Association of estrogen receptor ß polymorphisms with posterior tibial tendon dysfunction.

Posterior tibial tendon (PTT) dysfunction is three times more common in females, and some patients may have a predisposition without a clinically evident cause, suggesting that individual characteristics play an important role in tendinopathy. The present study investigated the association of rs4986938 (+ 1730G > A; AluI RFLP) and rs1256049 (- 1082G > A; RsaI RFLP) single nucleotide polymorphisms (SNPs) of estrogen receptor-beta (ER-ß) gene with PTT dysfunction. A total of 400 participants were recruited. The PTT dysfunction group: these patients underwent surgery, with PTT tendinopathy confirmed by histopathology and magnetic resonance image (MRI). The control group was composed of participants with no clinical or MRI evidence of PTT dysfunction. Each group was composed of 100 postmenopausal women, 50 premenopausal women, and 50 men. Genomic DNA was extracted from saliva samples, and genotypes were obtained by polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP). Concerning the ER-ß SNP rs4986938, there were significant differences in the frequencies of alleles between test and control groups of all the cases, only postmenopausal women and only men (p < 0.0001, p = 0.0016 and p = 0.0001). Considering the PTT dysfunction group and comparing postmenopausal women versus premenopausal women adding men, the analysis showed significant differences in the allelic distribution (p = 0.0450): the allele A in postmenopausal women is a risk factor. The ER-ß SNP rs1256049 did not show differences in the frequencies of alleles and genotypes between groups. The ER-ß SNP rs4986938, but not ER -ß SNPs rs1256049, may contribute to PTT insufficiency in the Brazilian population, with additional risk in postmenopausal women. Addition, in men the genetic factor could be more determinant.

Ankle fusion percutaneous home run screw fixation: Technical aspects and soft tissue structures at risk.

INTRODUCTION: The objective of this cadaveric study was to identify the number of attempts necessary for a perfect positioning of the ankle fusion home run screw and the neurovascular and tendinous structures at risk. METHODS: Eleven cadaveric limbs were used. Guidewires were percutaneously placed into the distal posterolateral aspect of the leg, under fluoroscopic guidance, with the ankle held in neutral position. Malpositioned guidewires were not removed and served as guidance for the following wires. The number of guidewires needed to achieve an acceptable positioning of the implant was noted. Neurovascular and tendinous injuries were assessed, and the shortest distance between the closest guidewire and the soft tissue structures was measured using a precision digital caliper. RESULTS: Mean number of guidewires needed to achieve acceptable positioning of the implant was 2.34 (SD 0.81, range 2-4). The mean distances between the closest guide pin and the soft tissue structures of interest were: Achilles tendon 5.35 mm (SD 2.74 mm); peroneal tendons 9.65 mm (SD 5.19 mm); posteromedial neurovascular bundle 12.78 mm (SD 7.14 mm). The sural bundle was in contact with the guide pin in 5/11 specimens (45.5%) and impaled in 3/11 specimens (27.3%). The average distance from the sural nerve bundle was 3.58 mm (SD 2.16 mm). CONCLUSIONS: The placement of percutaneous ankle fusion home run screws is technically demanding requiring multiple attempts for acceptable placement. Important tendinous and neurovascular structures are in close proximity to the guidewires. The sural bundle was either injured or in direct contact with the guide wire in approximately 73% of the cases. When using a home run screw, a mini-open approach is recommended. LEVEL OF EVIDENCE: Level V, cadaveric study.

Tibiofibular syndesmosis in asymptomatic ankles: initial kinematic analysis using four-dimensional CT.

AIM: To evaluate the reliability of ankle syndesmotic measurements and their changes during active motion using four-dimensional computed tomography (4DCT) examination in asymptomatic ankles. MATERIALS AND METHODS: 4DCT was performed on both ankles of patients with signs and symptoms of unilateral ankle instability. Ankles from the asymptomatic side of 10 consecutive patients were included in this analysis. Five ankle syndesmotic measurements were adopted from the available literature and performed by two fellowship-trained foot and ankle surgeons: (1) syndesmotic anterior distance (SAD); (2) syndesmotic posterior distance (SPD); (3) syndesmotic translation (ST); (4) syndesmotic tibiofibular angle (STFA); and (5) ankle tibiofibular angle (ATFA). A Monte Carlo simulation was also performed to obtain exact p-values with 99% confidence intervals. RESULTS: Excellent interobserver reliability was observed among the two readers for four out of five measurements (intra-class correlation coefficients [ICC]: 0.767-0.995, p<0.001-0.020). The ICC values for SAD were not statistically significant (ICC=0.548 and 0.569 for dorsi and plantarflexion respectively, p=0.1). Among the five measurements, only ST measurements had significant changes during active motion (median [interquartile range] for change: -0.70 mm [-1.6-0.10]; p=0.012). Of the above measurements, only the ST measurements demonstrated a negative linear association with the tibiocalcaneal angle during active motion (beta=-2.5, p=0.04). CONCLUSIONS: Reliable quantitative kinematic assessment of ankle syndesmosis can be performed using 4DCT examination. Syndesmotic measurements remain unchanged during ankle motion except for the syndesmotic translation, which tends to decrease during plantar flexion.

ERα PvuII and XbaI polymorphisms in postmenopausal women with posterior tibial tendon dysfunction: a case control study.

BACKGROUND: Posterior tibial tendon (PTT) insufficiency is considered as the main cause of adult acquired flat foot and is three times more frequent in females. High estrogen levels exert a positive effect on the overall collagen synthesis in tendons. We have previously demonstrated the association between some genetic single-nucleotide polymorphism (SNP) and tendinopathy. In the present study, we investigated the association of PvuII c454-397T>C (NCBI ID: rs2234693) and XbaI c454-351A>G (NCBI ID: rs9340799) SNPs in estrogen receptor alfa (ER-α) gene with PPT dysfunction. METHODS: A total of 92 female subjects with PTT dysfunction, with histopathological examination of the tendon and magnetic resonance image (MRI) evidence of tendinopathy, were compared to 92 asymptomatic females who presented an intact PPT at MRI for PvuII and XbaI SNPs in the ER-α gene. Genomic DNA was extracted from saliva and genotypes were obtained by polymerase chain reaction restriction fragment length polymorphism. RESULTS: The analysis of PvuII SNPs showed no significant differences in the frequency of alleles and genotypes between control and PTT dysfunction groups. The XbaI SNPs in the ER-α gene showed significant differences in the frequency of genotypes between control and test groups (p = 0.01; OR 95% 1.14 (0.55-2.33). CONCLUSIONS: The XbaI SNP in the ERα gene may contribute to tendinopathy, and the A/A genotype could be a risk factor for PTT tendinopathy in this population. The PvuII SNP studied was not associated with PTT tendinopathy.