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L Mosekilde

Publications and source records attributed to L Mosekilde.

At least 127 records · Page 7Linked to original sources

[Diuretics and osteoporosis].

Thiazide diuretics lower while loop diuretics promote calcium excretion by the kidney. Several studies have found thiazide use to be associated with higher bone mineral density and some have found that thiazides reduce the risk of hip fracture. The mechanisms by which thiazides favour preservation of the bones are uncertain. Thiazide use results in decreased renal calcium excretion and thiazide users have been shown to have lower levels of S-PTH and S-1,25-dihydroxy-vitamin D. The beneficial bone effects may result from a decrease in PTH-stimulated bone resorption and an associated reduction in the bone turn-over rate. Whether loop diuretics increases the bone turn-over by augmenting the urinary calcium excretion is more controversial as only few studies have been carried out on loop diuretics. However, in these studies the use of loop diuretics have been associated with decreased bone mineral density and increased risk of fractures. Future research should determine the minimal dose of thiazide therapy necessary to produce a sustained hypocalciuric effect and in addition the influence of diuretic dose on bone turn-over. Equally important is the need to evaluate potential unwanted effects of loop diuretics. In the mean time, thiazide diuretics may be used safely while some caution is necessary in the long term use of loop diuretics in patients who are prone to osteoporosis.

Aged↗

Components of variance when assessing the reproducibility of body composition measurements using bio-impedance and the Hologic QDR-2000 DXA scanner.

This study evaluated the reproducibility of measuring lean tissue mass (LTM), fat mass(FM(DXA)), bone mineral content (BMC) and density (BMD) with a Hologic QDR-2000 DXA scanner, and both fat free mass (FFM(bio)) and fat mass (FM(bio)) with an impedance meter. Furthermore, the study aimed to assess whether sheets and pillows significantly altered the DXA results. Fifty-one healthy volunteers aged 20-61 years were examined before and after repositioning (n = 20), removal of the sheets (n = 10), addition of two foam pillows (n = 11) or a regular pillow (n = 10). One to 7 days later a re-examination was performed (n = 35). Eight surgical patients were also scanned twice 1-7 days apart. The day to day coefficients of variation were about 1% for most measurements, though more than 2% for FM(DXA), and FM(bio). For total tissue mass, LTM, and BMC there was a significant biological day to day variance whereas for the other measurements the day to day variation could be accounted for by just measurement variance. Pillows systematically changed the estimates of bone mineral and soft tissue, but sheets did not.

Journal Article↗

A comparison of the effects of two anabolic agents (fluoride and PTH) on ash density and bone strength assessed in an osteopenic rat model.

The aim of this investigation was to compare the effects of sodium fluoride (NaF) and parathyroid hormone (PTH) on ash density and strength in an osteopenic rat model. The study comprised 66 female virgin rats divided into the following 11 groups, each comprising six animals: baseline controls; baseline ovariectomized (ovx); intact controls (5 and 16 weeks), ovx controls (5 and 16 weeks); ovx-treated with PTH (0.02 mg/kg per day, 5 and 16 weeks); ovx treated with NaF (10 mg/kg per day, 5 and 16 weeks); ovx-treated with NaF (1.0 mg/kg per day, 16 weeks). Ovariectomy was performed at 12 weeks of age, 14 weeks prior to start of treatment. Ash density, bone fluoride content, and biomechanical analyses were performed on femoral cortical bone, the right femoral neck, and the sixth lumbar vertebral body. ovx had no effect on cortical bone, whereas the femoral neck displayed a significantly lower bone strength in ovx baseline animals compared with intact baseline rats (p < 0.05). Vertebral ash density was found to be significantly decreased in ovx rats after 5 and 16 weeks (p < 0.05). Treatment with fluoride had little effect on the osteopenic rat skeleton. Cortical ash density was significantly lower than ovx and intact groups in the high-dose-treated rats after 5 (p < 0.01) but not after 16 weeks. High doses of fluoride for 16 weeks induced a significant increase in maximum load and normalized strength in cortical bone when compared with intact animals (p < 0.05), but not at the other bone sites. Cortical bone strength was not different from the ovx animals at either timepoint. In fluoride-treated animals, femoral neck bone strength, vertebral body bone strength, bone quality, and ash density were found to be at about ovx levels and, in the vertebral body, significantly lower than intact animals (p < 0.05, p < 0.01). In contrast, treatment with PTH increased ash density, bone strength, and bone quality to above ovx levels (p < 0.01), and above the level of the intact animals also, although significant values were reached for cortical bone strength only (p < 0.01). Additionally, biomechanical competence and ash density measurements were significantly higher in PTH-treated rats compared with fluoride-treated rats. In conclusion, this study has shown that PTH has a highly anabolic effect and is capable of effectively restoring ovx-induced loss of bone mass and biomechanical competence. In addition, in this osteopenic rat model, PTH proved much more advantageous than treatment with fluoride, which failed to restore the ovx-induced loss of bone strength.

Animals↗

No loss of biomechanical effects after withdrawal of short-term PTH treatment in an aged, osteopenic, ovariectomized rat model.

The aim of the study was to assess the biomechanical effects of short-term PTH treatment and withdrawal on bone mass and strength in an aged, osteopenic, ovariectomized (ovx) rat model. Additionally, the effect of sequential therapy with PTH and the bisphosphonate, risedronate, the effect of longterm PTH monotherapy, and the effect of long-term risedronate monotherapy were assessed. 96 4-month-old rats were randomized into nine groups. Eight groups were ovariectomized and one group was sham operated. 12 months after surgery, treatment regimens were initiated (OW) and were continued for either 2 weeks (2 W) or 12 weeks (12 W). The treatment regimens were as follows: (1) baseline ovx (OW); (2) ovx-saline (2 W); (3) ovx-PTH 1-34 (2 W); (4) intact-saline (12 W); (5) ovx-saline (12 W); (6) ovx-risedronate (12 W); (7) ovx-PTH 1-34 (12 W); (8) ovx-PTH 1-34 (2 W), followed by pause (10 W); and (9) ovx-PTH 1-34 (2 W), accompanied by risedronate (12 W). The effect of therapy (endpoint) was measured at three skeletal sites: vertebral bodies; femoral cortical bone; and femoral necks. The results revealed an anabolic, time-dependent effect of PTH 1-34 at all skeletal sites. No loss of anabolic effect was observed 10 weeks after discontinuation of 2 week PTH treatment in this rat model. Risedronate given in sequential therapy with PTH produced no significant effect on biomechanical properties at any skeletal sites when compared with 2 week PTH followed by a 10 week pause. However, when risedronate was given alone, a positive effect was seen at the vertebral site after a 12 week treatment. On the basis of this study with short-term PTH treatment of aged, osteopenic, ovariectomized rats, there seemed to be a significant effect of PTH on the biomechanical properties and no loss of effect even 10 weeks after PTH withdrawal.

Aging↗

Primary hyperparathyroidism: biochemical markers and bone mineral density at multiple skeletal sites in Danish patients.

Biochemical bone markers and bone mineral density (BMD) in spine, hip, and forearm were measured, before surgery, in 30 patients with mild to moderate primary hyperparathyroidism (PHP) (25 women and 5 men; mean age 54 +/- 12 years, range 26-73 years) and compared with normal controls. A group of 291 healthy adults (181 women and 110 men) served as controls for BMD. A smaller group of 30 normal individuals (25 women and 5 men; mean age 54 +/- 12 years; range 26-74 years) were used as matched normal controls. Parameters of bone formation (s-osteocalcin, s-alkaline phosphatase activity, and s-bone isoenzyme alkaline phosphatase activity) and bone resorption (s-type-1 collagen telopeptide) were considerably increased in patients with PHP compared with normal controls (p < 0.01 for all parameters). BMD was found to be reduced in the hip (trochanteric: 95.1 +/- 14.7% of expected, p < 0.05; intertrochanteric: 95.2 +/- 13.8% of expected, p < 0.05), and the forearm (proximal: 93.3 +/- 12.2% of expected, p < 0.05; mid: 91.8 +/- 11.6% of expected, p < 0.001; distal: 90.7 +/- 13.1% of expected, p < 0.001). Spine BMD was found significantly reduced in premenopausal (87.8 +/- 7.6% of expected, p < 0.05) but not in postmenopausal patients, and although normal women showed a decrease in spinal BMD with increasing age this was not found in the PHP women. Forearm BMD was reduced in both pre- and postmenopausal patients (distal forearm: 86.7 +/- 12.2% of expected, p < 0.05; 87.6 +/- 12.1% of expected, p < 0.01, respectively). It was concluded that Danish patients with mild or moderate PHP have only small reductions in BMD. The bone loss is mainly found in the appendicular skeleton.

Adult↗

Nondestructive determination of iliac crest cancellous bone strength by pQCT.

The close relationship between apparent bone density and compressive strength is well established. In clinical situations, histomorphometry and determination of the compressive strength on bone biopsies are destructive methods and require two separate biopsies from each patient. The aim of this study was to evaluate whether volumetric bone density measured by peripheral quantitative computed tomography (pQCT) could be used as a nondestructive method for estimating trabecular bone strength of iliac crest bone biopsies, thereby allowing the same biopsy to be used for subsequent histomorphometry. Materials consisted of trabecular bone samples prepared from unilateral transiliac crest bone samples obtained at autopsy [total 95 specimens; 41 females (21-90 years) and 54 males (23-87 years)]. From these, the apparent density of the cancellous bone was evaluated by pQCT in a 1-mm-thick slice in the middle of the biopsy and also by ash density measurement. Bone strength was measured by compression test. A strong power relationship was found between density measured by pQCT and compressive strength (r = 0.93, p < 0.00001). Likewise, there was a strong power relationship between ash density and compressive strength (r = 0.97, p < 0.00001). A linear correlation was found between pQCT measurement and ash density (r = 0.98, p < 0.00001), indicating a very high accuracy for the pQCT measurement. In conclusion, pQCT provides a very good estimate of cancellous bone strength. This nondestructive assessment of strength of iliac crest bone biopsies thereby enables biomechanical information as well as histomorphometric measurements to be obtained from the same biopsy.

Adult↗

Reliability of an image analysis system for quantifying the radiographic trabecular pattern.

A reliability evaluation technique was used to examine the reliability of an image analysis system of the trabecular pattern and to determine the contribution of three possible sources of error variance. Two series of radiographs were taken of 14 lumbar vertebral slices (28 radiographs). Every radiograph was placed on a viewing box for digitization four times by a single operator (112 positions of radiographs) and from every position of a radiograph an area of 15 mm x 15 mm was digitized twice (224 samples for analysis). Ten geometrical characteristics of the trabecular pattern were studied and its orientation was analyzed in 12 directions. Reliability was determined by calculating Cronbach's alpha. This design enabled dividing the measurement error (1-alpha) into fractions associated with the X-ray procedure, the operator and the system. Using this reliability evaluation technique, it was found that the orientation variables are more reliable than the geometric variables. It was found that effort to increase the reliability should be directed toward improving the technical procedure of this image analysis system. Also, repeated measurements will increase the reliability. The number of repeated measurements based on a desired reliability can be calculated. This procedure of evaluation gives the opportunity to select a source of error variance which have to be reduced to increase reliability most effectively.

Adult↗

Parathyroid hormone increases bone formation and improves mineral balance in vitamin D-deficient female rats.

The present study was designed to investigate whether enhanced bone formation due to intermittent PTH administration is dependent on vitamin D metabolites. Forty-eight female Sprague-Dawley rats were randomized into four groups: 1) vitamin D-sufficient, saline-injected (+D Sal); 2) vitamin D-sufficient, human (h) PTH-(1-38)-treated (+D PTH); 3) vitamin D-deficient, saline-injected (-D Sal); and 4) vitamin D-deficient, hPTH-(1-38)-treated (-D PTH) animals. The -D diet contained 2% calcium (Ca), 1.25% phosphorus (P), and 20% lactose to maintain normocalcemia and normophosphatemia despite vitamin D deficiency. The +D diet contained 0.8% Ca, 0.5% P, 20% lactose, and 1000 IU/kg vitamin D. After 45 days of either diet, the rats were injected with 50 microg/kg BW PTH or saline, s.c., daily for 2 weeks. Serum Ca, Mg, P, albumin, and creatinine were similar in all groups. PTH administration decreased endogenous PTH concentrations in the -D PTH compared with those in the - D Sal group. Serum alkaline phosphatase activity, bone mass measurements, dual energy x-ray absortiometric analysis of mineral density, and mechanical testing values in vertebrae and femora of the -D Sal animals did not significantly differ from those in +D Sal animals. Moreover, in both diet groups, PTH improved bone biochemical activity (as assessed by serum alkaline phosphatase), bone mass, mineral density, and biomechanical properties. These results indicate that mineral supply, more than vitamin D itself, may be important for normal bone mineralization and to enable PTH to enhance bone formation. A balance study performed during the last 3 days of the experiment revealed that PTH increased apparent intestinal magnesium absorption in the +D group only. Ca and P retention, however, were augmented in both diet groups after PTH treatment. In conclusion, in normocalcemic and normophosphatemic -D rats, PTH treatment reduced the increased endogenous hormone concentration and improved Ca and P retention. Furthermore, PTH may have a vitamin D-dependent influence on intestinal magnesium absorption. Finally, short term PTH treatment is anabolic in bone of vitamin D-deficient rats when adequate mineral amounts are provided in the diet.

Alkaline Phosphatase↗

Is skeletal responsiveness to thyroid hormone altered in primary osteoporosis or following estrogen replacement therapy?

Hyperthyroidism is characterized by increased bone turnover and resorptive activity. Similar changes in remodeling are seen in osteoporosis. To study the pathogenetic role of thyroid hormone in osteoporosis, we measured concentrations of free and total thyroid hormones and investigated the sensitivity of the skeleton toward thyroid hormones in 14 osteoporotic, 16 estrogen-treated, and 15 normal postmenopausal women with comparable thyroid status. Triiodothyronine (T3, 60 microg/day for 7 days) was administered to the three groups. The skeletal response was assessed by monitoring bone alkaline phosphatase (BAP), osteocalcin (BGP), and pyridinium cross-linked telopeptide domain of type I collagen (ICTP) in serum and urinary excretion of hydroxyproline (OHP), pyridinoline (PYR), and deoxypyridinoline (DPR) at days 0, 8, 15, and 57. Women on estrogen replacement therapy exhibited lower bone turnover than the normal postmenopausal women. Markers of bone formation were reduced by 19-43% and markers of resorption by 22-48%. The osteoporotic women displayed lower bone mass at the lumbar spine and the distal forearm (p < 0.01-0.001), but the levels of biochemical markers of bone formation and resorption were comparable to values obtained in the normal postmenopausal women. T3 stimulation caused significant increases (p values ranging between 0.05-0.001) in all three groups of the resorptive markers: ICTP (47%, 47%, 45%), OHP (29%, 30%, 33%), PYR (43%, 27%, 51%), and DPR (42%, 24%, 59%). Of the formative markers, only BGP increased significantly (32%, 40%, 47%) (p < 0.001). At day 57, however, all three formative markers increased compared with day 15 (p < 0.05-0.001). No significant differences in bone markers were demonstrated between groups. In the osteoporotic group, as the only group, serum calcium increased (p < 0.05) and serum PTH fell (p < 0.05). In conclusion, osteoporosis and estrogen substitution are not characterized by altered concentrations of thyroid hormones or responsiveness to thyroid hormones at the level of individual bone cells; however, altered responses pertaining to PTH and calcium were detected.

Absorptiometry, Photon↗

Inflammatory bowel disease and osteoporosis.

The relation between inflammatory bowel disease (IBD) and osteoporosis has received increasing attention during the past decade. The prevalence of low bone mass in patients with IBD has been reported to be more than 50%. The development of a quick non-invasive method to diagnose osteoporosis (dual-energy X-ray absorptiometry) provides a practical tool to identify the patient who needs special attention. The aetiology of the bone disease in patients with IBD has still not been elucidated, but corticosteroids may play a major role. Studies on the prevention/treatment of IBD-related osteoporosis are scarce. In a single uncontrolled study hormone replacement therapy proved effective in preventing bone loss in peri- and post-menopausal women with IBD. A placebo-controlled study showed that supplementation with calcium and vitamin D prevents bone loss in patients with Crohn's disease. The present paper reviews our current knowledge on the mechanisms and epidemiology of IBD-related bone disease.

Bone Density↗

[Apoptosis: cellular and clinical aspects].

Removal of damaged cells is essential for the maintenance of life in multicellular organisms. The process of self destruction, apoptosis, eliminates surplus or damaged cells as part of the pathophysiological defence system. Apoptosis is essential in structural and functional organogenesis during embryological development. The physiological regulation of tissue kinetics is a product of both cell proliferation and cell death. Internal and external regulatory stimuli regulate the balance between apoptosis and mitosis by genetic interaction. Apoptosis is characterized by condensation of chromatine as a result of DNA degradation, formation of blebs in the plasma and nuclear membranes, condensation of cytoplasma, formation of vesicular apoptotic bodies, and phagocytosis by neighbouring cells without inflammatory response. A number of observations indicate that programmed cell death plays an important role in the regulation of cytofunctional homeostasis and defense against accumulation of damaged cells, eg with DNA alterations. Dysregulation of the apoptotic gene program, eg by mutations, may not only lead to loss or degeneration of tissue, but also to hyperproliferative and tumorigenic disorders. New evidence indicates that apoptosis regulation is important both in aging processes and diseases such as: neuropathies, immunopathies, viral infections, cancer, etc. Pharmacological intervention designed to modulate apoptosis seems to raise new possibilities in the treatment of disease.

Apoptosis↗

[Apoptosis: molecular aspects].

Many signals and external stimuli regulate the apoptosis activity by interaction with the genome. These stimuli include morphogenetic signals, physiological factors, and environmental influence. The signals mediate their effect on cells with suitable receptors, relevant signalling pathways, and competence to execute the apoptosis cascade. Apoptosis is triggered indirectly by deprivation of survival factors, or directly by intercellular cell death signalling factors, and also by unbalanced intracellular messenger molecules, which are, more or less, involved in regulation of both programmed cell death and survival. Several genes are involved in regulation of cell survival and apoptosis: bcl-2/bax, p53, c-myc and transcription factors such as cdk, c-myc, c-fos and c-jun. Apparently, apoptosis could be triggered by increased or inhibited gene expression as well as biochemical reactions without changed gene expression. The morphological changes during apoptosis reflect a cascade of genetic and biochemical reactions in the cell. In the signal transduction pathway both secondary messenger Ca2+, different kinases, and polyamines are involved. Cysteine proteases cleave cytoskeletal proteins, endonucleases divide DNA into fragments, and transglutaminases cross-link macromolecules. Degradative enzymes such as proteases, endonucleases and transglutaminases are activated during apoptosis, leading to cellular collapse and formation of vesicular apoptotic bodies. Both increased and inhibited apoptosis activity may have pathological consequences. New therapeutic strategies aim to counteract dysregulation of apoptosis in specific tissues by pharmacological intervention. Thus there is a need for identification of molecules and gene products involved in regulation of apoptosis activity and clarification of the conditions where this knowledge may be used.

Apoptosis↗

Effects of recombinant human growth hormone and insulin-like growth factor-I, with or without 17 beta-estradiol, on bone and mineral homeostasis of aged ovariectomized rats.

This study aimed to evaluate whether recombinant human growth hormone (rhGH) or insulin-like growth factor-I (rhIGF-I) can reverse or prevent further bone loss in aged osteopenic ovariectomized (OVX) rats and to compare their effects with those of 17 beta-estradiol (E2). Twelve-month-old rats were OVX, remained untreated for 8 weeks, and subsequently received daily subcutaneous (SC) injections of rhGH (75 micrograms/day), rhIGF-I (250 micrograms/day), E2 (1.5 micrograms/day), and their respective combinations during 8 weeks, and were then compared with sham-operated, pretreatment OVX, and saline-treated OVX rats. A single sc injection of rhGH resulted in peak hGH concentrations after 90 minutes, with a half-life of 124 minutes; the highest plasma IGF-I concentrations were reached 45 minutes after rhIGF-I injection (+57% vs. baseline) with a gradual decline thereafter. Measurements included: biochemical parameters of bone remodeling (plasma osteocalcin and urinary pyridinolines); histomorphometry of proximal tibial metaphysis; DXA of femur; biomechanical analysis of femur and fifth lumbar vertebra (L5); plasma 1,25-dihydroxyvitamin D3 (1,25(OH)2D3), and calbindin-D9K in duodenal mucosa. Whereas all E2-treated OVX rats had much suppressed bone remodeling, rhGH or rhIGF-I had no effect on any biochemical or histomorphometrical parameter of remodeling. The bone mineral density (BMD) at the distal femoral metaphysis as well as parameters of strength at L5 were maintained at pretreatment values in OVX rats treated with E2, GH, or IGF-I, but not in saline-treated OVX rats; their effects were not additive, however. Trabecular bone volume in the tibial metaphysis was also higher in rats treated with these agents than in saline-treated rats, but this was more apparent at the primary than at the secondary spongiosa, suggesting that their mechanism of action is on primary spongiosa formation or breakdown. E2 alone was ineffective to augment the BMD at the femoral diaphysis; however, the diaphyseal BMD was 12-14% higher (p < 0.01) after 8 weeks of GH treatment than in pretreatment or saline-treated OVX rats and sham-operated rats, while IGF-I was less effective than GH, GH or IGF-I treatment had no effect on plasma 1,25(OH)2D3 or duodenal calbindin-D9K concentrations, but the combination of GH or IGF-I with E2 potentiated the effect of E2 to stimulate calbindin-D9K concentrations and urinary calcium excretion, indicating "hyperabsorption hypercalciuria." In conclusion, the administration of rhGH and rhIGF-I, like that of E2, into aged OVX rats prevents further loss of bone mass and strength at sites containing trabecular bone. In addition, rhGH increases cortical bone mass above pretreatment values.

Absorptiometry, Photon↗

Aluminium-induced bone disease in uremic rats: effect of deferoxamine.

We have previously established a rat model of chronic uremia, which is suitable to investigate the effect of various treatment modalities on renal osteodystrophy [1]. After four months subsequent to 5/6 nephrectomy, some animals were treated by gavage for 9 weeks with tap water (controls), or with aluminium (Al-citrate) 3 x 25 mg/week/kg b.wt +/- subsequent deferoxamine (DFO) 3 x 50 mg/week/kg b.wt. for 4 weeks. At termination of the study, serum clinical chemistry, femoral chemical composition and mechanical properties, calvarial parathyroid hormone (PTH)-elicited adenylate cyclase (AC) and phospholipase C (PLC) activities, cross-sectional femoral area, as well as bone histomorphometry, were analyzed. Animals given Al displayed moderately enhanced serum Al and bone Al accumulation, however, DFO-treatment did not fully alleviate bone Al retainment. A small increase in serum PTH was seen in all animals rendered uremic. Furthermore, a marked fall in serum alkaline phosphatase (ALP) below normal controls was observed in Al +/- DFO-treated animals compared with uremic controls. The uremic condition led to reduced femoral ratios of hydroxyproline (HYP) over Ca(2+) and phosphate (P(i)), while Al-intoxication alone enhanced femoral Hyp contents above values seen for normal controls. The protracted ureamia caused a deterioration of long bone resilience and brittleness, however, Al +/- DFO-treatment seemed to normalize the latter. Contrastingly, Al +/- DFO-gavage enhanced time to fracture. Uremic rats intoxicated with Al showed a complete loss of calvarial PTH-sensitive AC and PLC activities. DFO-treatment normalized PTH-elicited PLC, while PTH-susceptible AC remained super-normal. Al apparently exerts a long term down-regulation of both PTH-sensitive signaling systems as evidenced by studies of rat UMR 106 osteosarcoma cells in culture. The uremic condition enhanced endosteal bone resorption as shown by femoral shaft dimension analysis, while Al +/- DFO-treatment insignificantly reversed the condition. Finally, histomorphometrical analyses showed that DFO-administration tended to normalize aberrant trabecular bone volume, while rectifying both bone resorption and degree of mineralization. In conclusion, we assert that Al-intoxication hampers both processes (i.e. formation and resorption) of bone turnover, and that DFO-treatment to a certain extent prevents the uremia- and Al-induced bone disease in rats.

Adenylyl Cyclases↗

Cortical bone remodeling in autosomal dominant osteopetrosis: a study of two different phenotypes.

Previous analyses of cancellous bone remodeling in autosomal dominant osteopetrosis (ADO) have suggested a diminished osteoclastic resorption at the endocortical surface. Consequently, cortical width increases with age in both ADO type I and II. By means of histomorphometric methods, the remodeling cycle of the Haversian surface in the iliac crest has recently been reconstructed in normal individuals. The aim of the present investigation was to study cortical bone remodeling in ADO type I and II. Transcortical iliac crest bone biopsies obtained from 21 ADO patients were studied. Of these, 14 had ADO type I and seven had ADO type II. Twenty of the patients had received intravital double labeling with tetracycline before the biopsies were obtained. The static histomorphometric parameters for cortical bone mass and structure were compared with a control group of 21 sex- and age-matched individuals. Regarding the dynamic histomorphometric parameters for reconstruction of the cortical bone remodeling cycle, the ADO type I material was compared with control material from 14 sex- and age-matched individuals, whereas the ADO type II material was compared with control material from six sex-matched but younger individuals. Significant increases were seen in absolute as well as fractional cortical widths in both ADO types. Furthermore, an age-related increase was observed in both absolute and fractional cortical widths in ADO type I, whereas ADO type II was nonsignificant with regard to age. The fractional cancellous width was reduced in both type I and type II. However, only in ADO type I did the fractional cancellous width significantly correlate inversely with age. In the control group, neither cortical dimensions nor cancellous width correlated significantly with age. No significant differences were observed between patients and the control group in osteon dimensions; fractional resorptive, formative, or quiescent sites; resorptive or formative remodeling rates; remodeling periods; or activation frequency. An age-related increase in cortical porosity was seen in the group of normal individuals, but not in the two patient groups. The fractional remodeling space was increased in the ADO type II group. In conclusion, cortical dimensions are increased in both ADO type I and II and positively correlated to age in type I. However, cortical remodeling at the Haversian surface is essentially normal in both ADO type I and II. This could be explained by a defective endocortical bone resorption, as no periosteal accretion was observed, and because cancellous bone remodeling previously has been described to be normal.

Adult↗

Determination of connectivity density in human iliac crest bone biopsies assessed by a computerized method.

The aim of the present study was to design a computer program (based on the ConnEulor principle) for direct measurement of 3-D connectivity density in iliac crest bone sections, as used for conventional histomorphometry. We used the physical disector principle and developed an algorithm for nonlinear alignment of the disector pairs. 3-D connectivity was evaluated in transiliac specimens from 30 nonselected autopsy cases of 14 men (age range 20-84 years) and 16 women (age range 20-96 years). In order to visualize the findings from the disector pairs, 3-D reconstruction was performed for two of the iliac crest biopsies. The designed computer program aligns the two sections forming a disector pair and automatically depicts the differences between the images, thereby making correct, direct connectivity density measurements available for conventional bone research.

Adult↗