Faculty Bibliography

The history of limb-lengthening surgery can be traced back to the 19th Century. Since that time, the orthopaedic community has made tremendous progress in performing successful lengthening procedures. Among the important contributors to the field is Dr. Gavril Ilizarov. Because of advancements over the past century, limb lengthening has become a viable method of treating severe bony deformities and defects. This article, the second of a two-part series, reviews the principles of distraction osteosynthesis, including a thorough discussion of indications, instrumentation, and surgical technique.

The history of limb-lengthening surgery can be traced back to the nineteenth century. Since that time, the orthopaedic community has made tremendous progress in performing successful lengthening procedures. Among the important contributors to the field, Dr. Gavril Ilizarov remains one of the most significant innovators. Because of advancements over the past century, limb lengthening has become a viable method of treating severe bony deformities and defects. This article, the first of a two-part series, reviews the history of distraction osteosynthesis.

BACKGROUND: The recognition of the importance of femoro-acetabular impingement (FAI) as a potential cause of hip pain has been stimulated by major efforts to salvage hip joints by reconstruction to prevent or delay the need for replacement. A previous review addressed the nature of FAI, the various types, and how to make the diagnosis. When FAI occurs, the structure between the femur and acetabular rim, the labrum, is initially impinged upon and subsequently injured. METHOD: Injury to the labrum should be recognized when treating the osseous causes of FAI. Preserving or recovering labral function, enhancing hip stability and protecting the articular surface, is critical to restoring the hip to normal or near-normal mechanical and physiologic function. The present review collected the varied essential information about the labrum in a succinct manner, independent of treatment algorithms. RESULTS/CONCLUSION: Advanced knowledge of the labrum is presented, including the anatomy, circulation, histology, embryology, and neurology, as well as how the labrum tears, the types of tears, and how to make the diagnosis. The advantages and limitations of diagnostic magnetic resonance techniques are discussed, including magnetic resonance imaging (MRI), indirect magnetic resonance arthrography (i-MRA), and direct magnetic resonance arthrography (d-MRA). The review recognizes the complexity of the labrum and provides a greater understanding of how the labrum is capable of stabilizing the joint and protecting the articular surface of the hip. This information will act as a guide in developing treatment plans when treating FAI.

BACKGROUND: The recognition of the importance of femoral acetabular impingement (FAI) as a potential cause of hip pain has been stimulated by major efforts to salvage hip joints by reconstruction in order to prevent or delay the need for replacement. The purpose of this review is to define the nature of FAI, the various types, and how to make the diagnosis. METHODS: The review describes the characteristics of the hip that cause FAI and emphasizes understanding that the femoral and acetabular components normally function as a unit, complementing each other. RESULTSCONCLUSION: The methods of making the diagnosis of FAI and their limitations are described. If the acetabulum and femur are considered to be independent of each other, conflict may occur, hindering function, and not be apparent. The increasing frequency of making this diagnosis based on abnormal anatomy on one side of the joint, often in face of unclear physical findings, can bring the diagnosis into question. FAI seen in Perthes disease and acetabular dysplasia is explained. Knowing how to analyze the hip, being aware of the limitations of various available clinical and diagnostic studies, and recognizing the continued and ever-changing extensive body of literature is important and challenging. This primer is just the beginning.

BACKGROUND AND PURPOSE: Recent findings suggest that the noxious gas H(2)S is produced endogenously, and that physiological concentrations of H(2)S are able to modulate pain and inflammation in rodents. This study was undertaken to evaluate the ability of endogenous and exogenous H(2)S to modulate carrageenan-induced synovitis in the rat knee. EXPERIMENTAL APPROACH: Synovitis was induced in Wistar rats by intra-articular injection of carrageenan into the knee joint. Sixty minutes prior to carrageenan injection, the rats were pretreated with indomethacin, an inhibitor of H(2)S formation (DL-propargylglycine) or an H(2)S donor [Lawesson's reagent (LR)]. KEY RESULTS: Injection of carrageenan evoked knee inflammation, pain as characterized by impaired gait, secondary tactile allodynia of the ipsilateral hindpaw, joint swelling, histological changes, inflammatory cell infiltration, increased synovial myeloperoxidase, protein nitrotyrosine residues, inducible NOS (iNOS) activity and NO production. Pretreatment with LR or indomethacin significantly attenuated the pain responses, and all the inflammatory and biochemical changes, except for the increased iNOS activity, NO production and 3-NT. Propargylglycine pretreatment potentiated synovial iNOS activity (and NO production), and enhanced macrophage infiltration, but had no effect on other inflammatory parameters. CONCLUSIONS AND IMPLICATIONS: Whereas exogenous H(2)S delivered to the knee joint can produce a significant anti-inflammatory and anti-nociceptive effect, locally produced H(2)S exerts little immunomodulatory effect. These data further support the development and use of H(2)S donors as potential alternatives (or complementary therapies) to the available anti-inflammatory compounds used for treatment of joint inflammation or relief of its symptoms.

Objectives: We evaluated early complications of self-lengthening intramedullary nails during limb lengthening in patients with post-traumatic or growth-related limb length deficiencies. Patients and methods: A retrospective review was undertaken of all patients who underwent femoral lengthening using the Internal Skeletal Distractor (ISKD Orthofix, McKinney, Texas) device beginning September 2003 at our tertiary care center. Data from the radiographic and clinical records of 11 limbs in nine patients (mean age 24 years; range 16 to 33 years) were derived. Complications were recorded and compared to the demographic data. Results: Preoperative leg length discrepancies averaged 3.7 cm (range 2.5 to 4.8 cm) and postoperative lengthening averaged 3.1 cm (range 2.3 to 4.4 cm). The mean follow-up was 16 months (range 12 to 26 months). The nails were removed after a mean of 11.5 months (range 8 to 16 months). Complications were encountered with eight ISKD nails (72.7%). Of these, seven complications necessitated the patients returning to the operating room. The average time to reoperation was 21 days (range 4 to 37 days). Two patients had two complications per ISKD. In all, there were four nails which failed to advance and required re-osteotomy, three premature consolidations which required osteoclasis, and one runaway nail advancement of 3.0 mm/day compared to the target lengthening rate of 0.8-1.0 mm/day. Conclusion: We believe that binding at the osteotomy site was responsible for failure of nail advancement in patients in whom lengthening failed. In the light of the high complication rate, surgeons' vigilance during the postoperative period is crucial

Between 1994 and 1998, seven adolescents underwent hip arthrodesis with the use of an external fixator. Mean time of follow-up was 24.0 months after surgery. The duration of fixation and time to fusion were 6.6 months (range, 5-9.5 months) and 8.0 months (range, 5.2-15 months), respectively. At most recent follow-up, there was a significant improvement in the mean modified Harris hip score, in which the maximum score is 91 points after omitting 9 points for hip range of motion and deformity, from 25.7 before surgery to 66.7 after surgery (p < 0.01). The advantages of this procedure include (i) the ease and accuracy of obtaining the proper position for fusion, (ii) the ability to lengthen the affected leg at the same time, (iii) the diminished likelihood of compromising future hip operations, and (iv) the ability to ambulate and bear weight throughout the treatment course. We recommend this method of hip arthrodesis with external fixation for patients with intractable hip pain necessitating this procedure

Hypersensitivity to acetylcholinesterase inhibitors (anti-AChEs) causes severe nervous system symptoms under low dose exposure. In search of direct genetic origin(s) for this sensitivity, we studied six regions in the extended 22 kb promoter of the ACHE gene in individuals who presented adverse responses to anti-AChEs and in randomly chosen controls. Two contiguous mutations, a T-->A substitution, disrupting a putative glucocorticoid response element, and a 4-bp deletion, abolishing one of two adjacent HNF3 binding sites, were identified 17 kb upstream of the transcription start site. Allele frequencies for these mutations were 0.006 and 0.012, respectively, in 333 individuals of various ethnic origins, with a strong linkage between the deletion and the biochemically neutral H322N mutation in the coding region of ACHE. Heterozygous carriers of the deletion included a proband who presented with acute hypersensitivity to the anti-AChE pyridostigmine and another with unexplained excessive vomiting during a fourth pregnancy following three spontaneous abortions. Electromobility shift assays, transfection studies and measurements of AChE levels in immortalized lymphocytes as well as in peripheral blood from both carriers and non-carriers, revealed functional relevance for this mutation both in vitro and in vivo and showed it to increase AChE expression, probably by alleviating competition between the two hepatocyte nuclear factor 3 binding sites. Moreover, AChE-overexpressing transgenic mice, unlike normal FVB/N mice, displayed anti-AChE hypersensitivity and failed to transcriptionally induce AChE production following exposure to anti-AChEs. Our findings point to promoter polymorphism(s) in the ACHE gene as the dominant susceptibility factor(s) for adverse responses to exposure or to treatment with anti-AChEs