Human Femoral Cortical Bone Research Articles

Osteoblasts mediate interleukin 1 stimulation of bone resorption by rat osteoclasts.

A monocyte-derived factor with IL-1-like properties has recently been shown to cause resorption of bone in organ culture. We have investigated the action of IL-1 on disaggregated populations of osteoclasts, incubated alone or in the presence of osteoblastic cells, in an attempt to identify the target cell for IL-1 in bone, and to elucidate the mechanism by which IL-1 induces osteoclastic resorption. Osteoclasts were disaggregated from neonatal rat long bones and incubated on slices of human femoral cortical bone. Under these conditions, the majority of osteoclasts form distinctive excavations in the bone surface within 24 h, the volume of which can be quantified by computer-assisted morphometric and stereophotogrammetic techniques. IL-1 had no effect on bone resorption by osteoclasts alone, but when incubated in the presence of calvarial cells or cloned osteosarcoma cells, it induced a 3.8 (+/- 0.38)-fold increase in osteoclastic bone resorption, with significant enhancement at concentrations of greater than or equal to 30 pg/ml. The osteoblastic populations themselves did not resorb bone. The mechanism by which osteoblastic cells stimulate osteoclasts did not appear to depend upon PG synthesis; nor could we detect a diffusible substance in the medium of stimulated cocultures. These results indicate that IL-1 stimulates bone resorption through a primary action on osteoblasts, which are induced by IL-1 to transmit a short-range signal that stimulates osteoclastic bone resorption.

Osteoblastic Cells Mediate Osteoclastic Responsiveness to Parathyroid Hormone*

Indirect evidence suggests that cells of the osteoblastic lineage may mediate augmented osteoclastic bone resorption induced by PTH. To test this suggestion, osteoclasts were disaggregated from neonatal rat long bones and incubated on slices of human femoral cortical bone. Resorption was measured by computer-assisted morphometric and stereophotogram-metric quantification of osteoclastic excavations, identified in the scanning electron microscope after culture. We compared the effect of PTH on bone resorption by osteoclasts incubated alone with the effect of the hormone on resorption by osteoclasts cocultured with osteoblastic cells. PTH had no effect on bone resorption by osteoclasts alone, but in the presence of any of three osteoblast-containing cell populations, or in the presence of cloned, hormone-responsive osteosarcoma cells, PTH caused a 2- to 4-fold increase in osteoclastic resorption. Significant stimulation was observed at 10(-4) IU/ml PTH. None of the osteoblastic cell populations caused morphologically detectable bone resorption in the absence of osteoclasts. These results indicate that PTH acts primarily on osteoblasts, which are induced by the presence of the hormone to stimulate osteoclastic bone resorption.

Effect of substrate composition on bone resorption by rabbit osteoclasts.

Slices of human femoral cortical bone were prepared with a carborundum wheel. Osteoclasts were isolated from neonatal rabbit long bones and incubated on either untreated, demineralized or anorganic preparations of these bone slices. Anorganic bone showed extensive tracts of uninterrupted surface excavation after incubation, while untreated bone tended to show discontinuous excavations of smaller total volume; demineralized bone was not resorbed. The endosteal surface of adult rat calvaria was also used as a substrate for osteoclastic bone resorption. The endosteal surface was exposed and rendered acellular, and was used either without further treatment or after incubation in collagenase. Bone resorption occurred only in those calvaria pre-treated with collagenase. These experiments imply that osteoclastic contact with bone mineral rather than the endosteal surface is the stimulus that initiates bone-resorptive behaviour in osteoclasts. The mechanism by which osteoblasts induce osteoclastic bone resorption may be through the known ability of osteoblasts to secrete collagenase, which, by digestion of the unmineralized lamina limitans of endosteal surfaces, exposes bone mineral to osteoclastic contact.

Age-related changes in the orientation and particle size of the mineral phase in human femoral cortical bone.

It has previously been observed that after the third decade of life the tensile strength of bone decreases faster than its density [1], indicating that some microstructural change occurs in bone with advancing age. In order to try to elucidate this observation, the orientation and particle size of the mineral phase of bone have been studied with respect to age. Samples were taken from femora varying in age from 13 to 97 years. The results show that the degree of preferred orientation does not vary with age after the first decade of life. However, the percentage of small particles increased up to the fourth decade of life and thereafter decreased, a pattern of change similar to that observed for bone strength. It would seem to indicate that an increase in mineral particle size is a factor that contributes to the loss of bone strength and that an increased percentage of bone strength and that an increased percentage of large particles in the later years of life could, along with osteoporosis, help to explain the increased fragility in the bones of the elderly.

Age-related changes in the density and tensile strength of human femoral cortical bone.

In order to ascertain whether the intrinsic strength of human bone changes with age or not, we have determined the ultimate tensile strength and density of strips of femoral cortical bone. These femora were collected from cadavers varying in age from 13 to 97 years. The results show that both density and intrinsic strength of bone increase up to about the fourth decade of life and then decrease with age. However, the rate of decrease of strength is greater than that of density. This indicates that the density of bone is not the sole determining factor of its strength, and that some other factors play an important part.

Changes in the impact energy absorption of bone with age

The impact energy absorption of human femoral cortical bone decreases by a factor of about three between the ages of three and ninety. This decrease is associated with, and partially caused by, an increased mineralization of the bone. The porosity of the bone, which is highest at each end of the life span, is not dangerous in young bone but seems to exacerbate the effect of high mineralization in the old bone. Increased mineralization probably acts by decreasing the plastic deformation undergone before fracture starts. It may also make the process of crack travel less energetically expensive.

The crystallinity of bone mineral

The degree of crystallinity of human femoral cortical bone from 16 to 83 years of age was determined by various X-ray and infra-red methods. It was established that an X-ray integral index method and an infra-red peak comparison method were the most reliable. Both methods indicated that the crystallinity of bone material varies between 51 and 59%, with no significant change with age. A new X-ray line was noted at 2θ=43° in bone of age greater than 50 years.

Human femoral cortical bone: a preliminary report on the relationship between strength and density.

Tensile strength and density measurements were carried out on small samples of cortical bone taken from the lateral quadrant of the central region of the femoral diaphysis. A graph of strength against density shows that density is not the sole factor in determining bone strength, although there is a general trend of increasing strength with increasing density. Other factors must be taken into account to explain variation in bone strength.

Differences and relationships between the physical properties and the microscopic structure of human femoral, tibial and fibular cortical bone

AbstractCoefficients of correlation between certain physical properties and the histological components of the break area were calculated on an IBM 7090 computer for 56 femoral, 79 tibial and 37 fibular specimens of embalmed cortical bone of standardized size and shape. Strong positive correlations (0.01–0.02 significance level) were found between tensile strength and the percentage of interstitial lamellae in the break area; between hardness and the number of osteons/mm2; and between hardness and the percentage of osteons in the break area. Equally high negative correlations were found between tensile strength and percentage of osteons in the break area; between shearing strength and average area/osteon remnant; between elastic modulus and percentage of spaces in the break area; and an even higher correlation (0.001) between hardness and percentage of spaces in the break area. Negative correlations (at slightly more than 0.05 significance level) were found between shearing strength and modulus and average area/osteon. Osteons tend to reduce the tensile strength and elastic modulus of bone while interstitial lamellae tend to increase them. The probable reason is the relatively greater amount of cement lines, which are sites of weakness where failure can occur, in Haversian bone as compared with lamellar bone. The predominant orientation of collagen fibers and the amount and distribution of calcium may also be involved. These factors are now being investigated.