Arthroscopic Management of Elbow Osteoarthritis.

The incidence of osteoarthritis in the general population is low, but it can be seen in manual laborers, throwing athletes, and people dependent on crutches and wheelchairs. Patients often complain of pain at the terminal extents of motion, and imaging shows osteophyte formation at the tips of the coronoid and olecranon processes as well as thickening of the bone between the coronoid and the olecranon fossae. Recent advances in arthroscopic instrumentation and techniques have led to a growing interest in the arthroscopic treatment of elbow osteoarthritis. This article provides a review of basic arthroscopic elbow anatomy and the most common procedures, including diagnostic arthroscopy, loose body removal, and arthroscopic osteocapsular and ulnohumeral arthroplasty. As techniques advance, there might be interest in further procedures including arthroscopic-assisted interpositional arthroplasty. Although complications such as persistent drainage and nerve injury are frequently mentioned with elbow arthroscopy, the actual incidence of such complications remains low.

Relative Contribution of the Subsheath to Extensor Carpi Ulnaris Tendon Stability: Implications for Surgical Reconstruction and Rehabilitation.

PURPOSE: To identify the varying contributions of the proximal and distal portions of the subsheath of the extensor carpi ulnaris (ECU) to its stability, evaluate the correlation of ulnar groove depth and ECU subluxation, and observe the effect of forearm and wrist positions on ECU stability. METHODS: Extensor carpi ulnaris tendon position relative to the ulnar groove was measured in 10 human cadaveric specimens with the subsheath intact, partially sectioned (randomized to distal or proximal half), and fully sectioned. Measurements were obtained in 9 positions: forearm supinated, neutral, and pronated and wrist extended, neutral, and flexed. Ulnar groove depth was measured on all specimens. RESULTS: In 7 of 10 specimens with an intact subsheath, the ECU tendon subluxated out of the groove in at least 1 forearm-wrist position. We noted the subluxation of the ECU tendon in all wrist-forearm positions with the exception of pronation-extension in at least 1 specimen. For partial subsheath sectioning, tendon displacement markedly increased after distal subsheath sectioning but not after proximal sectioning. For full subsheath sectioning, wrist flexion produced subluxation in all forearm positions, and forearm supination produced subluxation in all wrist positions. Maximum displacement occurred in supination-flexion. There was no correlation between ulnar groove depth and ECU subluxation. CONCLUSIONS: Mild tendon subluxation occurred in the intact specimens in most tested positions. Two positions were remarkable for their consistency in maintaining the tendon within the groove: pronation-neutral and pronation-extension. In fully sectioned specimens, the greatest subluxation occurred in supination-flexion, with supination and flexion independently producing subluxation. Partial sectioning demonstrated that the distal portion of the subsheath played a more important role than the proximal portion in stabilizing the ECU. CLINICAL RELEVANCE: Subsheath repair or reconstruction should target the distal portion of the subsheath. During postinjury rehabilitation or following surgical reconstruction, combined forearm supination and wrist flexion should be avoided.

Attrition or rupture of digital extensor tendons due to carpal boss: report of 2 cases.

We present 2 cases that demonstrate the potential for tendon involvement in the presence of a carpal boss. In the first, a patient presented with tendon rupture without antecedent pain. In the second, pain and tendon irritation prompted magnetic resonance imaging that revealed tendon fraying, which was confirmed at surgery. These cases illustrate the potential for tendinous sequelae of a carpal boss. Advanced imaging may be considered when tendon irritation is clinically suspected. Attention to the possibility of tendon rupture in the setting of an otherwise asymptomatic carpal boss is advised.

ESET histone methyltransferase regulates osteoblastic differentiation of mesenchymal stem cells during postnatal bone development.

To investigate the effects of histone methyltransferase ESET (also known as SETDB1) on bone metabolism, we analyzed osteoblasts and osteoclasts in ESET knockout animals, and performed osteogenesis assays using ESET-null mesenchymal stem cells. We found that ESET deletion severely impairs osteoblast differentiation but has no effect on osteoclastogenesis, that co-transfection of ESET represses Runx2-mediated luciferase reporter while siRNA knockdown of ESET activates the luciferase reporter in mesenchymal cells, and that ESET is required for postnatal expression of Indian hedgehog protein in the growth plate. As the bone phenotype in ESET-null mice is 100% penetrant, these results support ESET as a critical regulator of osteoblast differentiation during bone development.

Mesenchyme-specific knockout of ESET histone methyltransferase causes ectopic hypertrophy and terminal differentiation of articular chondrocytes.

The exact molecular mechanisms governing articular chondrocytes remain unknown in skeletal biology. In this study, we have found that ESET (an ERG-associated protein with a SET domain, also called SETDB1) histone methyltransferase is expressed in articular cartilage. To test whether ESET regulates articular chondrocytes, we carried out mesenchyme-specific deletion of the ESET gene in mice. ESET knock-out did not affect generation of articular chondrocytes during embryonic development. Two weeks after birth, there was minimal qualitative difference at the knee joints between wild-type and ESET knock-out animals. At 1 month, ectopic hypertrophy, proliferation, and apoptosis of articular chondrocytes were seen in the articular cartilage of ESET-null animals. At 3 months, additional signs of terminal differentiation such as increased alkaline phosphatase activity and an elevated level of matrix metalloproteinase (MMP)-13 were found in ESET-null cartilage. Staining for type II collagen and proteoglycan revealed that cartilage degeneration became progressively worse from 2 weeks to 12 months at the knee joints of ESET knock-out mutants. Analysis of over 14 pairs of age- and sex-matched wild-type and knock-out mice indicated that the articular chondrocyte phenotype in ESET-null mutants is 100% penetrant. Our results demonstrate that expression of ESET plays an essential role in the maintenance of articular cartilage by preventing articular chondrocytes from terminal differentiation and may have implications in joint diseases such as osteoarthritis.

Madelung deformity.

Madelung deformity is a rare congenital anomaly of the wrist caused by asymmetric growth at the distal radial physis secondary to a partial ulnar-sided arrest. The deformity is characterized by ulnar and palmar curvature of the distal radius, positive ulnar variance, and proximal subsidence of the lunate. It more commonly occurs in females than males and typically affects both wrists. The deformity can occur in isolation or as part of a genetic syndrome. The pattern of inheritance varies, with some cases following a pseudoautosomal pattern and many others lacking a clear family history. Nonsurgical management is typically advocated in asymptomatic patients. Few studies exist on the natural history of the condition; however, extensor tendon ruptures have been reported in severe and chronic cases. Stiffness, pain, and patient concerns regarding wrist cosmesis have been cited as indications for surgery. Various techniques for surgical management of Madelung deformity have been described, but clear evidence to support the use of any single approach is lacking.

ESET histone methyltransferase is essential to hypertrophic differentiation of growth plate chondrocytes and formation of epiphyseal plates.

The ESET (also called SETDB1) protein contains an N-terminal tudor domain that mediates protein-protein interactions and a C-terminal SET domain that catalyzes methylation of histone H3 at lysine 9. We report here that ESET protein is transiently upregulated in prehypertrophic chondrocytes in newborn mice. To investigate the in vivo effects of ESET on chondrocyte differentiation, we generated conditional knockout mice to specifically eliminate the catalytic SET domain of ESET protein only in mesenchymal cells. Such deletion of the ESET gene caused acceleration of chondrocyte hypertrophy in both embryos and young animals, depleting chondrocytes that are otherwise available to form epiphyseal plates for endochondral bone growth. ESET-deficient mice are thus characterized by defective long bone growth and trabecular bone formation. To understand the underlying mechanism for ESET regulation of chondrocytes, we carried out co-expression experiments and found that ESET associates with histone deacetylase 4 to bind and inhibit the activity of Runx2, a hypertrophy-promoting transcription factor. Repression of Runx2-mediated gene transactivation by ESET is dependent on its H3-K9 methyltransferase activity as well as its associated histone deacetylase activity. In addition, knockout of ESET is associated with repression of Indian hedgehog gene in pre- and early hypertrophic chondrocytes. Together, these results provide clear evidence that ESET controls hypertrophic differentiation of growth plate chondrocytes and endochondral ossification during embryogenesis and postnatal development.