The history of orthopaedic use of nitinol compression staples.

INTRODUCTION: The use of nitinol continuous compression staples has shown clinical utility in the management of various orthopaedic injuries. While literature is most robust in the realm of foot/ankle and spine surgery, the use of nitinol staples has been documented in fixation of wrist, olecranon, patella, and pelvis fractures. METHODOLOGY: A narrative review was conducted by searching three online databases - PubMed, Web of Science, and Cochrane using the terms "Nitinol" and "Staple" published between 2003 and 2023. A total of 42 articles met inclusion/exclusion criteria and were included in this review. REVIEW: Literature outside of foot/ankle and spine surgery is largely limited to biomechanical studies, case reports, and finite element analyses. The literature is summarized within this review by anatomic location including foot/ankle, lower extremity, hand, upper extremity, spine, and pelvis. CONCLUSION: Existing literature demonstrates a diverse array of applications for nitinol continuous compression staples in both axial and appendicular orthopaedic care. Advantages of these implants include ease of application, ability to capture small bony fragments, continuous compression across a fracture or arthrodesis, and full coaptation which maximizes the surface area for healing and/or fusion.

Robotic Arm-Assisted Total Hip Arthroplasty to Correct Leg Length Discrepancy in a Patient With Spinopelvic Obliquity.

Leg length discrepancy is not an uncommon result of total hip arthroplasty and a major cause of patient dissatisfaction. Spinopelvic obliquity is a less-recognized cause of limb length differences in patients undergoing total hip arthroplasty. The robotic arm has recently been introduced to enhance implant positioning during surgery and to achieve more predictable leg length and offset goals. In this article, we illustrate the case of a patient who presented with a leg length discrepancy associated with significant spinopelvic obliquity. We show the use of the robotic arm total hip application to improve her pelvic obliquity and limb length discrepancy. This approach helped with the patient's symptoms and gait as well as her radiographic pelvic alignment.

An antibiotic depleted microbiome drives severe Campylobacter jejuni-mediated Type 1/17 colitis, Type 2 autoimmunity and neurologic sequelae in a mouse model.

The peripheral neuropathy Guillain-Barré Syndrome can follow Campylobacter jejuni infection when outer core lipooligosaccharides induce production of neurotoxic anti-ganglioside antibodies. We hypothesized that gut microbiota depletion with an antibiotic would increase C. jejuni colonization, severity of gastroenteritis, and GBS. Microbiota depletion increased C. jejuni colonization, invasion, and colitis with Type 1/17 T cells in gut lamina propria. It also stimulated Type 1/17 anti-C. jejuni and -antiganglioside-antibodies, Type 2 anti-C. jejuni and -antiganglioside antibodies, and neurologic phenotypes. Results indicate that both C. jejuni strain and gut microbiota affect development of inflammation and GBS and suggest that probiotics following C. jejuni infection may ameliorate inflammation and autoimmune disease.

Transplanted human fecal microbiota enhanced Guillain Barré syndrome autoantibody responses after Campylobacter jejuni infection in C57BL/6 mice.

BACKGROUND: Campylobacter jejuni is the leading antecedent infection to the autoimmune neuropathy Guillain-Barré syndrome (GBS), which is accompanied by an autoimmune anti-ganglioside antibody attack on peripheral nerves. Previously, we showed that contrasting immune responses mediate C. jejuni induced colitis and autoimmunity in interleukin-10 (IL-10)-deficient mice, dependent upon the infecting strain. Strains from colitis patients elicited T helper 1 (TH1)-dependent inflammatory responses while strains from GBS patients elicited TH2-dependent autoantibody production. Both syndromes were exacerbated by antibiotic depletion of the microbiota, but other factors controlling susceptibility to GBS are unknown. METHODS: Using 16S rRNA gene high-throughput sequencing, we examined whether structure of the gut microbial community alters host (1) gastrointestinal inflammation or (2) anti-ganglioside antibody responses after infection with C. jejuni strains from colitis or GBS patients. We compared these responses in C57BL/6 mice with either (1) stable human gut microbiota (Humicrobiota) transplants or (2) conventional mouse microbiota (Convmicrobiota). RESULTS: Inoculating germ-free C57BL/6 wild-type (WT) mice with a mixed human fecal slurry provided a murine model that stably passed its microbiota over >20 generations. Mice were housed in specific pathogen-free (SPF) facilities, while extra precautions of having caretakers wear sterile garb along with limited access ensured that no mouse pathogens were acquired. Humicrobiota conferred many changes upon the WT model in contrast to previous results, which showed only colonization with no disease after C. jejuni challenge. When compared to Convmicrobiota mice for susceptibility to C. jejuni enteric or GBS patient strains, infected Humicrobiota mice had (1) 10-100 fold increases in C. jejuni colonization of both strains, (2) pathologic change in draining lymph nodes but only mild changes in colon or cecal lamina propria, (3) significantly lower Th1/Th17-dependent anti-C. jejuni responses, (4) significantly higher IL-4 responses at 5 but not 7 weeks post infection (PI), (5) significantly higher Th2-dependent anti-C. jejuni responses, and (6) significantly elevated anti-ganglioside autoantibodies after C. jejuni infection. These responses in Humicrobiota mice were correlated with a dominant Bacteroidetes and Firmicutes microbiota. CONCLUSIONS: These data demonstrate that Humicrobiota altered host-pathogen interactions in infected mice, increasing colonization and Th-2 and autoimmune responses in a C. jejuni strain-dependent manner. Thus, microbiota composition is another factor controlling susceptibility to GBS.