Assessment of inducible fracture micromotion in distal radial fractures using radiostereometry.

OBJECTIVES: This study examined the potential for measuring dynamic inducible micromotion (DIMM) between fragments in healing distal radial fractures using radiostereometry (RSA). DESIGN: Prospective imaging study. SETTING: University teaching hospital. PATIENTS: Nine patients with low-impact distal radial fractures. INTERVENTION: Volar locked plating of the fracture with insertion of tantalum beads into bone fragments. RSA examinations at 1 day and then 2, 6, 26, and 52 weeks. Motion at the fracture site was induced by maximal voluntary hand grip using a Jamar dynamometer. Radiographs were analyzed using locally developed and UMRSA software. MAIN OUTCOME MEASUREMENTS: DIMM and migration were calculated as translations and rotations of the main distal segment. Clinical precision was assessed under repeatability conditions. RESULTS: Precision (as 95% error limit) ranged from 0.06 to 0.13 mm and 0.5 to 0.8 degrees for migration, and from 0.10 to 0.14 mm and 0.6 to 1.0 degrees for DIMM. DIMM was characterized by axial and dorsal compression with dorsiflexion. The median DIMM of patients reached a maximum at 2 weeks: mainly as 0.3 mm axial compression, 0.3 mm dorsal compression, and 2.5 degrees dorsiflexion. DIMM ceased by 26 weeks, indicating union of all fractures. Fracture collapse continued until the 26-week measurement, ranging between 0.2 and 2.8 mm axially. Instability of some intraosseous markers was observed. CONCLUSIONS: The precision of this RSA method was sufficient to observe inducible movements occurring during fracture healing. This has the potential for quantifying rates of fracture union and improving understanding of the available treatments.

Expression of Fhit, cell adhesion molecules and matrix metalloproteinases in atypical adenomatous hyperplasia and pulmonary adenocarcinoma.

Invasive parenchymal-type lung adenocarcinoma develops from atypical adenomatous hyperplasia (AAH), through an intermediate in situ stage of bronchioloalveolar carcinoma (BAC). We examined the expression of the putative tumour suppressor gene product Fhit, cell adhesion molecules CD44v6, E-cadherin and beta-catenin, and matrix metalloproteinase 2 and its inhibitor, TIMP-2, in a range of AAH lesions, BACs and invasive adenocarcinomas, to determine the changes in molecular expression associated with this form of neoplastic progression. Sections of formalin-fixed wax-embedded archival tissue were stained by standard Immunohistochemical techniques and scored semi-quantitatively, resulting in a grading of negative/low- or high-level staining. Fhit protein was retained at high levels in over 90% of AAH and 83% of BAC, but was found in only 6% of stromally invasive tumours (p < 0.0001). CD44v6 staining was high-level in 64% of AAH but fell to 26% in stromally invasive tumour (p = 0.007). E-cadherin and beta-catenin showed the opposite, with more high-level staining as adenocarcinoma developed (p < 0.001). High-level MMP-2 and TIMP-2 expression was relatively infrequent in AAH (32% and 40% respectively), rose in BAC (89% each) but fell in stromally invasive tumour (31% and 17% respectively) (p < 0.01). Unlike in central bronchial carcinogenesis, loss of Fhit expression is a relatively late event in this putative progression of lung adenocarcinogenesis, and has potential as a surrogate marker of invasion, which could be of value in screening patients for lung cancer. Loss of CD44v6 expression follows the convention of falling adhesion molecule expression as malignancy develops. Increased expression of E-cadherin and beta-catenin may reflect increased cell-cell contact as tissue architecture changes in the transition from AAH to adenocarcinoma. Loss of MMP-2 and TIMP-2 in stromally invasive tumour may reflect a particular role for MMP-2 at the BAC stage, with later down-regulation of this particular enzyme.