osteochondroma compressed the femoral artery and led to an acute onset of lower extremity ischaemia. Although trauma or vigorous exercise can cause vascular complications caused by osteochondroma, vascular insufficiency due to fracture of osteochondroma after a traumatic injury is extremely rare.