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Biomedical subjects

D B Burr

Publications and source records attributed to D B Burr.

At least 91 records · Page 5Linked to original sources

The Maquet procedure: effect of tibial shingle length on patellofemoral pressures.

The Maquet procedure--elevation of the anterior tibial tubercle--has been recommended for treatment of symptomatic osteoarthrosis of the patellofemoral joint. Although the operation was first described 30 years ago, it remains controversial, both on a clinical and on a biomechanical basis. In addition, deterioration of the long-term results has been suggested. One of the variables that has been ignored in both clinical and biomechanical studies has been tibial shingle length. In order to judge its effect, we examined contact pressures and areas in 15 cadaver knees with 7 and 20 cm tibial shingle lengths. We found significant patellofemoral pressure diminution only with 2 cm elevations. The short anterior tibial shingle with 2 cm of elevation tipped the patella on its superior pole, with a significant change in angle between the patella and the shingle. We suggest that this creates a potentially less than desirable biomechanical circumstance and believe it may explain the discrepancies among previously published reports.

Adult↗

Remodeling and the repair of fatigue damage.

This paper reviews the direct and indirect evidence for and against the idea that bone remodeling repairs fatigue damage. It defines experiments that should be performed to determine whether the accumulation and repair of fatigue damage is relevant to the pathogenesis of osteoporotic fracture. The experimental evidence favors the hypothesis that microdamage evokes local remodeling. The data suggest that the balance between the microdamage burden and bone repair is nearly constant. The indirect evidence comes from clinical observations that show positive relationships between depressed bone formation rate or prolonged remodeling period with bone fracture. More compelling indirect evidence comes from studies in which bone remodeling was pharmaceutically depressed, and fracture incidence rose in direct proportion. Data on microdamage accumulation were not collected in these studies. Conversely, some experimental evidence disputes a direct relationship between fatigue microdamage and repair. In these studies, increased amounts of bone microdamage in hyperadrenocortical dogs, and in irradiated dogs, could not be demonstrated even though bone fragility increased without associated osteopenia. Finally, the indirect evidence that argues that microdamage does not initiate repair is based on inference and does not provide an adequate test of the hypothesis. In balance, the current body of evidence favors the contention that bone remodeling repairs fatigue damage and thereby prevents fracture. Future studies should verify that microdamage accumulates when bone fracture occurs in conjunction with depressed remodeling activation frequency.

Animals↗

Physical activity and bone mass: exercises in futility?

Growing bone responds to low or moderate exercise through significant additions of new bone in both cortical and trabecular moieties and results in adaptation through periosteal expansion and endocortical contraction. Intracortical activation frequency declines in growing bone in response to exercise, reducing porosity and the remodelling space. These adaptations can be maintained into and throughout adulthood. Young bones have a greater potential for periosteal expansion than aging bone, allowing them to adapt more rapidly and efficiently to an acute need for increased strength, but a threshold level of activity exists above which some bones respond negatively by suppressing normal growth and modelling activity, reducing geometric, mechanical and material properties in cortical and trabecular bone. From cross-sectional studies, differences in bone mass between exercising and non-exercising adults are generally less than 10%, but do not account for exercise history which may be very important, and often fail to consider important confounding variables. There is sufficient longitudinal data to demonstrate that moderate to intensive training can bring about modest increases of about 1-3% in bone mineral content (BMC) of men and premenopausal women. In young adults very strenuous training may increase BMC of the tibia up to 11% and its bone density (BD) by 7%, but may represent periosteal woven bone formation in response to excessive strain. Some evidence shows that exercise can also add bone mass to the post-menopausal skeleton, although the amounts are site-specific and relatively modest. Increases as high as 5-8% can be found after 1-2 years of intensive exercise, but additions of bone to the femur and radius are generally less than 2%, well within the range of the remodelling space and measurement precision. Although increases in bone mass of the post-menopausal skeleton may be extremely modest, physical activity is important to preserve bone mass and muscle function. Detraining reduces any bone mass increase to pre-existing values so that long-term benefits are only retained with continuing exercise. Most importantly, the amount of bone gain that can be achieved appears dependent primarily on the initial bone mass suggesting that individuals with extremely low initial bone mass may have more to gain from exercise than those with moderately reduced bone mass.

Animals↗

Microcracks in articular calcified cartilage of human femoral heads.

The purpose of this work was to determine whether microcracks occur in calcified cartilage in vivo, and to use histological techniques to separate these from artifacts caused by processing. Six femoral heads without disease were split in the frontal plane. Sections from one slab were cut to 150 microns and stained with basic fuchsin. The other slab was stained en bloc, and sections were cut to 150 microns after staining. Sections were examined microscopically, and microcrack density was calculated. Data show that microcracks occur routinely in calcified cartilage from nondiseased femoral heads of aged humans, and that they can be separated from processing artifact. Their physiological significance is unknown, but it is possible that microcracks may trigger vascular invasion of subchondral bone and may play a role in the initiation and progression of osteoarthrosis.

Aged↗

Estimated intracortical bone turnover in the femur of growing macaques: implications for their use as models in skeletal pathology.

Although macaques have been used widely to study the dynamics of bone remodeling, there have been few comparisons to skeletal tissue turnover in humans. This study analyzes variation in bone microstructure with respect to gender, age, and body weight in growing macaques to determine whether the pattern of osteonal remodelling in macaques is like that in analogous bones of humans. Histomorphometric measurements were made on femoral midshaft cross-sections of 54 macaques from the Cayo Santiago skeletal collection. These data show that variation in bone microstructure occurs independent of gender, age, and body weight in macaques. Moreover, intracortical bone turnover in the macaque femur is much slower than in humans, making them poor models to study the effects of weightlessness, but good models to study low turnover skeletal dysplasias.

Age Factors↗

Effect of groove on bone fracture toughness.

When testing for the effects of bone orientation on mode I fracture toughness, compact tension specimens are grooved with a V-notch to provide a crack guide. The effect of grooving on the expressions for the critical stress intensity factor (Kc) and the critical strain energy release rate (Gc) for mode I fracture toughness was investigated. Experiments were performed using grooved and ungrooved bovine compact tension specimens. The results indicate that the standard expression used to determine Kc for a compact tension specimen requires modification. The thickness (B) must be modified to account for the thickness between the grooves (Bn). The thickness used in the standard expression is replaced by an effective thickness written as (BBn)0.5. It was also found that the thickness between the grooves should be used in the standard formula for Gc.

Animals↗

Collagen fiber orientation and geometry effects on the mechanical properties of secondary osteons.

The effects of collagen fiber orientation and osteon geometry on the mechanical properties of secondary osteons under axial compression/tension and combined loadings (compression, bending and torsion) were investigated using a composite-beam finite-element model. Three cross-sectional shapes of secondary osteons were studied to show the effect of geometry. The results of stiffness are presented using the tension and compression properties for each lamella. The model shows that the mechanical properties of osteons are enhanced in bending and torsion when collagen fibers are oriented within 30 degrees of the loading axis. Osteons with alternating lamellar orientation are not well adapted to resist torsional moments, but alternate collagen fiber orientation has virtually no effect on the bending stiffness of osteons. Fiber orientation affects the mechanical properties less significantly when osteons are non-circular. Collagen fiber orientation and osteon geometry interact to determine the mechanical behavior of the osteon, and may act in a compensatory manner in the adaptive process.

Adult↗

Do different fluorochrome labels give equivalent histomorphometric information?

Substances that bind calcium are given to determine where and how fast bone is forming. Several vital dyes are used (tetracycline, calcein, alizarin, xylenol), but it is not known whether the histomorphometric results they provide are equivalent. This work tests whether different fluorochrome labels give the same results when they are quantitatively measured. Twelve-week-old rats (n = 58) were divided into six groups and given double labels IP of calcein, tetracycline HCl, alizarin complexone, or xylenol using a 1-7-1 scheme. Two other groups received either calcein followed by tetracycline, or tetracycline followed by calcein. Our results show that (a) tetracycline hydrochloride leads to a significant underestimation of mineralizing surface when given as the second label, probably because of its weak fluorescence; (b) there were no differences among any of the non-tetracycline labels for any of the histomorphometric measurements; (c) there was no evidence of osteoblast suppression with any label; and (d) there was no evidence that tetracycline caused increased osteoblast resting periods.

Animals↗

Morphologic and morphometric changes in synovial membrane associated with mechanically induced osteoarthrosis.

We sought to determine whether synovial leukocytic inflammation is a primary event in mechanically induced osteoarthrosis. Repetitive impulse loading (50 ms duration at 60 Hz for 40 minutes each day) was applied to the right hindlimbs of 24 New Zealand white rabbits for 3, 6, or 9 weeks. The synovial membrane from the medial suprapatellar area was examined qualitatively using transmission electron microscopy and quantitatively using light microscopic morphometry. The results indicate that synovial inflammation is not a primary event in this mechanically induced osteoarthrosis, but synovial hyperplasia occurs prior to histologically evident cartilage destruction at 6-9 weeks.

Animals↗

Mechanical determinants of osteoarthrosis.

The joint is an organ and functions as a mechanical bearing created of biological materials. In the joint, as in all connective tissues, there is a relationship between mechanical factors and tissue behavior. Therefore, it is not surprising that joint health and osteoarthrosis are reflections of both mechanical and biological factors. Osteoarthrosis is not a disease, but organ failure caused initially by mechanical factors. The biological changes follow. There is no habitual pathophysiological cascade. Osteoarthrosis is best thought of not as a common final pathway, but as a common end stage. The hypotheses that in osteoarthrosis substructural disorganization of the matrix proceeds chondrocytic enzyme production, that impulsive loading is an essential factor in the progressive cartilage destruction, and that tidemark advancement and horizontal cartilage splitting are the primary mechanisms in progressive cartilage loss are discussed.

Animals↗

Patterns of skeletal histologic change through time: comparison of an archaic native American population with modern populations.

This paper compares patterns of histologic change in an archaic Native American population with those in modern white populations. Histologic sections were removed from core biopsies taken from the anterior femoral cortex of an archeologic sample of Pecos Indians. The data demonstrate many microstructural similarities between the Pecos and modern populations, even though they were genetically and culturally distinct. Pecos women had small Haversian canals and large osteon mean wall thickness, with no clear evidence of an intracortical bone volume deficit even in the older age groups, although significant marrow cavity expansion occurred in both males and females with age. No striking relationships were found between bone tissue changes and gross geometric changes with age. The data suggest that a more active life-style is associated with greater osteon mean wall thickness or osteon population density, but that it alone does not protect against significant bone loss on the cortical-endosteal surface.

Adult↗

Bone and cartilage changes following experimental varus or valgus tibial angulation.

The purpose of this work was to determine whether subchondral bone changes are an integral part of the development of osteoarthrosis of the knee following experimentally created tibial angulation. Thirty degree varus or valgus proximal tibial osteotomies were created in female New Zealand white rabbits. Bone and cartilage changes were assessed grossly, radiologically, and histologically. Thirty-four weeks following osteotomy, severe cartilage changes, including osteophytes, fibrillation, derangement of cell columns, and cloning, were evident on the overloaded condyle, accompanied by increased subchondral bone density. The pattern of cartilage deterioration was different from that found in other experimental, mechanically induced arthroses. We conclude that osteoarthrosis is a final common pathway for mechanically induced joint failure, and that progressive cartilage change is associated with increased subchondral bone density.

Animals↗

Regional patterns of bone loss and altered bone remodeling in response to calcium deprivation in laboratory rabbits.

This study explores the effects of a calcium-deficient diet on patterns of bone remodeling, and examines regional differences in the amount of bone lost. Skeletally mature female rabbits (n = 6) were fed a calcium-deficient diet (0.10% Ca2+ and 0.50% P) for 14 weeks. A separate group of rabbits (n = 4) were fed a maintenance diet (1.2% Ca2+ and 0.45% P). Bone mineral content, serum calcium, and serum phosphorus were measured each week during the experimental period. Following sacrifice, the L3 vertebra, femoral head, proximal tibial metaphysis, and tibial midshaft were analyzed histomorphometrically. Rabbits had 20% less vertebral bone after only 14 weeks of a calcium-deficient diet. As in human postmenopausal osteoporosis, bone loss in calcium-deficient rabbits occurs in the trabecular bone of the lumbar spine before that in the trabecular bone of the lower extremity. Calcium-deficient diets alone do not lead to increased osteoid volume or thickness. Because bone loss is relatively rapid and because the pattern of loss is similar in some respects to that found in humans, adult rabbits may provide an attractive model of calcium deficiency osteoporosis in a skeletally mature mammal in which remodeling is predominant over modeling.

Animals↗

Long-term fatigue behavior of compact bone at low strain magnitude and rate.

Fatigue behavior of compact bone at physiological strain ranges was examined in vitro. Standardized specimens of bovine compact bone were cyclically loaded in uniaxial tension of 0-1200 or 0-1500 microstrain for up to 13-37 million cycles to study the long-term fatigue properties. All specimens exhibited fatigue during the first several million cycles of loading, evidenced by a gradual decrease of specimen modulus during this initial loading period; mean modulus loss for all specimens was approximately 6%. After this initial stiffness loss, specimen modulus stabilized and did not change again for the duration of the loading. Osteonal bone specimens lost significantly more stiffness than primary bone specimens during the early loading history, but neither microstructural type progressed to fatigue failure. These data suggest that some fatigue of compact bone is a realistic expectation of the normal loading environment, but this fatigue does not progress to fatigue failure within a physiologically reasonable number of cycles when tested in vitro at strain magnitudes like those measured in living animals. Implications for fatigue/stress fractures in vivo are discussed.

Animals↗

Experimental stress fractures of the tibia. Biological and mechanical aetiology in rabbits.

We have shown that stress fractures can be induced in the tibial diaphysis of an animal model by the repeated application of non-traumatic impulsive loads. The right hind limbs of 31 rabbits were loaded for three to nine weeks and changes in the bone were monitored by radiography and bone scintigraphy. The presence of stress fractures was confirmed histologically in some cases. Most animals sustained a stress fracture within six weeks and there was a positive correspondence between scintigraphic change and radiological evidence. Microscopic damage was evident at the sites of positive bone scans. The progression, location, and time of onset of stress fractures in this animal model were similar to those in clinical reports, making the model a useful one for the study of the aetiology of stress fractures.

Animals↗

Validity of the bulk-staining technique to separate artifactual from in vivo bone microdamage.

Frost's bulk-staining technique clearly separates artifactual cracking in bone from that caused by mechanical loading in vivo. One-centimeter sections of human rib were either bulk stained before preparation of a thin section (experimental) or stained after grinding to a thickness of 150 microns (control). Microdamage produced before preparation can be separated from that caused by the preparation itself. Moreover, the technique does not cause additional artifactual cracking through dehydration. This technique provides a valid way to test hypotheses about the role that microdamage creation or its repair plays in skeletal pathology.

Aged↗

Errors in bone remodeling: toward a unified theory of metabolic bone disease.

Recent evidence suggests that skeletal adaptation is organized by a functional unit that includes cells of diverse origin working in coordination. Genetic and metabolic factors control and regulate the processes of modeling and remodeling, only rarely acting on the isolated individual functions of specific cell lines. Errors in the genetic or metabolic regulation of the functional unit affect the entire process of skeletal adaptation rather than specific elements of it. Viewed in this way, some metabolic bone diseases can be understood as relatively simple errors in factors that control the coordinated activities of the entire functional unit. This paper reviews the modeling and remodeling processes and demonstrates how abnormal morphological characteristics of bone tissue can be viewed as products of specific errors in the adaptive process.

Aging↗