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. (C) 2019 The Japanese Orthopaedic Association. Published by Elsevier B.V. All rights reserved.

Purpose: Advances in small arthroscopy have enabled a minimally invasive surgery for thumb carpometacarpal joints. However, surgery is often difficult using standard CM-radial (CM-R) and CM-ulnar portals ( CM-U). Here, we describe the clinical applications and complications associated with using thenar portal (TP) and standard portals.Methods: Arthroscopic surgeries of thumb carpometacarpal joint were performed in 21 patients including 15 patients with osteoarthritis and six Bennett's fracture-dislocations. Complications and the frequency of use associated with each portal were evaluated.Results: Complications associated with the CM-R portal comprised paresthesia due to damage of the radial nerve branches in two patients. No nerves were damaged but the operation scar became tender at the TP in three patients. The CM-R was used at a lower frequency when the TP was utilized.Conclusion: The clinical use of TP may decrease the risk of radial sensory nerve damage through decreasing frequency of use of the CM-R that is located near the nerve. (C) 2015 Elsevier Masson SAS. All rights reserved.

Advances in small arthroscopy have enabled a minimally invasive surgery for thumb carpometacarpal joints. However, surgery is often difficult using standard CM-radial (CM-R) and CM-ulnar portals (CM-U). Here, we describe the clinical applications and complications associated with using thenar portal (TP) and standard portals. Arthroscopic surgeries of thumb carpometacarpal joint were performed in twenty-one patients including fifteen patients with osteoarthritis and six Bennett's fracture-dislocations. Complications and the frequency of use associated with each portal were evaluated. Complications associated with the CM-R portal comprised paresthesia due to damage of the radial nerve branches in two patients. No nerves were damaged but the operation scar became tender at the TP in three patients. The CM-R was used at a lower frequency when the TP was utilized. The clinical use of TP may decrease the risk of radial sensory nerve damage through decreasing frequency of use of the CM-R that is located near the nerve. IV.

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.

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.

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.

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.

Introduction: Intervertebral disc (IVD) degeneration is characterized biochemically by the degradation of the extracellular matrix (mainly, proteoglycans and collagens). Recent studies suggest these changes in macromolecular assemblies are induced by matrix-degrading enzymes, such as the matrix metalloproteinases (MMPs), ADAMTS [1, 2] and serine proteinases [3] under the stimulation of proinflammatory cytokines [e.g., interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α)]. Proteinase-activated receptor 2 (PAR2) is one of a unique subfamily of G protein-coupled receptors that are activated by several serine proteinases (e.g., elastase) [4]. The activation of PAR2, via protease cleavage and exposure of the tethered ligand, is known to exert an inflammatory reaction with upregulation of cytokines in several cell types [5]. The expression of PAR2 was also identified in articular cartilage and was thought to contribute to the pathogenesis of osteoarthritis [6]. Recent data indicated that PAR2 was expressed in rat IVD cells and, importantly, its expression was upregulated by IL-1β [7]. We hypothesized that PAR2 is expressed in IVD cells and is involved in the regulatory mechanism of IVD degeneration. The expression of PAR2 in the human IVD remains unknown. The purpose of this study was (1) to determine if human IVD cells express PAR2, and (2) to quantify the PAR2-expressing cells in human IVD tissues of early stage and advanced stages of degeneration. Materials and Methods: Human disc tissue: Human lumbar IVDs were obtained from (a) cadaveric human spines (10 donors, 12 discs) and (b) tissues obtained from spine surgery (6 patients, 6 discs) (Total: 18 discs; mean age: 64.2 years [range 43-76]; MRI: Thompson grade: average 3.1 [range 1-4]). Tissue preparation for histology: The specimens were fixed in 4% paraformaldehyde and then embedded in paraffin. 5-μm-thick sections were stained with Safranin-O and hematoxylin and eosin (H-E). Serial sections adjacent to the sections stained with Safranin-O/H-E were used for immunohistochemical analysis. Immunohistochemistry: The specimens were incubated with a mouse monoclonal anti-human PAR2 antibody overnight at 4°C. Mouse IgG was used as an isotype control. Color was developed with an immuno-peroxidase polymer. Immunoblotting for PAR2: Two IVD tissues (mean age 48.5 years; range 46-51) obtained from surgery were used for western blot analysis. The specimens were homogenized and lysed with RIPA buffer, including protease inhibitors, for seven days at 4°C. Proteins (30 μg per well) were separated by SDS-PAGE (7.5% acrylamide) under reducing conditions, followed by western blotting using the antiPAR2 antibody. Quantification of PAR2 expression: Human IVDs were divided into two groups; early stage degeneration (Early group, MRI: Thompson grades 1 and 2) and advanced stage degeneration (Advanced group, grades 3 and 4). The number of samples used in each group was as follows: early group (NP: n = 6, AF: n = 11); advanced group (NP: n = 6, AF: n = 12). PAR2-immunoreactive cells were divided into three groups according to the intensity of staining (none: -; moderate: +1; strong: +2). Under light-microscopy, five visual fields (x200) on each sample were randomly chosen, and the total number of cells and PAR2-positive cells were manually counted. The percentage of PAR2-immunoreactive cells was calculated as follow; the number of PAR2-positive cells/total number of cells x 100 (%). Statistical Analysis: The evaluation of statistical differences between the groups was determined by the unpaired student t-test. P values less than 0.05 were considered significant. Results: PAR2 expression in human IVD tissues: Immunoreactivity to the anti-PAR2 antibody was clearly identified in human IVD cells, showing a punctuate cytoplasmic staining pattern (Fig. 1). PAR2-immunoreactive cells were distributed in both AF (anterior and posterior) and NP tissues. Immunoblotting for PAR2: A single protein band with a molecular mass of about 55 kDa was found (Fig. 2). Quantification of PAR2-expressing cells: The percentage of PAR2-immunoreactive cells in the AF was significantly elevated in the advanced group compared to the early group; a similar trend but with no statistical difference was found in the NP (AF: early: 8.8 ± 9.9%, advanced: 32.5 ± 24.5%, p<0.01 / NP: early: 19.5 ± 13.7%, advanced: 30.6 ± 24.0%, p = 0.36) (Fig. 3). The proportion of PAR2immunoreactive cells exhibiting a strong staining pattern in the AF was significantly increased in the advanced group compared with the early group (p<0.05); this was not seen in the NP (p = 0.77).