Metallosis is a combined chemical and toxic reaction which, if the wear of a metal implant is large, may cause extensive reaction of synovial membrane and thus triggering the loosening. We present a case of a 72 year-old man, who underwent to a cemented unicompartimental porous metal coated knee implant because affected by rheumatoid arthritis complicated by osteonecrosis of medial femoral condyle of the knee. Four years after replacement, the patient presented symptoms included moderate swelling, pain, synovitis inability to bear full weight as well as grinding; plain radiographs shows well fixed implant and not finding of loosening of prosthesis; arthroscopy revealed the diagnosis of metallosis. The specimens of synovial tissue were prepared to observation to light and electron microscopy. Total synovialectomy and revison with total knee replacement were successful in relieving the symptoms. Arthroscopy examination revealed a posterior break of tibial component, source of the release of multiple metal beads; we observe alsogray black discoloration of hypertofic and hyperplastic synovium pannus like; metal beads were detected in the joint space soft tissue and were also embedded in the articulating surface of the tibia component. Microscopic examination shows metal debris as black aggregates and a diffuse sheet like proliferation inside histiocytes of villous membrane. Ultrastructural study demonstrate that the presence of metallic fragments, measuring less than 0.3 micron in diameter is predominantly concentrated inside the macrophage’s phagolisosomes. Delivery of large number of metal beads from implant and the release of smallest size metal debris play a pivotal role in the development of a foreign body granulomatous reaction. The failure of unicompartimental prosthesis has been accellerated by unperformed sinoviectomy during the first implant; the cells of synovial membrane are continuosly activated, by wear of implant material, to phagocitate and to secrete inflammatory response.
The compressive stiffness of cartilage is primarlly determined by proteoglycan, whereas the tensile properties are determined by collagen fibres. The first alteration in cartilage structure during cartilage degeneration is the decrease in proteoglycan content and increase in interstitial water; consequently, cartilage becomes softer and cartilage stiffness decreases. The pupose of our study was to evaluate arthroscopically the compressive stiffness of cartilage in different areas of living human knee joints. Detection of softening is revealed in vivo by using an indentation instrument (artscan 200). The instrument is composed of a measurement rod joined to the handle; in the distal end of the rod, there is an inclined flat surface with a separate plane –ended cylindrical indenter. During measurement the distal end of the instrument is pressed against the articular surface while the indenter imposes constant deformation on the cartilage. The maximal indenter force, by which the tissue resists the constant deformation, is measured with strain gauge transducers. We performed indenter tests in knees joints in which cartilage was diagnosed as normal; stiffness of articular cartilage was also measured during arthroscopy in knees before ACL reconstruction, in knees with closed chondromalacia (ICRS grade 0–1) and in osteochondral lesions (ICRS OCD grade 1) and the data compared with areas of normal cartilage.
