Arthroscopic ligamentoplasty for osteoarthritis of the thumb carpometacarpal joints: Clinical and radiological outcomes with a minimum 2-year follow-up.

BACKGROUND: We reported a new technique for arthroscopic ligamentoplasty for the thumb carpometacarpal osteoarthritis (CMC-OA) along with a minimum of 2 years of results. METHODS: Twenty-nine thumbs with CMC-OA in stages II and III according to the Eaton and Glickel classification, were treated by arthroscopic ligamentoplasty. The procedure included partial trapeziectomy followed by ligamentoplasty similar to the Thompson technique. We evaluated pain VAS; DASH; grip and pinch strength; thumb abduction range of motion, and radiographic examination preoperatively and every 3 months until 1 year after surgery, and every 6 months thereafter. The mean duration of the follow-up was 3.2 years with a range of 2.0-6.0 years. RESULTS: Pain, VAS, and DASH were significantly improved at 3 months after surgery than those preoperatively. Further, the strength of grip, tip, and key pinch significantly increased at 9, 9, and 12 months after surgery, respectively. Additionally, these improvements were maintained until the final follow-up. The range of motion tended to decrease in both palmar and radial abduction, although the differences were not significant. Radiographic examination after surgery showed that the ratio of trapezial space was significantly reduced because of surgical excision of the trapezium. However, there were no significant differences in the results between each follow-up time and the final follow-up. Moreover, the ratio of subluxation on the plain X-ray was significantly improved and maintained until the final follow-up. The parameters of clinical and radiographic outcomes, except motion, were significantly improved, even in patients with including those in stage III and with greater than 1/3 subluxation of the 1st metacarpal base on plain radiography. CONCLUSION: Arthroscopic ligamentoplasty was effective for pain relief and improvement of grip and pinch strength for the patients with symptomatic CMC-OA. LEVEL OF EVIDENCE: Therapeutic study/Level IV.

Extracting Symptom Names and Disease-Symptom Relationships from Web Texts Using a Multi-Column Convolutional Neural Network.

We propose a method to create large-scale Japanese medical dictionaries that include symptom names and information about the relationship between a disease and its symptoms using a large web archive that includes large amounts of text written by non-medical experts. Our goal is to develop a diagnosis support system that makes a diagnosis according to the natural language (NL) inputs provided by patients. To achieve this, two medical dictionaries need to be constructed: one that includes a wide variety of symptom names expressed in NL and another that includes information about the relationship between a disease and its symptoms. Dictionaries will then be used to predict the patient's disease via two developed methods that extract symptom names and disease-symptom relationships. Both methods retrieve sentences using WISDOM X and then apply neural classifiers to them. Our experimental results show that our methods achieved 93.8% and 88.3% in the F1-score, respectively.

Tissue renin-angiotensin system in the intervertebral disc.

STUDY DESIGN: Immunohistochemical and biochemical analyses of the rat intervertebral disc (IVD) tissue renin-angiotensin system (tRAS). OBJECTIVE: To examine the expression and function of tRAS in the rat IVD. SUMMARY OF BACKGROUND DATA: Angiotensin II (Ang II), the major effector of tRAS, is a hormone that contributes to inflammation and fibrosis in many organs. The expression of tRAS in the rat IVD has not been determined. METHODS: tRAS expression in rat and bovine IVDs was examined using real-time polymerase chain reaction (rat) and immunohistochemistry (rat and bovine). Rat annulus fibrosus cells in monolayer culture were used to examine the biological role of tRAS in vitro. The effect of Ang II peptide on extracellular matrix metabolism was assessed by real-time polymerase chain reaction. RESULTS: mRNA of tRAS components, including angiotensin converting enzyme, Ang II, Ang II receptor type 1, Ang II receptor type 2, and Cathepsin D (a renin-like enzyme), was clearly confirmed by real-time polymerase chain reaction analysis. In rat and bovine annulus fibrosus and nucleus pulposus cells in monolayer culture, immunohistochemical analysis showed that each tRAS component was clearly expressed. In rat IVD tissues, immunoreactivity to each antibody for tRAS components was also observed. Proliferation of rat annulus fibrosus cells was mildly stimulated by Ang II peptide. Ang II peptide also had minor stimulatory effect on the expression of the extracellular matrix components, growth factors, and catabolic proteins. CONCLUSION: Our results demonstrate for the first time that the tRAS components necessary to activate tRAS have been found in the normal rat IVD at both mRNA and protein levels. To elucidate the association between tRAS and the process of IVD degeneration, the expression and function of tRAS in the human degenerated IVD should be examined in a future study.

Expression of proteinase-activated receptor-2 in the intervertebral disc.

STUDY DESIGN: Immunohistochemical and biochemical analyses of proteinase-activated receptor-2 (PAR-2) in rat and human intervertebral discs (IVDs). OBJECTIVES: To examine the expression and function of PAR-2 in rat IVD cells, and to determine if PAR-2 is expressed in human IVDs. SUMMARY OF BACKGROUND DATA: PAR-2 is a G protein-coupled receptor that contributes to the regulation of inflammatory reactions and the pathophysiology of inflammatory diseases, including arthritis. The expression of PAR-2 in the IVD has not been determined. METHODS: PAR-2 expression by rat IVD cells and tissues was examined using immunohistochemistry and western blot. Rat anulus fibrosus cells in monolayer culture were used to examine the biologic role of PAR-2 in vitro. The effect of PAR-2-activating peptide (PAR-2AP) on the catabolic cascade was assessed by western blot and real-time PCR. The expression of PAR-2 by human IVD tissues at different stages of degeneration was determined by immunohistochemical analyses. RESULTS: PAR-2 was expressed by rat IVD cells and in both anulus fibrosus and nucleus pulposus tissues, PAR-2 expression was up-regulated by interleukin-1beta (IL-1beta). PAR-2AP significantly increased the release of IL-1beta into the medium. Although PAR-2AP had no direct effect on matrix metalloproteinase-3 (MMP-3) and MMP-13 mRNA levels, treatment with PAR-2AP significantly up-regulated the mRNA levels of a disintegrin and metalloproteinase with thrombospondin motif-4. The simultaneous administration of PAR-2AP and IL-1beta synergistically up-regulated the mRNA levels of a disintegrin and metalloproteinase with thrombospondin motif-4, MMP-3, and MMP-13. The expression of PAR-2 was identified in human IVD tissues. The number of PAR-2-expressing cells was significantly elevated in advanced stages of IVD degeneration compared with those in early stages of degeneration. CONCLUSION: Our results demonstrate for the first time that IVD cells express PAR-2. The expression of PAR-2 is regulated by IL-1beta stimulation. PAR-2 activation accelerates the expression of matrix-degrading enzymes. PAR-2 may play an important role in the cytokine-mediated catabolic cascade and consequently may be involved in IVD degeneration.

Pathomechanism of entrapment neuropathy in diabetic and nondiabetic rats reared in wire cages.

To examine the pathomechanism of entrapment neuropathy associated with diabetes with special emphasis on the roles of mast cells and Tenascin-C using a rat model of Streptozotocin-induced diabetes. The roles of mast cells and Tenascin-C in development of tarsal tunnel syndrome were analyzed electrophysiologically and histologically in 20 male Ws/Ws-/-rats (mast cell deficient) and 20 of their male wild type counterparts (12-16 weeks old; 250-300 g). Rats were assigned randomly to one of the following three groups; diabetic group and nondiabetic group reared in cages with a wire grid flooring; non-diabetic group in cages with sawdust covered plastic flooring. No significant role for mast cells in entrapment neuropathy was found in the rats with streptozotocin-induced diabetes. Distal latency was prolonged in diabetic rats compared with nondiabetic rats, and positively correlated with increases in blood glucose levels. Tenascin-C expression levels in the endoneurium at the tarsal tunnel in diabetic rats were found to be correlated with distal latency. The anti-alpha-smooth muscle actin (alpha-SMA) positive myofibroblast was scattered in nerve fascicles overexpressing Tenascin-C. It seems likely that Tenascin-C expressing myofibroblasts constrict axons by inducing collagen contraction of the endoneurium. Our data indicate that metabolic and phenotypic abnormalities of endoneurium and perineum lie behind the vulnerability of diabetic patients to entrapment neuropathy.

Metal concentrations in the serum and hair of patients with titanium alloy spinal implants.

STUDY DESIGN: A retrospective study of serum and hair metal concentrations in patients with titanium alloy spinal implants was performed. OBJECTIVE: To determine the incidence and possible causes of abnormal metal concentrations. SUMMARY OF BACKGROUND DATA: Several studies have demonstrated that metal debris are present in the tissues surrounding titanium alloy spinal implants. However, few studies suggest that metals dissolve, circulate in the body fluid, and accumulate in remote organs. METHODS: Titanium, aluminum, and vanadium concentrations in serum and hair were measured after surgery in 46 patients with titanium alloy spinal implants (12 patients in the implant failure group and 34 patients in the no implant failure group) and 20 patients without spinal implants (control group). All the subjects were examined again 1 year after the first examination or implant removal. RESULTS: Of the 46 patients with titanium alloy spinal implants, 16 patients (34.8%) exhibited abnormal serum metal concentrations and 11 patients (23.9%) exhibited abnormal hair metal concentrations. In the control group, three patients (15%) exhibited only abnormal serum and metal aluminum concentrations at the first examination. In both of the two patients who exhibited abnormal serum titanium concentrations and then had their spinal implants removed, the serum and hair titanium levels decreased to beneath the reference value limit in 1 year after the removal. Comparison of the implant failure and no implant failure groups showed no significant differences in the incidence of abnormal serum concentrations of titanium, aluminum, or both metals. Therefore, serum metal concentrations did not seem to be a useful indicator of hardware loosening or implant failure. CONCLUSIONS: Approximately one third of patients with titanium alloy spinal implants exhibited abnormal serum or hair metal concentrations at a mean time of mean 5.1 years after surgery. Titanium or aluminum may travel to distant organs after dissolution of metals from the spinal implants.