Reports of differing failure rates of total hip prostheses made of various metals prompted us to measure the size of metallic and polyethylene particulate debris around failed cemented arthroplasties. We used an isolation method, in which metallic debris was extracted from the tissues, and a non-isolation method of routine preparation for light and electron microscopy. Specimens were taken from 30 cases in which the femoral component was of titanium alloy (10), cobalt-chrome alloy (10), or stainless steel (10). The mean size of metallic particles with the isolation method was 0.8 to 1.0 microns by 1.5 to 1.8 microns. The non-isolation method gave a significantly smaller mean size of 0.3 to 0.4 microns by 0.6 to 0.7 microns. For each technique the particle sizes of the three metals were similar. The mean size of polyethylene particles was 2 to 4 microns by 8 to 13 microns. They were larger in tissue retrieved from failed titanium-alloy implants than from cobalt-chrome and stainless-steel implants. Our results suggest that factors other than the size of the metal particles, such as the constituents of the alloy, and the amount and speed of generation of debris, may be more important in the failure of hip replacements.
Biochemical and histochemical studies have indicated that there is specific cellular activity in the region of the calcification front of articular cartilage implying that a regulation process takes place there. Using scanning and transmission electron microscopy and light microscopy to examine tissue sections of both undecalcified and decalcified articular cartilage in the region of the calcification front, we have looked at its morphology with particular reference to its cellular control. Our observations show that physiological calcification is an active process under cellular control and is related to the presence of extracellular membrane-bound matrix vesicles.
The thickness of the calcified zone of the articular cartilage and the number of tidemarks at the junction between articular cartilage and bone has been determined in specimens from 41 femoral heads and 42 humeral heads from cadavers aged between 25 and 93. The thickness of the calcified zone decreased with age but the number of tidemarks increased, particularly over the age of 60. These observations suggest that remodelling of the bone ends occurs and that this process is accelerated with increasing age.
A quantitative study of the vascularity and a qualitative study of the remodelling of the calcified cartilage and subchondral bone end-plate of adult human femoral and humeral heads were performed with respect to age. In the femoral head the number of vessels per unit area was found to fall 20% from adolescence until the seventh decade and in the humeral head 15% until the sixth decade. Thereafter an increase was noted in the femur but none in the humerus. More vessels were present at all ages in the more loaded areas of the articular surfaces: 25% more for the femur and 15% more for the humerus. The degree of active remodelling by endochondral ossification declined 50% from adolescence until the seventh decade in the femoral head, and 30% until the sixth decade in the humeral head, rising thereafter to levels comparable to those found at young ages. More remodeling was noted in the more loaded areas at all ages.
1. A predictable pattern of degeneration occurs on both the femoral head and the acetabulum and this pattern is age dependent. 2. The degenerative areas on the femoral head are related to habitual non-use. 3. The hip is shown to be anatomically incongruent, and the dome of the acetabulum, a predictable area of degeneration, is shown also to be an area of habitual non-use. 4. The possible relationships between age-dependent degenerative changes and senile degenerative joint disease is discussed and the importance of changing geometry stressed.
1. Serial slices of articular cartilage obtained at necropsy from apparently normal femoral condyles of individuals between the ages of twenty-six and sixty were examined chemically, by electron microscopy and for permeability. 2. The most superficial layer was shown by chemical analysis and electron microscopy to have the highest collagen content, which fell sharply with distance from the articular surface. On the other hand the glycosaminoglycan content was very low in the superficial layers but increased with depth. This variation was found in all specimens tested but the absolute levels of collagen and of glycosaminoglycans were widely different. There was no correlation of chemical composition with age. 3. Collagen fibrils in the superficial layer were of much smaller diameter than in the deeper zones. 4. Hydraulic permeability was shown to depend more on glycosaminoglycan than on collagen content, although it varied inversely with both these factors. 5. The results obtained demonstrate clearly the close relation between the physical properties of cartilage and its chemical composition.
The collagen framework of articular cartilage is disposed, as in other connective tissues, to resist tension forces within the material. In this paper the fine structure of articular cartilage, as demonstrated by polarised light microscopy and electron microscopy, is related to the gross anatomy and to the naked eye changes of chondromalacia and fibrillation.
1. We have shown that the permeability of cartilage is the same in necropsy specimens as in the living animal. We have concluded that studies of material transport into cartilage carried out on necropsy specimens validly reflect 2. We have studied the effect of agitation of the fluid in which cartilage is immersed upon the rate of diffusion of substances into cartilage and have found that agitation increases the rate of penetration up to three or four fold. We believe that it may be inferred from this fact that the nutrition of cartilage is partly dependent on joint movement. 3. We have examined the permeability of the bone-cartilage interface to water and solutes and have found that in the adult no detectable material transfer occurs across this zone. In the child on the other hand the bone-cartilage interface appears to be permeable to water and solutes. 4. We have measured the diffusion coefficient of glucose in cartilage and have hence estimated the depth of cartilage which can be adequately supplied with glucose from the synovial fluid in the presence and absence of agitation. 5. We have examined both experimentally and theoretically the possible effect of intermittent loading on the rate of penetration of substances into cartilage. We have concluded that at low pressures intermittent loading contributes little to the material transfer into cartilage. At high pressures intermittent loading does lead to the transport of solutes into cartilage but it cannot significantly increase the rate of transfer above that attributable to normal diffusion. Loading cartilage surfaces for prolonged periods of time without allowing intermittent relaxation would be expected to lead to decreased diffusion, without any absorption of fresh fluid attributable to the action of a pump, and would thus result in an overall decrease in the rate of penetration of substances into cartilage.
