Normal Cartilage Surface Research Articles

Management of Bone Cyst of Talar Body by Endoscopic Curettage, Nanofracture, and Bone Graft Substitute

Large bone cyst of the talar body is frequently associated with an osteochondral lesion. The talar bone cyst can be an incidental radiologic finding. However, when the talus is extensively destroyed, there is a risk of pathologic fracture and damage to the articular cartilage, leading to persistent swelling and pain of the subtalar joint and ankle joint. Open debridement and bone grafting frequently requires extensive soft-tissue dissection or even different types of malleolar osteotomy for proper access to the lesion. The purpose of this Technical Note is to describes the technique of endoscopic curettage, nanofracture, and filling the cyst with injectable bone graft substitute. This minimally invasive approach has minimal disruption of the normal cartilage surface.

Arthroscopic Curettage and Bone Grafting of Bone Cysts of the Talar Body

Talar bone cysts can develop as a result of osteochondral lesions of the talus. This can be a source of deep ankle pain. Open debridement and bone grafting of the bone cysts requires extensive soft tissue dissection and malleolar osteotomy. Removal of normal cartilage of the talus is frequently required to approach the bone cysts. Alternatively, the cysts can be grafted arthroscopically with minimal disruption of the normal cartilage surface. The key to success is careful preoperative planning with a computed tomogram of the ankle. Bone cyst of the posterior half of the talar body can be grafted via posterior ankle endoscopy. Bone cyst of the anterior half of the talar body can be debrided and grafted via anterior talar osseous portals. The purpose of this technical note is to describe a minimally invasive approach of curettage and bone grafting of the talar bone cysts with preservation of the articular surfaces.

Effects of hyaluronic acid and γ-globulin concentrations on the frictional response of human osteoarthritic articular cartilage.

Synovial fluid plays an important role in lubricating synovial joints. Its main constituents are hyaluronic acid (HA) and γ–globulin, acting as boundary lubricants for articular cartilage. The aim of the study was to demonstrate the concentration-dependent effect of HA and γ–globulin on the boundary-lubricating ability of human osteoarthritis (OA) cartilage. Normal, early and advance stage articular cartilage samples were obtained from human femoral heads and in presence of either HA or γ–globulin, cartilage frictional coefficient (µ) was measured by atomic force microscopy (AFM). In advanced stage OA, the cartilage superficial layer was observed to be completely removed and the damaged cartilage surface showed a higher µ value (∼0.409) than the normal cartilage surface (∼0.119) in PBS. Adsorbed HA and γ–globulin molecules significantly improved the frictional behavior of advanced OA cartilage, while they were ineffective for normal and early OA cartilage. In advanced-stage OA, the concentration-dependent frictional response of articular cartilage was observed with γ–globulin, but not with HA. Our result suggested that HA and γ–globulin may play a significant role in improving frictional behavior of advanced OA cartilage. During early-stage OA, though HA and γ–globulin had no effect on improving frictional behavior of cartilage, however, they might contribute to disease modifying effects of synovial fluid as observed in clinical settings.

Appearance of Subchondral Bone in Computed Tomography Is Related to Cartilage Damage in Osteochondral Lesions of the Talar Dome

Osteochondral lesions of the talar dome (OLT) involve the articular cartilage and/or subchondral bone. The subchondral bone plate plays an important role in cartilage metabolism. We hypothesized that the findings of subchondral bone on CT image would be related to the cartilage damage of OLT. The purpose of this study was to evaluate the relationship between the arthroscopic and CT findings focused on subchondral bone. Thirty-one ankles diagnosed as OLT were analyzed. All patients underwent CT, MRI, and arthroscopic surgery. The CT findings for both the cystic and fragment lesions were classified into 3 types. The 3 types for the cystic lesion ankles were irregular shape, round shape with sclerotic wall, and irregular shape with opening to an articular cavity. The 3 types for the fragment lesion were no bone absorption, bed absorption without fragment absorption, and bed sclerosis and fragment absorption. The subchondral bone findings on CT were compared with International Cartilage Repair Society (ICRS) grades and arthroscopic grading. All round and sclerotic cystic lesions revealed cartilaginous flap lesions with a nearly normal cartilage surface. An irregular shape with opening revealed an unstable lesion with severely damaged cartilage. As for fragment lesions, no absorption revealed a stable lesion with a nearly normal cartilage surface. Bed absorption revealed an unstable lesion with a nearly normal cartilage surface. Fragment absorption with bed sclerosis showed an unstable lesion with severely damaged cartilage. There was a significant difference between CT findings and ICRS grade or arthroscopic findings (both P < .01), while there was no significant difference with MRI grading. The diagnosis of cartilage status by CT was better than MRI. CT findings for OLT based on subchondral bone related to cartilage damage. This study showed that CT was a useful tool for evaluating cartilage damage in OLT. Level III, comparative case series.

Polymorphonuclear leukocyte adhesion to articular cartilage is inhibited by cartilage surface macromolecules.

The present studies deal with polymorphonuclear neutrophil (PMN) adhesion inhibitory properties of cartilage surface proteoglycans. Normal human PMN were used in adhesion experiments with bovine cartilage surfaces exposed to neutrophil elastase and reconstituted with fibronectin (Fn) or on plastic-bound Fn. An extract of cartilage surface small proteoglycans (SE) and purified fibromodulin (FM), decorin (DCN), biglycan (BGN), and aggrecan (AGN) on the surface of normal cartilage were used to test for inhibition of Fn-dependent cell adhesion. The PMN did not adhere to intact articular cartilage surfaces, whereas significant adhesion was measured using cartilage explants digested with elastase and reconstituted with Fn. Incubation of elastase-treated, Fn-reconstituted cartilage with 45 microg/ml SE inhibited PMN adhesion by 50.7 +/- 5.8% (P < 0.0001). Addition of 50 microg/ml purified FM to the reconstituted articular surfaces inhibited cell adhesion by 71.2 +/- 13.9% (P < 0.0001). Inhibition of PMN adhesion to plastic-bound Fn was seen with 1.7 microg/ml SE (20.4 +/- 8.0%). Maximal inhibition of 67.4 +/- 14.8% (P < 0.01) was obtained with 17.0 microg/ml SE. With FM, concentrations of 4.3 microg/ml resulted in 34.7 25.2 inhibition (P < 0.001), and maximal inhibition of 66.3 16.2% (P < 0.01) was obtained with 43.0 microg/ml. Similar results were obtained with purified bovine DCN and BGN. The main component of cartilage matrix, AGN, failed to inhibit cell adhesion significantly. The results indicate that macromolecules normally present on articular cartilage surfaces act as a barrier to PMN adhesion. Since cartilage surface proteins are susceptible to breakdown by proteases from synovial fluid inflammatory cells, we postulate that the degradation of this barrier may be responsible for increasing PMN adhesion and subsequent cartilage damage in inflammatory arthritis.

Phospholipid composition of articular cartilage boundary lubricant

The mechanism of lubrication in normal human joints depends on loading and velocity conditions. Boundary lubrication, a mechanism in which layers of molecules separate opposing surfaces, occurs under severe loading. This study was aimed at characterizing the phospholipid composition of the adsorbed molecular layer on the surface of normal cartilage that performs as a boundary lubricant. The different types of phospholipid adsorbed onto the surface of cartilage were isolated by extraction and identified by chromatography on silica gel paper and mass spectroscopy. The main phospholipid classes identified were quantified by a phosphate assay. Gas chromatography and electrospray ionization mass spectrometry were used to further characterize the fatty acyl chains in each major phospholipid component and to identify the molecular species present. Phosphatidylcholine (41%), phosphatidylethanolamine (27%) and sphingomyelin (32%) were the major components of the lipid layer on the normal cartilage surface. For each lipid type, a mixture of fatty acids was detected, with a higher percentage of unsaturated species compared to saturated species. The most abundant fatty acid observed with all three lipid types was oleic acid (C18:1). Additional work to further quantify the molecular species using electrospray ionization mass spectrometry is recommended.

Finite Element Analyses of Repaired Articular Surfaces

The response to a compressive load of a repaired cartilage surface, consisting of full-thickness repair tissue adjacent to normal cartilage, was predicted by the u-p finite element method and compared to that of a normal cartilage surface under the same loading conditions. By individually varying the aggregate modulus, permeability and Poisson's ratio for the repair tissue, analyses were performed to assess the contributions of each to the changes in mechanical behaviour. In comparing the repaired to normal surfaces, the presence of a softer repair tissue resulted in increased axial and decreased radial deformations at any given time point, while a repaired surface with an increased permeability compressed more easily due to the increased fluid flow and caused equilibrium to occur sooner. For smaller Poisson's ratio, the axial deformation was not different from normal if the aggregate modulus was the same as normal; however, the radial expansion was reduced as the repair tissue experienced a larger volume change. These results indicate that the presence of repair tissue in a joint surface can have a strong influence on the mechanical behaviour of the surface.

Scanning Electron Microscopy of Human Articular Cartilage

Specimens of human normal and osteoarthritic cartilage obtained during surgical procedures were washed with normal saline to remove gross debris and synovial fluid, fixed in 0.1% glutaraldehyde in Ringer's solution for periods varying between one and four hours, dehydrated in graded acetone solutions and air dried. They were coated with a layer of carbon(100A°) and gold palladium alloy(200A°) and examined in a JSM-U3 SEM.The articular surface of normal cartilage appeared undulated and was composed of a dense irregular network of fibers approximately 0.1 micron thick.(Fig.1) Ridges on the surface measuring between 2 and 6 microns in width were frequently noted in a parallel, intersecting, or random pattern.