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PubMed2006

Bone remodeling is different in metaphyseal and diaphyseal-fit uncemented hip stems.

Femoral component stability in uncemented total hip arthroplasties depends on periprosthetic bone remodeling. Stem design is an important factor influencing bone remodeling, however the design that promotes the most bone remodeling is unclear. We examined metaphyseal and diaphyseal-fit stems to determine the effect of stem design on bone remodeling and stability. Twenty-three patients who had total hip arthroplasties (28 hips) with metaphyseal-fit stems were matched with 27 patients (32 hips) who had uncemented total hip arthroplasties with diaphyseal-fit stems. We assessed preoperative radiographs for canal fill, canal shape, and bone quality. We then assessed postoperative radiographs for periprosthetic bone remodeling including spot welds, cortical hypertrophy, and pedestal formation. Patients were examined clinically using a modified Harris hip score. Patients with metaphyseal stems had increased cortical hypertrophy 1 year postoperatively. However, there was no functional difference 2 years postoperatively. Both stem designs resulted in bone remodeling by 2 years postoperatively with similar clinical results.

Adult↗
PubMedDate not supplied

Increased bone remodeling in first-episode major depressive disorder.

OBJECTIVE: Bone mineral density is decreased in patients with depressive disorder. This study evaluated biochemical bone remodeling markers in patients having their first depressive episode who had not taken psychotropic medications to evaluate possible pathogenic mechanisms implicated in the loss of bone mineral density in early states of this illness. METHODS: Serum osteocalcin, parathyroid hormone, bone alkaline phosphatase, telopeptide, collagen type I C-terminal propeptide, cross-laps, and 25-hydroxyvitamin D levels were measured in 19 depressive patients and 19 age-matched healthy women. In addition, serum cortisol and interleukin-6 were determined. Patients were assessed with the Schedules for Clinical Assessment in Neuropsychiatry interview and met criteria for a single depressive episode. RESULTS: Depressed patients had increased levels of osteocalcin (p = .003), an osteoblastic marker; telopeptide (p = .01), an osteoclastic marker; and cross-laps (p = .000), another osteoclastic marker. Parathyroid hormone was lower in patients (p = .02), whereas the rest of the markers were comparable between patients and healthy control subjects. Serum cortisol was higher in depressed patients than in control subjects (p = .003), but cortisolemia and interleukin-6 did not show any relationship with bone markers in patients. Clinical severity of the illness and weight loss due to depression in patients did not correlate with bone remodeling markers. CONCLUSIONS: These data suggest that an increase in bone remodeling not due to vitamin D deficiency induces a release of calcium from bone and inhibition of parathyroid hormone secretion.

Adult↗
PubMed2006

Bone remodelling after total hip arthroplasty using an uncemented anatomic femoral stem: a three-year prospective study using bone densitometry.

PURPOSE: To evaluate the clinical, radiological, and densitometric changes in the bone-remodelling patterns of femoral stems aligned in neutral, valgus, or varus positions. METHODS: Between February and October 2000, 70 patients underwent unilateral total hip arthroplasty for primary osteoarthritis using an uncemented Anatomique Benoist Girard (ABG) II stem. 69 patients (30 males and 39 females) with a mean age of 59 years (range, 38-76 years) and a mean body weight of 79.3 kg (range, 29-110 kg) completed 3 years' follow-up on bone remodelling. The clinical, radiological, and densitometric changes of the neutral, valgus, and varus groups were evaluated, and the difference in bone-remodelling patterns between the 3 groups was analysed. RESULTS: 54 patients had neutrally placed stems, while varus and valgus malalignment occurred in 6 and 9 patients, respectively. Clinical and radiological evaluations were very similar among the 3 groups. Only densitometry could detect traceable changes resulting from the differing biomechanics of the neutral, varus, and valgus stem alignments. CONCLUSION: The ABG II stem design made moderate errors in alignment biomechanically tolerable. Alignment defects had no clinical consequences and resulted in minimal differences in bone remodelling.

Absorptiometry, Photon↗
PubMed1991

[The age dependence of traumatically induced bone remodeling as studied in the bone scintigram].

Two independent groups of patients were studied by bone scintigraphy to demonstrate age-dependent changes in the appearance time of fractures: 83 patients with 123 fractures of the spine showed neither by multiple regression analysis nor by separation into two subgroups (younger and older than 55 years) a clinically significant difference by scintimetric evaluation. A second group of 162patients with multiple trauma demonstrated no age dependence of the rate of additional bone lesions shown by scintigraphy. Instead a clear dependence on the site of the lesion and the time after trauma was found: fractures of the shafts of long bones and fractures of the pelvis and spine showed up significantly later than fractures in the neighbourhood of the distal joints. 12-14 days after a trauma all fractures may be detected with a high accuracy independently from the fracture site (except for fractures of the skull which did not show up at all in most cases). Thus, the differences in the appearing time of fractures are not age- but site-dependent.

Adolescent↗
PubMed1994

[Local factors in bone remodeling. II. Factors stimulating bone resorption].

In this article, author gives a surveillance of factors, locally produced in bone tissue, which stimulate bone resorption. Production of local factors in bone tissue cells is initiated by various hormones, including some systemic hormones. Some new hypothesis about relation of systemic hormones activity and local bone tissue factors production are described including hypothesis about function of estrogens on bone.

Animals↗
PubMed2002

Nutrition and molecular markers of bone remodelling.

PURPOSE OF REVIEW: Molecular markers of bone remodelling are noninvasive and comparatively inexpensive tools to evaluate the two major processes of bone renewal: bone formation and bone resorption. Over the past 10 years, research has generated a number of novel and specific bone markers that enable us to investigate those processes even more closely. RECENT FINDINGS: It has been known for some time that nutritional and lifestyle factors are of great importance in the development and maintenance of normal bone mass and remodelling. Recent studies suggest that hypovitaminosis D is frequent in children and adolescent persons, and may affect their bone health. Clearly, chronic eating disorders such as anorexia nervosa are associated with high rates of bone resorption and bone loss, and increased fracture risk. In obese patients weight loss is associated with changes in both bone mineral density and bone remodelling, although the pathogenesis of these changes is ill defined. SUMMARY: Nutritional and lifestyle factors influence bone mass and remodelling. Malnutrition, vitamin D deficiency, chronic and acute eating disorders, and diet-induced weight loss often induce high rates of bone resorption and bone loss.

Biomarkers↗
PubMed2006

Advanced glycation end product modification of bone proteins and bone remodelling: hypothesis and preliminary immunohistochemical findings.

BACKGROUND: The process of bone remodelling is disturbed in the development of osteoporosis. OBJECTIVE: To investigate if proteins in osteoporotic bone are modified by advanced glycation end products (AGEs), and whether these alterations are related to measures of bone remodelling based on histomorphometric findings. METHODS: Bone specimens taken from the iliac crest by bone biopsy of eight osteoporotic patients were investigated by histomorphometry and by immunohistochemical staining with the AGEs imidazolone and N(epsilon)-carboxymethyllysine. RESULTS: Both AGEs were found in all bone specimens. The intensity of staining correlated with patient age. The percentage of bone surface covered with osteoblasts showed a significantly negative correlation with the staining intensity of both AGEs. CONCLUSIONS: It is known that AGEs can regulate proliferation and differentiation of osteoblastic cells and that AGE-specific binding sites are present in cultured osteoblast-like cells. Moreover, AGE induced biological effects in these cells might be mediated by RAGE (receptor of AGE) or by other AGE receptors in different stages of osteoblast development. The inverse relation between AGE staining intensity and the percentage of bone surface covered with osteoblasts in the trabecular bone may provide evidence that AGE modification of bone proteins disturbs bone remodelling.

Adult↗
PubMed1992

An analytical and numerical study of the stability of bone remodelling theories: dependence on microstructural stimulus.

The origin of unstable bone remodelling simulations using strain-energy-based remodelling rules was studied mathematically in order to assess whether the unstable behavior was due to the mathematical rules proposed to characterize the processes, or to the numerical approximations used to exercise the mathematical predictions. A condition which is necessary for the stability of a strain-energy-based remodelling theory was derived analytically using the calculus of variation. The analytical result was derived using a simple elastic model which consists of a long beam loaded by an axial force and a bending moment. This loading situation mimics the coupling between local density and global density distributions seen in vivo. A condition necessary for a stable remodelling scheme is arrived at, but the conditions necessary to guarantee a stable remodelling scheme are not. In this remodelling scheme, the elastic modulus is proportional to volumetric density raised to an exponent n, and the microstructural stimulus is taken as the strain energy density divided by volumetric density raised to an exponent m. In order for a remodelling scheme to be stable in this loading situation, m must be greater than n. Finite-difference time-stepping is used to verify the predictions of the analytical study. These numerical studies appear to confirm the analytical studies. Physiologic interpretation of the behavior found with n greater than m indicates that this type of unstable behavior is unlikely to be observed in vivo. Since numerical approximations are not made in deriving this stability condition, we conclude that the mathematical rules proposed to characterize bone remodelling based on strain energy density should meet this condition to be relevant to physiologic bone remodelling.

Bone Density↗
PubMed1985

Bone remodeling in response to in vivo fatigue microdamage.

It has been suggested that osteonal remodeling is triggered by bone microdamage. The validity of this theory rests on the assumption that loading within the physiological range will produce substantial microdamage with relatively few load cycles. The object of the first experiment was to determine threshold values required to consistently produce fatigue microdamage in vivo. The left forelimb of five groups of dogs, characterized by different strain levels and different numbers of load cycles, were loaded in three point bending. The number of microscopic fields which contained some microdamage was calculated as a percentage of the total number of fields. This experiment indicated that loads producing strains as low as 1500 microstrain on the radius and 1400 microstrain on the ulna for 10,000 cycles will produce significant bone microdamage. A second experiment was performed to verify this threshold and to determine whether microcracks are associated with the initiation of bone remodeling. Procedures in this experiment were the same as those in the first, except that all dogs were loaded in such a way as to produce strains on the radius of 1500 microstrain for 10,000 cycles, and the dogs were sacrificed 1-4 days after loading. The loaded limb demonstrated significantly more microdamage than the control limb (p = 0.03). Moreover, we observed 44 times as many microcracks in association with resorption spaces as expected by chance alone. These data support the hypothesis that fatigue microdamage is a significant factor in the initiation of intracortical bone remodeling.

Animals↗
PubMed1992

Expression of growth hormone receptor by immunocytochemistry in rat molar root formation and alveolar bone remodeling.

Growth hormone (GH) may regulate tooth formation and bone remodeling associated with tooth eruption. This study reports the distribution of growth hormone receptor/binding protein in developing rat molars and adjacent alveolar bone by immunocytochemistry using well-characterized anti-growth hormone receptor monoclonal antibodies. These tissues represent an excellent model for studying the ontogenic changes that occur in odontogenic and osteogenic cells, as these cells are found in linear arrays displaying the various stages of morphological and functional differentiation, and differentiated function. Immunoreactivity was first seen in precementoblasts in contact with the epithelial root sheath, and preodontoblasts. However, growth hormone receptor immunoreactivity was associated primarily with the cytoplasm of odontogenic and osteogenic cells forming their respective matrices. Thus, cementoblasts and odontoblasts at sites of new matrix formation showed intense immunoreactivity whereas cementocytes and mature odontoblasts at later stages of tooth development were nonreactive. Osteoblasts engaged in intramembranous ossification in the alveolar bone were positive, although osteocytes and endosteal cells were immunonegative. Osteoclasts at sites of alveolar bone remodeling resorption were also immunopositive. These patterns of receptor expression parallel the ontogenic sequences of odontogenic and osteogenic cells and suggest that GH promotes the functional state of these cells. Our results also imply that GH may influence differentiation or differentiated functions associated with odontogenesis, osteogenesis, and bone remodeling independent of systemic insulin-like GF-I.

Alveolar Process↗
PubMed2003

Bone remodeling markers: assessment of fracture risk and fracture risk reduction.

There is an increasing repertoire of laboratory tests available for assessing the bone remodeling process. Biochemical markers of bone remodeling can be measured in serum or urine, and have a number of potential roles in the management of fracture risk. Differences in remodeling between individuals might be related to fracture risk and could be used to target therapy. Change in remodeling with therapy could be related to fracture risk reduction and the choice of therapy could be influenced by knowledge of bone remodeling. Biochemical therapeutic monitoring may improve patient understanding and therapeutic adherence. The rate of bone remodeling is weakly predictive of fracture risk in individuals who are not receiving therapy; however, it is not clear whether this is independent of other risk factors. There is increasing evidence that change in bone mineral density does not explain fracture risk reduction with antiresorptive therapies, and that therapeutic benefit might be explained by change in bone turnover. Additional studies and information are required to allow these scientific advances to be translated into cost-effective and validated clinical protocols. Optimizing the precision and accuracy of bone turnover assessment remains an important priority.

Absorptiometry, Photon↗
PubMed2006

Bone remodeling in post-menopausal osteoporosis.

Bone mass in the skeleton is dependent on the coordinated activities of bone-forming osteoblasts and bone-resorbing osteoclasts in discrete bone multi-cellular units. Remodeling of bone in these units is important not only for maintaining bone mass, but also to repair microdamage, to prevent accumulation of too much old bone, and for mineral homeostasis. The activities of osteoblasts and osteoclasts are controlled by a variety of hormones and cytokines, as well as by mechanical loading. Most importantly, sex hormones are very crucial for keeping bone mass in balance, and the lack of either estrogen or testosterone leads to decreased bone mass and increased risk for osteoporosis. The prevalence of osteoporotic fractures is increasing dramatically in the Western part of the world and is a major health problem in many countries. In the present review, the cellular and molecular mechanisms controlling bone remodeling and the influence of sex hormones on these processes are summarized. In a separate paper in this issue, the pathogenesis of post-menopausal osteoporosis will be compared with that of inflammation-induced bone remodeling, including the evidence for and against the hypothesis that concomitant post-menopausal osteoporotic disease influences the progression of periodontal disease.

Animals↗
PubMed1997

[Biochemical markers of bone remodeling in assessment of osteoporosis].

The diagnostic significance of biochemical markers of bone remodelling is limited and it should always be evaluated together with results of other methods. Unlike bone densitometry, biochemical markers do not reflect bone mass and cannot be therefore used in diagnosis of osteoporosis. Markers enable for differential diagnostics of metabolic and neoplastic bone diseases and can be used for assessment of activity of bone disease and its monitoring. Different markers reflect aspects of bone remodelling. The sensitivity and specificity of the markers differ according to the type of bone disease and its treatment. The application of markers in monitoring treatment in individual patients requires an acceptable long-term biological variability of the marker (C.V. < 12%). In postmenopausal osteoporosis, osteocalcin measurements suffice in assessment of activity of the disease and for monitoring treatment. Lack of improvement in the marker can indicate poor compliance of the patient, a diagnostic error or an and-organ resistance to treatment. The biochemical measurement predicts changes in bone mass about one year prior to bone densitometry, thus enabling for decision concerning urgency of therapeutic intervention. In individual patients, however, a single measurement of a biochemical marker cannot be used to predict long-term changes in bone mass. Osteokalcin is cleared from the circulation by kidney and cannot be used to assess bone remodelling in chronic renal failure patients. This is not true with bone-specific alkaline or acid phosphatase isoenzymes. Low serum osteocalcin concentrations have special significance in hypercortisolism. Considering their high cost, the markers should be clinically applied under specified indications and only when standardised.

Biomarkers↗
PubMed2000

The central regulation of bone remodeling.

For a long time bone remodeling has been thought to be mainly an autocrine-paracrine phenomenon. Yet bone resorption mechanisms are under the control of hormones, suggesting that the same might be true for bone formation. The recent development of molecular endocrinology uncovers a common, central regulation of bone formation, body weight and reproduction mediated by leptin.

Animals↗
PubMed1980

Haversian bone-remodeling measurements in young Beagles.

Haversian bone remodeling was measured in Beagles (8.9 to 9.9 months of age) from a colony of laboratory-raised animals. The data were compared with data in published age-related curves. There was no marked dissimilarity between the measurements of haversian bone-remodeling values in Beagles from different sources.

Age Factors↗