Operative Fixation of a Humeral Shaft Periprosthetic Fracture After IlluminOss: A Case Report.

CASE: An 82-year-old man sustained a periprosthetic fracture after IlluminOss photodynamic bone stabilization system (PBSS) stabilization for an impending pathologic fracture. Nonoperative management was unsuccessful, and he subsequently underwent operative fixation, which featured lag screw fixation of the spiral distal humeral shaft fracture and osteotomy followed by plate fixation of the pathologic humeral shaft fracture. CONCLUSION: This is the first article to report this complication with IlluminOss PBSS stabilization and details regarding revision surgery.

Factors affecting fixation of the glenoid component of a reverse total shoulder prothesis.

The semiconstrained design of the reverse arthroplasty allows loads from the humerus to challenge the fixation of the glenoid component to the scapula. We examined some of the factors affecting the quality of glenoid screw fixation, including the density of the material into which the screws are placed, the purchase of individual screws, and the direction of loading in relation to screw placement. Loads were applied by the humeral component to glenoid components with different conditions of fixation. The load to failure for each set of conditions was measured and compared statistically. Load to failure was less when the glenoid component was fixed to material of lesser density. Each screw contributed to the quality of fixation; the screw nearest the point of load application made the largest contribution. Load to failure was less when the load was colinear with a line through the nonlocking holes in the base plate compared to colinear with a line through the locking holes. In performing a reverse total shoulder, surgeons should emphasize secure intraosseous placement of the fixation screws in the best quality bone available. The placement of the inferior screw appears to be the most critical.

Intramedullary reaming for press-fit fixation of a humeral component removes cortical bone asymmetrically.

Periprosthetic humeral fractures are major complications of shoulder arthroplasty. Bone removal during surgical reaming is a risk factor for these fractures. Although it is recognized that the endosteal surface of the humerus is asymmetrical whereas the reamers are symmetrical, to our knowledge, the effect of cylindrical reaming on the pattern of cortical bone removal during reaming has not been previously studied. The medullary canals of 10 cadaveric humeri (mean age, 73 years) were reamed in a manner similar to that used during humeral arthroplasty. Cortical dimensions were obtained from computed tomography scans before and after reaming. In unreamed humeri, the anterior-posterior endocortical diameter was 20% smaller than the medial-lateral diameter. The average medial-lateral diameter (15.6 +/- 2.3 mm) was significantly greater than the anterior-posterior diameter (12.5 +/- 1.9 mm) at 13 cm distal to the tuberosity (P < .00005). Successive cylindrical reaming preferentially thinned the anterior and posterior cortices. This bone loss would not be apparent on anterior-posterior radiographs. Intramedullary reaming to obtain substantial cortical contact asymmetrically removes cortical bone in a manner that may increase the risk of periprosthetic fracture.

Principles for the evaluation and management of shoulder instability.

During use of the normal shoulder, the humeral head is centered within the glenoid and the coracoacromial arch. When the shoulder cannot maintain this centered position during use, it is unstable. An unstable shoulder prevents normal function of the upper extremity. Shoulder instability is not the same as joint laxity. Joint laxity is a property of normal joints and allows the shoulder to attain its full range of functional positions. The concavity of the glenoid and the coracoacromial arch along with the passive and active forces that press the humeral head into the glenoid and the coracoacromial arch maintain the head in its centered position. This concavity-compression mechanism is dependent on the integrity of the glenoid and the coracoacromial arch, muscular compression, and restraining ligaments of the shoulder. Loss of any of these elements due to developmental, degenerative, traumatic, or iatrogenic factors may compromise the ability of the shoulder to center the humeral head in the glenoid.

Deltoidplasty: outcomes using orthobiologic augmentation.

Iatrogenic deltoid injury can result in severe shoulder dysfunction and pain. We used an augmentation patch (porcine submucosa) concomitantly to assist in deltoid repair. We prospectively studied 14 patients (mean age, 57.9 years). All underwent deltoidplasty for postoperative deltoid dehiscence with the orthobiologic patch placed around the detached deltoid and subsequent transosseous repair to the acromion (mean follow-up, 30 months [range, 24-62 months]). Ten patients underwent concomitant revision rotator cuff repair. All patients had undergone at least 1 previous operation. All improved postoperatively with regard to pain, function, or both. The mean pain level (out of 10) decreased (from 5.4 to 1.2); strength (out of 5) improved (from 3.2 to 4.4), forward elevation increased (from 93.1 degrees to 132.5 degrees), external rotation improved (from 30.8 degrees to 54.3 degrees), and internal rotation improved (from L1 to T9). Improvements were found for the mean Simple Shoulder Test score (out of 12) (from 3.6 to 7.1), Disabilities of the Arm, Shoulder and Hand score (from 68.8 to 28.8), and American Shoulder and Elbow Surgeons score (from 38.3 to 69.4). Recurrent deltoid dehiscence occurred in 2 patients (14%). Deltoid dehiscence remains an unsolved issue associated with shoulder reconstruction. Augmenting deltoid repair can improve function and diminishes pain after failed rotator cuff surgery. Careful revision surgical technique and rehabilitation might provide quality outcomes in this patient population.

An instrument to measure skeletal burden and predict functional outcome in fibrous dysplasia of bone.

UNLABELLED: An instrument to measure skeletal burden in fibrous dysplasia was developed. Biological and clinical relevance was shown by correlating skeletal burden scores with bone markers, quality of life, and ambulatory status. Childhood scores predict adult ambulatory status, and scores were unaffected when bone markers decreased with bisphosphonate treatment or aging. INTRODUCTION: Fibrous dysplasia (FD) is a skeletal disease with a broad clinical expression. There is no objective method to assess the extent of skeletal involvement or predict outcome. We developed an instrument to measure skeletal burden that correlates with physical function, health-related quality of life (HRQL), and ambulatory status. MATERIALS AND METHODS: Seventy-nine patients with FD underwent bone scintigraphy. The skeletal burden score was derived from a weighted score based on the regional measurement using bone scintigraphy to estimate the amount of FD in anatomical segments. Six readers scored 20 scans twice to determine the inter- and intrareader agreement. To assess biological significance, scores were correlated with bone markers. To assess functional outcome, scores on the SF-36 (adults) or CHQ-PF50 (children) were correlated with skeletal burden scores. In a group of patients who had bone scans as children and adults (n = 6), the ability to predict ambulatory status was tested. Skeletal burden scores were assessed in patients before and after treatment with pamidronate (n = 5). RESULTS: The inter- and intrareader agreement of burden scores were r = 0.96, and 0.98, respectively (p < 0.001 for both). The scores correlated with markers of bone metabolism and HRQL (Spearman rho, 0.54-0.67 p < 0.001 and -0.43, p = 0.001, respectively). The mean score of patients who ambulated unassisted was significantly lower than those requiring assistance (p < 0.001 unassisted versus crutch and/or wheelchair). In unassisted ambulators, younger patients had higher scores, suggesting high childhood scores may predict adulthood impairment. In six patients with childhood and adulthood scans, childhood scores >30 predicted assisted ambulation in adulthood. There was a negative correlation between bone markers and age (Spearman rho, -0.42 to -0.70; p < 0.001), but not age and skeletal burden score. Pamidronate treatment decreased serum alkaline phosphatase but had no effect on the skeletal burden score. CONCLUSIONS: This is a validated and reliable instrument for the measurement of skeletal burden of FD and is able to predict functional outcome.

Fracture incidence in polyostotic fibrous dysplasia and the McCune-Albright syndrome.

UNLABELLED: In patients with polyostotic fibrous dysplasia of bone, the peak incidence of fractures is during the first decade of life, followed by a decrease thereafter. Phosphaturia is associated with an earlier incidence and increased frequency of fractures. INTRODUCTION: Fibrous dysplasia (FD) is a disorder involving either one (monostotic) or several bones (polyostotic FD [PFD] and sometimes is associated with cafe-au-lait hyperpigmentation of the skin and one or more hyperfunctioning endocrinopathies (McCune-Albright syndrome [MAS]). Both PFD and MAS are often associated with phosphaturia. Although fractures occur frequently in PFD/MAS, fracture incidence and the effect of age and co-existing metabolic abnormalities (endocrinopathy and/or phosphaturia) on fractures are ill defined. MATERIALS AND METHODS: We reviewed the medical records and examined the endocrine and phosphorus metabolism of 35 patients with PFD/MAS. We report on the age at which extremity fractures occurred and their location and treatment. The results of endocrine and phosphorus metabolism testing and associations between age of first fractures, number of fractures, fracture rate, and metabolic abnormalities were noted. RESULTS: The average follow-up was 14.2 years (range, 2-39 years), during which 172 fractures occurred. The number and sites of fractures were 103 femoral, 25 tibial, 33 humeral, and 11 forearm. Twenty-seven patients had PFD with one or more endocrinopathies and/or phosphaturia, and eight had PFD alone. The endocrinopathies included precocious puberty (n = 19), hyperthyroidism (n = 9), growth hormone excess (n = 6), and one patient each with Cushing syndrome and primary hyperparathyroidism. Twelve patients had phosphaturia. The peak rate of fractures occurred between 6 and 10 years of age and decreased thereafter. Patients with metabolic abnormalities sustained their first fracture at an earlier age (6.9 versus 16.6 years, p < 0.005) and had a higher lifetime rate of fractures (0.29 versus 0.08 fractures/year), relative to patients with PFD alone. Phosphaturia was the single metabolic dysfunction associated with both an earlier age of first fracture (5.1 versus 16.6 years, p < 0.05) and a greater lifetime fracture rate (0.35 versus 0.08 fractures/year, p < 0.05). CONCLUSIONS: The occurrence of extremity fractures in FD peaks between 6 and 10 years of age and declines thereafter. Fractures occur earlier and more frequently in the presence of phosphaturia. These data have implications for long-term prognosis, clinical management, and interpretation of therapeutic interventions.

Characterization of gsp-mediated growth hormone excess in the context of McCune-Albright syndrome.

McCune-Albright syndrome (MAS) is a disorder characterized by the triad of café-au-lait skin pigmentation, polyostotic fibrous dysplasia of bone, and hyperfunctioning endocrinopathies, including GH excess. The molecular etiology of the disease is postzygotic activating mutations of the GNAS1 gene product, G(s)alpha. The term gsp oncogene has been assigned to these mutations due to their association with certain neoplasms. The aim of this study was to estimate the prevalence of GH excess in MAS, characterize the clinical and endocrine manifestations, and describe the response to treatment. Fifty-eight patients with MAS were screened, and 22 with stigmata of acromegaly and/or elevated GH or IGF-I underwent oral glucose tolerance testing. Twelve patients (21%) had GH excess, based on failure to suppress serum GH on oral glucose tolerance test, and underwent a TRH test, serial GH sampling from 2000-0800 h, and magnetic resonance imaging of the sella. We found that vision and hearing deficits were more common in patients with GH excess (4 of 12, 33%) than those without (2 of 56, 4%). Of interest, patients with a history of precocious puberty and GH excess who had reached skeletal maturity achieved normal adult height despite a history of early epiphyseal fusion. All 9 patients tested had an increase in serum GH after TRH, 11 of 12 (92%) had hyperprolactinemia, and all 8 tested had detectable or elevated nighttime GH levels. Pituitary adenoma was detected in 4 of 12 (33%) patients. All patients with elevated IGF-I levels were treated with cabergoline (7 patients), long-acting octreotide (LAO; 8 patients), or a combination of cabergoline and LAO (4 patients). In six of the seven patients (86%) treated with cabergoline, serum IGF-I decreased, but not to the normal range. In the eight patients treated with LAO alone, IGF-I decreased, and, in four, returned to the normal range. The remaining 4 patients were treated with a combination of cabergoline and LAO. For them, symptoms of GH excess diminished, and IGF-I decreased further, but did not enter the normal range. GH excess is common in MAS and results in a distinct clinical phenotype characterized by inappropriately normal stature, TRH responsiveness, prolactin cosecretion, small or absent pituitary tumors, a consistent but inadequate response to treatment with cabergoline, and an intermediate response to LAO.