Delayed unions and nonunions of stress fractures in athletes

From 1971 to 1985, 369 athletes presented to us with stress fractures. Of these patients, 10% (37) were treated for development of delayed unions or nonunions. Twenty-seven of the patients were male and 10 were female. Their mean age was 23.1 years (range, 17 to 39). About half of the athletes were involved in endurance sports. The diagnostic criteria for a delayed union or nonunion were clinical and radiological evidence. There was a diagnostic delay of about 3.5 months in the series. Plain radiographs, tomography, and isotope scans were used in the diagnosis. Special radiographic views were also used. In 15 cases (10 hallux sesamoid bone fractures, 1 midtibial shaft fracture, 1 metatarsal V base fracture, 1 tarsal navicular fracture, 1 olecranon fracture, and 1 proximal tibial shaft fracture) nonoperative treatment was used. Operative treatment was used 22 times (5 sesamoid fractures, 5 midtibial fractures, 5 metatarsal V base fractures, 3 tarsal navicular fractures, 3 olecranon fractures, and 1 proximal tibial shaft fracture). Results were good or excellent in 32 cases (86.5%), moderate in 4 cases, and poor in 1 case.     

Array comparative genomic hybridization analysis of olfactory neuroblastoma.

Olfactory neuroblastoma is an unusual neuroectodermal malignancy, which is thought to arise at the olfactory membrane of the sinonasal tract. Due to its rarity, little is understood regarding its molecular and cytogenetic abnormalities. The aim of the current study is to identify specific DNA copy number changes in olfactory neuroblastoma. Thirteen dissected tissue samples were analyzed using array comparative genomic hybridization. Our results show that gene copy number profiles of olfactory neuroblastoma samples are complex. The most frequent changes included gains at 7q11.22-q21.11, 9p13.3, 13q, 20p/q, and Xp/q, and losses at 2q31.1, 2q33.3, 2q37.1, 6q16.3, 6q21.33, 6q22.1, 22q11.23, 22q12.1, and Xp/q. Gains were more frequent than losses, and high-stage tumors showed more alterations than low-stage olfactory neuroblastoma. Frequent changes in high-stage tumors were gains at 13q14.2-q14.3, 13q31.1, and 20q11.21-q11.23, and loss of Xp21.1 (in 66% of cases). Gains at 5q35, 13q, and 20q, and losses at 2q31.1, 2q33.3, and 6q16-q22, were present in 50% of cases. The identified regions of gene copy number change have been implicated in a variety of tumors, especially carcinomas. In addition, our results indicate that gains in 20q and 13q may be important in the progression of this cancer, and that these regions possibly harbor genes with functional relevance in olfactory neuroblastoma.     

Rupture of the distal biceps tendon. A report of 19 patients treated with anatomic reinsertion, and a meta-analysis of 147 cases found in the literature

We present a series of 19 avulsions of the distal tendon of the biceps brachii muscle after a follow-up of 2 to 11 years. Ten patients with delayed diagnosis and treatment (3 weeks to 5 months) were compared with nine patients treated early (within 8 days after injury). Excellent or good results at follow-up were obtained in 9 of 10 patients in the delayed-treatment group and in all 9 patients in the early-treatment group. Nine of 10 patients in the delayed-treatment group and all patients in the early-treatment group had been able to return to their preinjury levels of activity. For reference, a meta-analysis of 147 cases reported previously was performed. Ninety percent of the patients treated with an anatomic reinsertion had excellent or good results after an average follow-up of 3 years, while similar results after 3 years were seen in 60% of the patients who had nonanatomic tendon reinsertion and in 14% of the patients who were treated nonoperatively. The delay of up to 3 years between injury and anatomic reinsertion had not compromised the result. From these data we concluded that anatomic reinsertion of the avulsed distal biceps tendon to the radius is the preferred treatment in acute as well as chronic injuries.     

Avulsion fractures in athletes.

34 cases of avulsion fractures are described. Each fracture took place during athletic training or competition. Excepting six sportsmen participating in a general fitness programme, every patient was an active competitive athlete. There were six women and 28 men; their average age was 20.1 years, raised by a few middle-aged "fitness sportsmen". Most avulsion fractures took place in sprinters and hurdlers; next were middle and long distance renner, footballers, fitness joggers, skiers and ice-hockey players. The most usual location of a fracture was the anterior pelvic spines; avulsion fractures were also detected in various parts of lower limbs. There were fewer avulsion fractures in the area of the trunk and upper extremities. Roetgenologically, the diagnosis of an avulsion fracture is generally easy to make. However, the diagnosis is facilitated by knowing the mechanism of the injury, the technique of the athletic event, and some of the training methods. Generally, a fracture heals well, even if it requires both sufficient immobilisation and some delay in resuming physical exertion.     

p53Mutations and Presence of HPV DNA Do Not Correlate with Radiosensitivity of Gynecological Cancer Cell Lines

Objective.The correlation betweenp53tumor suppressor gene mutations and the presence of high-risk human papillomavirus (HPV) DNA with thein vitroradiosensitivity of gynecological malignancies was studied in 26 cell lines derived from gynecological cancers of 23 patients.Methods.Comparison of the intrinsic radiosensitivity was performed with mean inactivation dose (D?) determined with the 96-well plate clonogenic assay.p53mutations were investigated with polymerase chain reaction and single-strand conformation polymorphism (PCR–SSCP) analysis and direct DNA sequencing, and the presence of HPV DNA was studied with PCR using HPV consensus primers.Results. p53mutations were found in 6 of 10 vulvar squamous cell carcinoma (SCC) lines. Nine vulvar and 1 vaginal SCC cell lines were HPV DNA negative and 1 vulvar cell line was HPV 16 positive. All 4 cervical SCC lines were HPV positive and possessed the wild-typep53.Three cell lines expressed HPV 16 and 1 HPV 68. Among 10 endometrial cancer cell lines, 2 cell lines with mutantp53and 1 HPV 16 positive cell line were found. No correlation could be demonstrated between inactivation of thep53gene and radiosensitivityin vitro;the cell lines were evaluated as one group or according to their anatomical origin or histology.Conclusion.Our results indicate that inactivation of thep53gene through mutation or binding with HPV DNA does not increase the resistance of gynecological malignancies to ionizing radiationin vitro.     

Biallelic inactivation of fumarate hydratase (FH) occurs in nonsyndromic uterine leiomyomas but is rare in other tumors

Germline mutations in the fumarate hydratase (FH) gene at 1q43 predispose to dominantly inherited cutaneous and uterine leiomyomas, uterine leiomyosarcoma, and papillary renal cell cancer (HLRCC syndrome). To evaluate the role of FH inactivation in sporadic tumorigenesis, we analyzed a series of 299 malignant tumors representing 10 different malignant tumor types for FH mutations. Additionally, 153 uterine leiomyomas from 46 unselected individuals were subjected to and informative in loss of heterozygosity analysis at the FH locus, and the five (3.3%) tumors displaying loss of heterozygosity were subjected to FH mutation analysis. Although mutation search in the 299 malignant tumors was negative, somatic FH mutations were found in two nonsyndromic leiomyomas; a splice site change IVS4 + 3A>G, leading to deletion of exon four, and a missense mutation Ala196Thr. The occurrence of somatic mutations strongly suggests that FH is a true target of the 1q43 deletions. Although uterine leiomyomas are the most common tumors of women, specific inactivating somatic mutations contributing to the formation of nonsyndromic leiomyomas have not been reported previously. Taking into account the apparent risk of uterine leiomyosarcoma associated with FH germline mutations, the finding raises the possibility that also some nonsyndromic leiomyomas may have a genetic profile that is more prone to malignant degeneration. Our data also indicate that somatic FH mutations appear to be limited to tumor types observed in hereditary leiomyomatosis and renal cell cancer.