Outcomes after a Grammont-style reverse total shoulder arthroplasty?

BACKGROUND: The purpose of this study was to determine the factors associated with outcomes after reverse total shoulder arthroplasty (RTSA). METHODS: We retrospectively evaluated all RTSAs performed by the senior author between January 1, 2007, and November 1, 2017. We evaluated pain visual analog scale (VAS), Simple Shoulder Test (SST), and American Shoulder and Elbow Surgeons Standardized Shoulder Assessment Form (ASES) scores and complication and reoperation rates at a minimum of 2-year follow-up. We evaluated preoperative and 2-week postoperative radiographs for glenoid inclination (GI), medialization as distance between the center of the humeral head or glenosphere and the line of the deltoid, and distalization via the acromial-greater tuberosity distance. We performed inter- and intrarater reliabilities via intraclass correlation coefficients (ICCs) and conducted a multivariable analysis. RESULTS: We included 230 RTSAs in the analysis, with 70% follow-up at a median of 3.4 years. Reliability was acceptable with all ICCs >.678. Increased postoperative GI was significantly associated with increased VAS pain postoperatively (P = .008). Increased distalization was associated with an increased rate of complications and reoperations (P = .032). Younger age (P = .008), female gender (P = .009), and lower body mass index (BMI) (P = .006) were associated with worse ASES scores. Female gender (P < .001) and lower BMI (P = .039) were associated with worse SST scores. Female gender (P = .013) and lower BMI (P = .005) were associated with worse VAS-pain scores. CONCLUSION: Age, gender, and BMI are associated with outcome after RTSA. In this retrospective analysis of a Grammont-style RTSA, superior inclination is associated with increased pain postoperatively, whereas excessive arm lengthening is associated with increased risk for complication or reoperation.

Double-loaded suture anchors in the treatment of anteroinferior glenohumeral instability.

HYPOTHESIS: The purpose of this study was to determine the clinical outcomes of arthroscopic labral repair for anteroinferior glenohumeral instability with the use of double-loaded suture anchors. METHODS: This study evaluated a series of consecutive patients treated after the senior author changed from single- to double-loaded suture anchors for the treatment of anteroinferior glenohumeral instability with a minimum follow-up period of 2 years. We collected the following outcomes at final follow-up: visual analog scale pain score, Simple Shoulder Test score, American Shoulder and Elbow Surgeons score, and instability recurrence data. RESULTS: A total of 41 consecutive patients underwent arthroscopic labral repair with double-loaded anchors, of whom 30 (71%) were able to be contacted at a minimum of 2 years postoperatively. These patients included 4 contact or collision athletes (13%). The patients had an average of 12 ± 13 prior dislocations over an average period of 56 ± 57 months preoperatively. Mean glenoid bone loss measured 16% ± 10%, and 67% (18 of 27 patients) had glenoid bone loss ≥ 13.5%. Intraoperatively, 3.2 ± 0.4 anchors were used. No posterior repairs or remplissage procedures were performed. At an average of 6.7 ± 2.7 years' follow-up, the visual analog scale pain score was 0.8 ± 1.4; Simple Shoulder Test score, 11 ± 2; and American Shoulder and Elbow Surgeons score, 90 ± 14. Patients with bone loss < 13.5% had a 0% redislocation rate and 11% subluxation rate, whereas those with bone loss ≥ 13.5% had a 6% reoperation rate, 22% redislocation rate, and 22% subluxation rate. CONCLUSION: Arthroscopic labral repair with double-loaded anchors provides satisfactory clinical results at early to mid-term outcome assessment when glenoid bone loss is <13.5%.

A pilot trial of text-delivered peer network counseling to treat young adults with cannabis use disorder.

Approximately 1.8 million young adults aged 18 to 25 had a Cannabis Use Disorder (CUD) in the past year. Unfortunately, engaging young adults in treatment is very challenging. Creative approaches to treat cannabis disorders such as integrating mobile technology with evidence-based treatments are warranted. In light of these challenges, we developed a text message-delivered version of Peer Network Counseling (PNC-txt), which is a substance use intervention that focuses on peer relations. PNC-txt engages participants in 16 automated, personalized text interactions over 4weeks. We conducted a randomized controlled trial to test the efficacy of PNC-txt against a waitlist control group with 30 treatment seeking young adults (ages 18-25) who met DSM-5 criteria for CUD. Self-report and urine analyses were used to test outcomes at the three-month follow-up. The PNC-txt group significantly reduced their cannabis use related problems as well as cannabis cravings, compared to the control group. PNC-txt participants also had a significantly greater percentage with urines negative for cannabis metabolites compared to controls. Moderation analysis showed that CUD severity level moderated treatment, suggesting that PNC-txt is more effective for participants with medium and high levels of CUD severity. All effect sizes ranged from medium to large. Results from this pilot trial are promising and warrant further research on PNC-txt for addressing cannabis use disorder.

Involvement of Wnt, Eda and Shh at defined stages of sweat gland development.

To maintain body temperature, sweat glands develop from embryonic ectoderm by a poorly defined mechanism. We demonstrate a temporal cascade of regulation during mouse sweat gland formation. Sweat gland induction failed completely when canonical Wnt signaling was blocked in skin epithelium, and was accompanied by sharp downregulation of downstream Wnt, Eda and Shh pathway genes. The Wnt antagonist Dkk4 appeared to inhibit this induction: Dkk4 was sharply downregulated in ß-catenin-ablated mice, indicating that it is induced by Wnt/ß-catenin; however, its overexpression repressed Wnt target genes and significantly reduced gland numbers. Eda signaling succeeded Wnt. Wnt signaling was still active and nascent sweat gland pre-germs were still seen in Eda-null mice, but the pre-germs failed to develop further and the downstream Shh pathway was not activated. When Wnt and Eda were intact but Shh was ablated, germ induction and subsequent duct formation occurred normally, but the final stage of secretory coil formation failed. Thus, sweat gland development shows a relay of regulatory steps initiated by Wnt/ß-catenin - itself modulated by Dkk4 - with subsequent participation of Eda and Shh pathways.

Forkhead transcription factor FoxA1 regulates sweat secretion through Bestrophin 2 anion channel and Na-K-Cl cotransporter 1.

Body temperature is maintained in a narrow range in mammals, primarily controlled by sweating. In humans, the dynamic thermoregulatory organ, comprised of 2-4 million sweat glands distributed over the body, can secrete up to 4 L of sweat per day, thereby making it possible to withstand high temperatures and endure prolonged physical stress (e.g., long-distance running). The genetic basis for sweat gland function, however, is largely unknown. We find that the forkhead transcription factor, FoxA1, is required to generate mouse sweating capacity. Despite continued sweat gland morphogenesis, ablation of FoxA1 in mice results in absolute anihidrosis (lack of sweating). This inability to sweat is accompanied by down-regulation of the Na-K-Cl cotransporter 1 (Nkcc1) and the Ca(2+)-activated anion channel Bestrophin 2 (Best2), as well as glycoprotein accumulation in gland lumens and ducts. Furthermore, Best2-deficient mice display comparable anhidrosis and glycoprotein accumulation. These findings link earlier observations that both sodium/potassium/chloride exchange and Ca(2+) are required for sweat production. FoxA1 is inferred to regulate two corresponding features of sweat secretion. One feature, via Best2, catalyzes a bicarbonate gradient that could help to drive calcium-associated ionic transport; the other, requiring Nkcc1, facilitates monovalent ion exchange into sweat. These mechanistic components can be pharmaceutical targets to defend against hyperthermia and alleviate defective thermoregulation in the elderly, and may provide a model relevant to more complex secretory processes.

Shh is required for Tabby hair follicle development.

In embryonic Eda mutant ("Tabby") mice, the development of one of the two major types of hair, "primary" hair fails, but other "secondary" hairs develop in normal numbers, though shorter and slightly aberrant. In Tabby mice, Shh is undetectable in skin early on, but is activated during secondary hair formation. We inferred that Shh may be involved in primary hair formation, activated normally by Eda, and also possibly in secondary hair formation, activated by an Eda-independent pathway. Varying the dosage of Shh now supports these inferences. In Shh knockout mice, mice were totally hairless: primary and secondary hair follicle germs were formed, but further progression failed. Consistent with these findings, when Shh loss was restricted to the skin, secondary hair follicle germs were initiated on time in Tabby mice, but their subsequent development (down-growth) failed. An Shh transgene expressed in Tabby skin could not restore induction of primary hair follicles, but restored normal length to the somewhat aberrant secondary hair that was formed and prolonged the anagen phase of hair cycling. Thus, Shh is required for primary and secondary hair down-growth and full secondary hair length, but is not itself sufficient to replace Eda or make fully normal secondary hair.

Dkk4 and Eda regulate distinctive developmental mechanisms for subtypes of mouse hair.

The mouse hair coat comprises protective "primary" and thermo-regulatory "secondary" hairs. Primary hair formation is ectodysplasin (Eda) dependent, but it has been puzzling that Tabby (Eda(-/y)) mice still make secondary hair. We report that Dickkopf 4 (Dkk4), a Wnt antagonist, affects an auxiliary pathway for Eda-independent development of secondary hair. A Dkk4 transgene in wild-type mice had no effect on primary hair, but secondary hairs were severely malformed. Dkk4 action on secondary hair was further demonstrated when the transgene was introduced into Tabby mice: the usual secondary follicle induction was completely blocked. The Dkk4-regulated secondary hair pathway, like the Eda-dependent primary hair pathway, is further mediated by selective activation of Shh. The results thus reveal two complex molecular pathways that distinctly regulate subtype-based morphogenesis of hair follicles, and provide a resolution for the longstanding puzzle of hair formation in Tabby mice lacking Eda.