Anatomical Structures at Risk in Percutaneous Distal Bunionette Correction.

Bunionette deformity is an incredibly pervasive issue in our society with almost a quarter of individuals being affected by it. As it is so common, there are numerous techniques and approaches to correct the deformity. Currently, there is a growing trend that favors percutaneous osteotomy of the bunionette. As there are multiple osteotomy sites, there are anatomical considerations that must be made at each one. The purpose of this study was to investigate the anatomic structures at risk during distal osteotomy of bunionette deformity using a Shannon burr. Using 11 fresh cadaver specimens, the fifth metatarsal was accessed through a carefully marked portal. A Shannon burr was employed for the osteotomy. Dissections were performed to assess potential damage to critical structures, including the lateral dorsal cutaneous nerve (LDCN), abductor digiti minimi (ADM), and extensor digitorum longus (EDL). Measurements were taken from the osteotomy site to each structure. The distal osteotomy site was on average greater than 8 mm from the EDL and ADM, whereas it was 1.64 mm from the LDCN. The Shannon burr made contact with and transected the LDCN on 2 occasions. However, previous studies have highlighted potential anatomical variations of the LDCN that arise distally. The study underscored the challenges posed by minimally invasive approaches to treating bunionette deformity and highlighted the need for cautious consideration when using percutaneous methods.Level of Clinical Evidence: 5.

Ligamentous Augmentation to Prevent Proximal Junctional Kyphosis and Failure: A Biomechanical Cadaveric Study.

STUDY DESIGN: Biomechanical cadaveric study (level V). OBJECTIVE: To evaluate the effectiveness of polyethylene bands looped around the supra-adjacent spinous process (SP) or spinal lamina (SL) in providing strength to the cephalad unfused segment and reducing junctional stress. BACKGROUND: Proximal junctional kyphosis (PJK) is a pathologic kyphotic deformity adjacent to posterior spinal instrumentation after fusion constructs. Recent studies demonstrate a mismatch in stiffness between the instrumented construct and nonfused adjacent levels to be a causative factor in the development of PJK and proximal junction failure. To our knowledge, no biomechanical studies have addressed the effect of different methods of polyethylene band placement at the proximal junction. MATERIALS AND METHODS: Twelve fresh frozen cadavers were divided into 3 groups of 4: pedicle screw-based instrumentation from T10 to L5 ("control"), T10-L5 instrumentation with a polyethylene band to the T9 "SP," T10-L5 instrumentation with 2 polyethylene bands to the T9 "SL." Specimens were tested with an eccentric (10 mm anterior) load at 5 mm/min for 15 mm or until failure occurred. Failure was defined by the inflection point on the load versus deformation curves. Linear regression was utilized to evaluate the effect of augmentation on the load-to-failure. Significance was set at 0.05. RESULTS: Fractures occurred in all specimens tested. The mean peak load to failure was 2148 N (974-3322) for the SP group, and 1248 N (742-1754) for the control group (P > 0.05) and 1390 N (1080-2004) for the SL group. No difference existed between the control group and the SP group in terms of fracture level (P > 0.05). Net kyphotic angulation shows no differences among these 3 groups (P > 0.05). CONCLUSION: Although statistical significance was not achieved, ligament augmentation to the SP increased mean peak load-to-failure in a cadaveric PJK model.

Anatomical Structures at Risk in Percutaneous Preparation Talonavicular Fusion.

BACKGROUND: The stability of the hindfoot greatly relies on the integrity of the talonavicular joint. Pathologies affecting this joint often necessitate fusion. Our study explores the risks posed to neurovascular and tendon structures during simulated percutaneous talonavicular joint preparation for fusion. METHODS: In 9 fresh cadaver specimens, the talonavicular joint was accessed through two portals. A 2-mm Shannon burr was employed for joint surface preparation with distraction provided by a pin-based distractor. Dissections were performed to assess potential damage to critical structures, including the dorsalis pedis artery, superficial and deep peroneal nerves, extensor hallucis longus (EHL), and tibialis anterior (TA) tendons. RESULTS: The dorsal portal site was found to be significantly closer to important structures compared to the medial portal site. The Shannon burr made contact with various structures, with a single transection identified for both deep and superficial peroneal nerve branches. During the dorsal portal site approach, potential injury to the EHL tendon was identified as concern. CONCLUSION: This study sheds light on the potential risks associated with percutaneous dorsal and medial joint preparation approaches using a Shannon burr.Level of Evidence:Level V, mechanism-based reasoning..

Osmosensing by WNK Kinases.

With No Lysine (K) WNK kinases regulate electro-neutral cotransporters that are controlled by osmotic stress and chloride. We showed previously that autophosphorylation of WNK1 is inhibited by chloride, raising the possibility that WNKs are activated by osmotic stress. Here we demonstrate that unphosphorylated WNK isoforms 3 and 1 autophosphorylate in response to osmotic pressure in vitro, applied with the crowding agent polyethylene glycol (PEG)400 or osmolyte ethylene glycol (EG), and that this activation is opposed by chloride. Small angle x-ray scattering of WNK3 in the presence and absence of PEG400, static light scattering in EG, and crystallography of WNK1 were used to understand the mechanism. Osmosensing in WNK3 and WNK1 appears to occur through a conformational equilibrium between an inactive, unphosphorylated, chloride-binding dimer and an autophosphorylation-competent monomer. An improved structure of the inactive kinase domain of WNK1, and a comparison with the structure of a monophosphorylated form of WNK1, suggests that large cavities, greater hydration, and specific bound water may participate in the osmosensing mechanism. Our prior work showed that osmolytes have effects on the structure of phosphorylated WNK1, suggestive of multiple stages of osmotic regulation in WNKs.

A Phosphorylated Intermediate in the Activation of WNK Kinases.

WNK kinases autoactivate by autophosphorylation. Crystallography of the kinase domain of WNK1 phosphorylated on the primary activating site (pWNK1) in the presence of AMP-PNP reveals a well-ordered but inactive configuration. This new pWNK1 structure features specific and unique interactions of the phosphoserine, less hydration, and smaller cavities compared with those of unphosphorylated WNK1 (uWNK1). Because WNKs are activated by osmotic stress in cells, we addressed whether the structure was influenced directly by osmotic pressure. pWNK1 crystals formed in PEG3350 were soaked in the osmolyte sucrose. Suc-WNK1 crystals maintained X-ray diffraction, but the lattice constants and pWNK1 structure changed. Differences were found in the activation loop and helix C, common switch loci in kinase activation. On the basis of these structural changes, we tested for effects on in vitro activity of two WNKs, pWNK1 and pWNK3. The osmolyte PEG400 enhanced ATPase activity. Our data suggest multistage activation of WNKs.