Anatomical Cadaver Study of the Hotchkiss Over-the-Top Approach for Exposing the Anteromedial Facet of the Ulnar Coronoid Process: Critical Measurements and Implications for Protecting the Median Nerve.

PURPOSE: To measure distances from anatomical landmarks to the median nerve, and estimate the length of the flexor-pronator/flexor carpi ulnaris (FCU) detachment necessary to expose the anteromedial facet of the ulnar coronoid process (UCP) using the Hotchkiss over-the-top approach. METHODS: Dissections were made of 20 fresh-frozen cadaveric upper limbs. Measurements were made of the shortest distance from the medial epicondyle to the median nerve, the distance from the medial epicondyle to the median nerve in line with the flexor-pronator/FCU interval, the shortest distance from the apex of the UCP to the median nerve, and the length of the flexor-pronator/FCU detachment necessary to expose the anteromedial facet of the UCP. Measurements were also made of the length of the ulnar insertion of the brachialis muscle and the shortest distances from the proximal and distal insertions of the brachialis muscle to the median nerve. RESULTS: The distances and lengths were as follows: medial epicondyle to median nerve, 31 ± 3 mm; in line with the flexor-pronator/FCU interval, 43 ± 5 mm; from the apex of the UCP to the median nerve, 7 ± 2 mm; the detachment necessary to expose the UCP, 47 ± 6 mm; the ulnar insertion of the brachialis muscle, 27 ± 4 mm; and the proximal and distal insertions of the brachialis muscle to the median nerve, 14 ± 2 mm and 5 ± 1 mm, respectively. CONCLUSIONS: The length of the flexor-pronator/FCU detachment necessary to expose the anteromedial facet of the UCP was similar to the distance from the medial epicondyle to the median nerve in line with the flexor-pronator/FCU interval. The distance from the distal insertion of the brachialis muscle to the median nerve was 5 mm. CLINICAL RELEVANCE: The results of our study provide information on important points for surgeons to consider when performing distal exposure using the Hotchkiss over-the-top approach.

Anatomic cadaveric study of the extensile extensor digitorum communis splitting approach for exposing the ulnar coronoid process.

BACKGROUND: The extensile extensor digitorum communis (EDC) splitting approach can access the ulnar coronoid process (UCP), which can be used to treat terrible triad injuries. The present study anatomically examined the extensile EDC splitting approach for exposing the UCP. METHODS: Twenty fresh frozen cadaveric upper limbs were dissected. The splitting length of the EDC and detachment length of the extensor carpi radialis brevis (ECRB)-extensor carpi radialis longus (ECRL)-brachioradialis (BR) origin were measured to expose the UCP. The distance between the most distal site of the EDC splitting and the point at which the posterior interosseous nerve (PIN) crosses the anterior aspect of the radial shaft, and the distance between the most proximal site of the ECRB-ECRL-BR origin detachment and the point at which the radial nerve crosses the anterior aspect of the humeral shaft were measured. RESULTS: The splitting length of the EDC was 45.4 ± 4.8 mm, the detachment length of the ECRB-ECRL-BR origin was 30.2 ± 4.7 mm, the distance between the distal site of the EDC splitting and PIN was 10.6 ± 6.1 mm (minimum distance, 1.1 mm), and the distance between the proximal site of the ECRB-ECRL-BR origin detachment and the radial nerve was 49.5 ± 9.7 mm (minimum distance, 31.7 mm). CONCLUSIONS: The extensile EDC splitting approach can sufficiently expose the UCP. However, splitting must be performed carefully because the most distal site of the EDC splitting is close to the point at which the PIN crosses the anterior aspect of the radial shaft (average distance, 10 mm; minimum distance, 1 mm).

A Cadaver Study of Median-to-Radial Nerve Transfer for Radial Nerve Injuries.

PURPOSE: To assess the anatomic feasibility of a median-to-radial nerve transfer in cadaver limbs and to quantify the number of axons present in the cut ends of the involved donor and recipient nerves. METHODS: Ten fresh frozen cadaveric upper limbs were dissected. We investigated whether the flexor carpi radialis (FCR) branch/flexor digitorum superficialis (FDS) branch (donor nerve) reached the posterior interosseous nerve (PIN)/extensor carpi radialis brevis (ECRB) branch (recipient nerve) without tension. We also investigated the length of the transected supinator fascia for FCR-posterior interosseous nerve transfer and the FDS-ECRB positional relationship using the epicondyle line and the midline of the forearm as axes. The findings were used for these 2 types of nerve transfer with evaluation closer to the target muscles. The distance between the point at which the FDS and ECRB branches met and the point at which the ECRB branch entered the muscle was measured. After nerve coaptation, the axon number was determined by histological evaluation. RESULTS: In all limbs, the FCR and FDS branches reached the PIN and the ECRB branch without tension. The transected supinator fascia was 17 (3-25) mm long. The point at which the FDS branch reached the ECRB branch [corrected] was 48 (23-65) mm distal to the epicondyle line and approximately 23 (18-27) mm radial to the midline of the forearm. The distance between the point at which the FDS and ECRB branches met and the point at which the ECRB branch entered the muscle was 27 (17-40) mm. The mean axon numbers were FCR, 1501 (932-3022); PIN, 5162 (4325-7732); FDS, 885 (558-962); and ECRB, 548 (433-723). CONCLUSIONS: The FCR branch could be transferred to the PIN [corrected] and the FDS to the ECRB branch in all limbs without tension. CLINICAL RELEVANCE: We provide anatomical and histological information for median-to-radial nerve transfer.

Accuracy of specimen-specific nonlinear finite element analysis for evaluation of radial diaphysis strength in cadaver material.

The feasibility of a user-specific finite element model for predicting the in situ strength of the radius after implantation of bone plates for open fracture reduction was established. The effect of metal artifact in CT imaging was characterized. The results were verified against biomechanical test data. Fourteen cadaveric radii were divided into two groups: (1) intact radii for evaluating the accuracy of radial diaphysis strength predictions with finite element analysis and (2) radii with a locking plate affixed for evaluating metal artifact. All bones were imaged with CT. In the plated group, radii were first imaged with the plates affixed (for simulating digital plate removal). They were then subsequently imaged with the locking plates and screws removed (actual plate removal). Fracture strength of the radius diaphysis under axial compression was predicted with a three-dimensional, specimen-specific, nonlinear finite element analysis for both the intact and plated bones (bones with and without the plate captured in the scan). Specimens were then loaded to failure using a universal testing machine to verify the actual fracture load. In the intact group, the physical and predicted fracture loads were strongly correlated. For radii with plates affixed, the physical and predicted (simulated plate removal and actual plate removal) fracture loads were strongly correlated. This study demonstrates that our specimen-specific finite element analysis can accurately predict the strength of the radial diaphysis. The metal artifact from CT imaging was shown to produce an overestimate of strength.

Accuracy of specimen-specific nonlinear finite element analysis for evaluation of distal radius strength in cadaver material.

BACKGROUND: Distal radius fracture, which often occurs in the setting of osteoporosis, can lead to permanent deformity and disability. Great effort has been directed toward developing noninvasive methods for evaluating the distal radius strength, with the goal of assessing fracture risk. The aim of this study was to evaluate distal radius strength using a finite element model and to gauge the accuracy of finite element model measurement using cadaver material. METHODS: Ten wrists were obtained from cadavers with a mean age of 89.5 years at death. CT images of each wrist in an extended position were obtained. CT-based finite element models were prepared with Mechanical Finder software. Fracture on the models was simulated by applying a mechanical load to the palm in a direction parallel to the forearm axis, after which the fracture load and the site at which the fracture began were identified. For comparison, the wrists were fractured using a universal testing machine and the fracture load and the site of fracture were identified. RESULTS: The fracture load was 970.9 N in the finite element model group and 990.0 N in the actual measurement group. The site of the initial fracture was extra-articular to the distal radius in both groups. The finite element model was predictive for distal radius fracture when compared to the actual measurement. CONCLUSION: In this study, a finite element model for evaluation of distal radius strength was validated and can be used to predict fracture risk. We conclude that a finite element model is useful for the evaluation of distal radius strength. Knowing distal radius strength might avoid distal radius fracture because appropriate antiosteoporotic treatment can be initiated.

Additional decompression at adjacent segments leads to adjacent segment degeneration after PLIF.

PURPOSE: Adjacent segment degeneration (ASD) is one of the major complications of lumbar fusion. Several previous retrospective studies reported ASD after PLIF. However, few reports evaluated whether decompression surgery combined with fusion surgery increases the rate of complications in adjacent segments. The purpose of the current study was to investigate the degeneration in decompressed adjacent segments after PLIF. METHODS: A total of 23 patients (12 men, 11 women; average age, 58.6) who underwent PLIF surgery [1 level (n = 9), 2 levels (n = 8), 3 levels (n = 4), 4 levels (n = 2)] were included. Additional adjacent decompression above or below the level of interbody fusion was performed at 25 levels and no adjacent decompression was performed at 15 levels. We retrospectively investigated ASD by X-ray films of all 40 adjacent segments (above and below fusion level) and clinical outcomes of all 23 cases. RESULTS: Of the 40 adjacent segments, 19 (47.5%) showed ASD and 9 (22.5%) showed symptomatic ASD. In the 19 segments with ASD, ASD occurred in 16 of 25 (64.0%) segments at decompressed sites compared with 3 of 15 (20.0%) non-decompressed sites. The ratio of ASD in adjacent segments was significantly higher at decompressed sites than at non-decompressed sites (p < 0.01). CONCLUSION: ASD occurs frequently in association with additional decompression above or below the level of PLIF. In cases in which the adjacent segments require decompression, a surgical strategy that preserves as much of the posterior complex as possible should be selected.

The effect of Anti-NGF receptor (p75 Neurotrophin Receptor) antibodies on nociceptive behavior and activation of spinal microglia in the rat brachial plexus avulsion model.

STUDY DESIGN: We measured the response of the behavior and spinal glial activation to anti-nerve growth factor receptor (p75 neurotrophin receptor [p75NTR]) antibodies in the rat brachial plexus avulsion (BPA) model. OBJECTIVE: The aim of this study was to investigate the effect of anti-p75NTR antibodies on nociceptive behavior and activation of spinal microglia in the rat BPA model. SUMMARY OF BACKGROUND DATA: Tanezumab (anti-nerve growth factor antibody) treatment is associated with pain reduction and improvement in function, but with several complications. METHODS: Thirty male Wistar rats were used. In the BPA group, the C8-T1 roots were avulsed from the spinal cord with forceps at the lower trunk level and 10 µL of saline was applied locally (n = 10). In the anti-p75NTR group, the C8-T1 roots were avulsed and 10 µL of anti-p75NTR antibody was applied locally (n = 10). In a sham-operated group, the lower trunk was simply exposed (n = 10). Mechanical hyperalgesia and pain-induced walking patterns were measured using von Frey filaments (Stoelting, Wood Dale, IL) and the CatWalk gait analysis (Noldus Information Technology, the Netherlands) system every third day for 3 weeks. Activation of astrocytes and microglia was immunohistochemically examined in the spinal cord using anti-glial fibrillary acidic protein (GFAP) and anti-Iba1 antibodies both 7 and 21 days after surgery. RESULTS: Animals in the BPA group displayed significant mechanical hyperalgesia that continued through day 21 compared with animals in the sham-operated group, and mechanical hyperalgesia in the anti-p75NTR group was significantly improved 6 days after the operation. Regarding pain-induced gait analysis via CatWalk, animals in the BPA group displayed a significantly greater pain-like gait pattern than the p75 group for up to 3 weeks. Levels of GFAP-immunoreactive astrocytes and Iba1-immunoreactive microglia in the anti-p75NTR group were significantly reduced compared with the BPA group. CONCLUSION: Our results suggest that p75NTR contributes to neuropathic pain associated with BPA, and that inhibition of p75NTR reduces neuropathic pain. LEVEL OF EVIDENCE: N/A.

Comparison of material-related complications after bilateral sagittal split mandibular setback surgery: biodegradable versus titanium miniplates.

PURPOSE: The aim of the present prospective study was to compare material-related complications using biodegradable and titanium miniplates after bilateral sagittal split mandibular setback surgery. PATIENTS AND METHODS: The subjects included 200 Japanese adults (67 men and 133 women, age range 18 to 45 years) with jaw deformities diagnosed as mandibular prognathism. All patients were prospectively and consecutively randomized to 2 study groups, receiving biodegradable or titanium fixation plates. Of the 200 patients, 110 underwent bilateral sagittal split ramus osteotomy with a biodegradable fixation plate and 90 underwent bilateral sagittal split ramus osteotomy with a titanium metal plate. The clinical records and radiologic findings of the patients were reviewed, and the incidence of material-related complications was compared. RESULTS: The incidence of postoperative complications and breakage in the biodegradable group was 8.2% (9 cases) and in the titanium group was 3.3% (3 cases). No statistically significant difference in the incidence of complications was found between the 2 groups. Fractures of the biodegradable plate occurred at a significantly greater frequency in patients with asymmetry than in patients without asymmetry. CONCLUSION: Biodegradable plates were reliable with minimal material-related complications. However, the use of biodegradable plates should be recommended for minimally loaded situations.

mPGES-1-expressing bone marrow-derived cells enhance tumor growth and angiogenesis in mice.

Microsomal prostaglandin (PG) E synthase 1 (mPGES-1) is a major PGE synthase and has recently been reported to be expressed at high levels in several cancer types. We previously reported that the PGE receptor EP3 is expressed in bone marrow (BM) derived cells, enriched in stromal tissue, and enhances the potential for tumor angiogenesis. In the present study, we examined the role of mPGES-1-expressing BM cells on tumor angiogenesis using BM chimeric mice. After lethal radiation, wild-type (WT) BMs were excised and replaced with BM cells isolated from mPGES-1 knockout mice (mPGES-1(-/-)). Lewis lung carcinoma cell were implanted subcutaneously and the levels of neoangiogenesis were measured tumor growth in mPGES-1(-/-) BM chimeric mice was significantly reduced compared to that observed in WT BM chimeric mice. Tumor-associated angiogenesis as measured by histological analysis was localized to tumor stroma, and was significantly lower in mPGES-1(-/-) BM chimeric mice compared to that in WT BM chimeric mice. Tumor sections probed by immunohistochemistry revealed that vascular endothelial growth factor (VEGF) that was present in the stromal tissue was markedly reduced in mPGES-1(-/-) BM chimeric mice compared to WT BM chimeras. These results suggest that the recruitment of mPGES-1-expressing BM cells to tumor-associated stromal tissue is crucial for tumor growth and angiogenesis, and correlates with gene expression of host VEGF in stroma. Taken together, these data suggest that regulation of mPGES-1-expressing BM cell recruitment to the site of primary tumors may be a novel strategy for the treatment of solid tumors.

COX-2 and prostaglandin EP3/EP4 signaling regulate the tumor stromal proangiogenic microenvironment via CXCL12-CXCR4 chemokine systems.

Bone marrow (BM)-derived hematopoietic cells, which are major components of tumor stroma, determine the tumor microenvironment and regulate tumor phenotypes. Cyclooxygenase (COX)-2 and endogenous prostaglandins are important determinants for tumor growth and tumor-associated angiogenesis; however, their contributions to stromal formation and angiogenesis remain unclear. In this study, we observed that Lewis lung carcinoma cells implanted in wild-type mice formed a tumor mass with extensive stromal formation that was markedly suppressed by COX-2 inhibition, which reduced the recruitment of BM cells. Notably, COX-2 inhibition attenuated CXCL12/CXCR4 expression as well as expression of several other chemokines. Indeed, in a Matrigel model, prostaglandin (PG) E2 enhanced stromal formation and CXCL12/CXCR4 expression. In addition, a COX-2 inhibitor suppressed stromal formation and reduced expression of CXCL12/CXCR4 and a fibroblast marker (S100A4) in a micropore chamber model. Moreover, stromal formation after tumor implantation was suppressed in EP3-/- mice and EP4-/- mice, in which stromal expression of CXCL12/CXCR4 and S100A4 was reduced. The EP3 or EP4 knockout suppressed S100A4+ fibroblasts, CXCL12+, and/or CXCR4+ stromal cells as well. Immunofluorescent analyses revealed that CXCL12+CXCR4+S100A4+ fibroblasts mainly comprised stromal cells and most of these were recruited from the BM. Additionally, either EP3- or EP4-specific agonists stimulated CXCL12 expression by fibroblasts in vitro. The present results address the novel activities of COX-2/PGE2-EP3/EP4 signaling that modulate tumor biology and show that CXCL12/CXCR4 axis may play a crucial role in tumor stromal formation and angiogenesis under the control of prostaglandins.

Host prostaglandin EP3 receptor signaling relevant to tumor-associated lymphangiogenesis.

Prostaglandin E(2) (PGE(2)) and prostaglandin E (EP) receptor signaling pathways have been implicated in the promotion of tumor growth and angiogenesis. However, little is known about their roles in lymphangiogenesis during tumor development. The present study evaluates whether endogenous PGE(2) exhibits a critical role in tumor-associated lymphangiogenesis. Treatment of male C57BL/6 mice with a cyclooxygenase-2 inhibitor, celecoxib, for seven days resulted in a 52.4% reduction in tumor size induced by subcutaneous injection of murine Lewis lung cells. Celecoxib treatment down-regulated the expression of vascular endothelial growth factor receptor (VEGFR)-3 in stromal tissues by 73.9%, and attenuated expression of podoplanin, a marker for lymphatic endothelial cells. To examine the role of host PGE receptor signaling, we tested four kinds of EP receptor knockout mice. At Day 7 after tumor cell implantation, EP3 receptor knockout mice, but not EP receptor knockout mice lacking EP1, EP2, or EP4, exhibited a 53.3% reduction in tumor weight, which was associated with a 74.5% reduction in VEGFR-3 mRNA expression in tumor stromal tissues. At Day 14, VEGFR-3 expression in EP3-/- mice remained significantly lower than that of their wild-type (WT) counterparts. The expression of VEGF-C in the tumor stromal tissues in EP3-/- mice were also reduced by 22.1% (Day 7) and 44.1% (Day 14), respectively. In addition, the level of immunoreactive podoplanin in the tumor tissues from EP3-/- mice was less than that of WT. These results suggest that host EP3 receptor signaling regulates tumor-associated lymphangiogenesis by up-regulating expression of VEGF-C and its receptor, VEGFR-3, in tumor stromal tissues. Host EP3 blockade together with COX-2 inhibition may be a novel therapeutic strategy to suppress tumor-associated lymphangiogenesis.