Concentration profiling of minerals in iliac crest bone tissue of opium addicted humans using inductively coupled plasma and discriminant analysis techniques.

Opium addiction is one of the main health problems in developing countries and induces serious defects on the human body. In this work, the concentrations of 32 minerals including alkaline, heavy and toxic metals have been determined in the iliac crest bone tissue of 22 opium addicted individuals using inductively coupled plasma-optical emission spectroscopy (ICP-OES). The bone tissues of 30 humans with no physiological and metabolomic diseases were used as the control group. For subsequent analyses, the linear and quadratic discriminant analysis techniques have been used for classification of the data into "addicted" and "non-addicted" groups. Moreover, the counter-propagation artificial neural network (CPANN) has been used for clustering of the data. The results revealed that the CPANN is a robust model and thoroughly classifies the data. The area under the curve for the receiver operating characteristic curve for this model was more than 0.91. Investigation of the results revealed that the opium consumption causes a deficiency in the level of Calcium, Phosphate, Potassium and Sodium in iliac crest bone tissue. Moreover, this type of addiction induces an increment in the level of toxic and heavy metals such as Co, Cr, Mo and Ni in iliac crest tissue. The correlation analysis revealed that there were no significant dependencies between the age of the samples and the mineral content of their iliac crest, in this study. The results of this work suggest that the opium addicted individuals need thorough and restricted dietary and medical care programs after recovery phases, in order to have healthy bones.

The effect of dietary phosphorus and calcium level, phytase supplementation, and ileal infusion of pectin on the chemical composition and carbohydrase activity of fecal bacteria and the level of microbial metabolites in the gastrointestinal tract of pigs.

Two experiments with growing pigs were conducted to determine the effects of dietary P and Ca level, phytase supplementation, and ileal pectin infusion on ileal and fecal P and Ca balance, chemical composition of fecal mixed bacterial mass (MBM), and bacterial metabolic activity. Pigs (initial BW = 30 kg) were fitted with simple T-cannulas at the distal ileum. They were fed a low-P corn-soybean meal control diet (3 g of P/kg) or the control diet supplemented with monocalcium phosphate (MCP; 7 g of P/kg; Exp. 1) or 1,000 FTU phytase/kg (Exp. 2). The daily infusion treatments consisted of 60 g of pectin dissolved in 1.8 L of demineralized water or 1.8 L of demineralized water as the control infusion, infused via the ileal cannula. In each experiment, 8 barrows were assigned to 4 dietary treatments according to a double, incomplete 4 x 2 Latin square. The dietary treatments in Exp. 1 were the control (Con-) diet with water infusion; the control (Con+) diet with pectin infusion; the MCP diet with water infusion; and the MCP diet with pectin infusion. In Exp. 2, the pigs received the same Con- and Con+ treatments as in Exp. 1 and, in addition, the phytase-supplemented diet in combination with water or pectin infusion. After a 15-d adaptation period, feces were collected for 5 d followed by ileal digesta collection for 24 h. In Exp. 1, supplemental MCP increased (P

Effect of common antinutritive factors and fibrous feedstuffs in pig diets on amino acid digestibilities with special emphasis on threonine.

Most feedstuffs contain antinutritive factors (ANF) such as insoluble fibers, lignins, tannins, and lectins. Intake of these ANF has the ability to reduce nutrient digestibility and to increase endogenous protein losses, such as through increased intestinal mucus secretion. The objective of this experiment was to determine the apparent ileal digestibilities (AID) of AA of 6 ANF-enriched diets to estimate endogenous protein loss associated with these ingredients in diets for young pigs. Forty-two 10-kg BW pigs fitted with a simple T-cannula at the distal ileum were randomly assigned to 1 of 7 casein-based diets with: no supplement (control), 100 g/kg of canola meal (CM), 100 g/kg of wheat bran (WB), 150 g/kg of barley (BR), 22.5 g/kg of lignin (LG), 15 g/kg of kidney beans [as a lectin (LE) source], and 15 g/kg of tannins (TN). All diets were formulated to be similar in N, indispensable AA, and caloric contents. After a 7-d adaptation to the test diets, N balance was conducted for 5 d, followed by 24 h of collection of digesta for analyses of AA. Pigs fed BR had 17% lower ADG and 15% lower feed conversion ratio (P < 0.05) compared with control and CM pigs. Pigs fed diets containing WB and BR had lower N retention as a percentage of absorbed N compared with all other groups (P = 0.03). The AID for CP was lower in BR, WB, and LE pigs compared with control. Of the AA, AID of Thr was notably lowest in BR, WB, and TN pigs (P < 0.05). The standardized ileal digestibility was lower in WB and BR pigs for most indispensable AA. Altogether, these data suggest that hemicellulose fiber, at concentrations typical in commercial swine diets, reduces AID of AA by increasing endogenous losses. Understanding the differential effects of ANF on endogenous losses of individual dietary AA will improve the accuracy of diet formulation.

Evidence that treatment with risedronate in women with postmenopausal osteoporosis affects bone mineralization and bone volume.

Risedronate is used in osteoporosis treatment. Postmenopausal women enrolled in the Vertebral Efficacy with Risedronate Therapy trial received either risedronate (5 mg/day) or placebo for 3 years. Subjects received calcium and vitamin D supplementation if deficient at baseline. Lumbar spine bone mineral density (BMD) was measured at baseline and at 3 years. Quantitative back-scattered electron imaging (qBEI) was performed on paired iliac crest biopsies (risedronate, n = 18; placebo, n = 13) before and after treatment, and the mineral volume fraction in the trabecular bone was calculated. Combining dual-energy X-ray absorptiometric values with the mineral volume fraction for the same patients allowed us to calculate the relative change in trabecular bone volume with treatment. This showed that the effect on BMD was likely to be due partly to changes in matrix mineralization and partly due to changes in bone volume. After treatment, trabecular bone volume in the lumbar spine tended to increase in the risedronate group (+2.4%, nonsignificant) but there was a significant decrease (-3.7%, P < 0.05) in the placebo group. Calcium supplementation with adequate levels of vitamin D led to an approximately 3.3% increase in mineral content in the bone material independently of risedronate treatment. This increase was larger in patients with lower matrix mineralization at baseline and likely resulted from correction of calcium/vitamin D deficiency as well as from reduced bone remodeling. Combining BMD and bone mineralization density distribution data show that in postmenopausal osteoporosis 3-year treatment with risedronate preserves or may increase trabecular bone volume, unlike placebo. This analysis also allows, for the first time, separation of the contributions of bone volume and matrix mineralization to the increase in BMD.

Calcium, phosphorus, and amino acid digestibility in low-phytate corn, normal corn, and soybean meal by growing pigs.

Nine growing barrows were equipped with a T-cannula in the distal ileum and used to determine apparent ileal (AID) and apparent total-tract digestibility (ATTD) coefficients of Ca and P in low-phytate corn, normal corn, soybean meal, and in diets where soybean meal was mixed with low-phytate corn or normal corn. The AID and the standardized ileal digestibility coefficients (SID) of CP and AA also were determined. The animals (initial BW = 29.3 +/- 1 kg) were allotted to a 9 x 9 Latin square with nine diets and nine periods. Three diets contained low-phytate corn, normal corn, and soybean meal as their sole source of CP, AA, Ca, and P, respectively. Three additional diets were identical to these diets except that limestone and monosodium phosphate were added. Two diets contained low-phytate corn or normal corn and soybean meal, limestone, and monosodium phosphate, and the final diet was a N-free diet. The AID and ATTD of Ca were higher (P < 0.05) for low-phytate corn than for normal corn (70.0 and 69.1% vs. 47.4 and 49.6%, respectively). The AID and ATTD for Ca in soybean meal (50.9 and 46.7%, respectively) did not differ from values for normal corn but were lower (P < 0.05) than for low-phytate corn. The AID and ATTD for P from low-phytate corn (56.5 and 54.5%, respectively) were greater (P < 0.05) than from normal corn (28.3 and 28.8%, respectively), whereas soybean meal had intermediate AID and ATTD for P (37.2 and 38.0%, respectively). The AID and ATTD of P increased (P < 0.05) when monosodium phosphate was added to normal corn (44.9 and 49.8%, respectively) and soybean meal (49.6 and 46.2%, respectively), but adding monosodium phosphate to low-phytate corn, did not alter either AID (49.7%) or ATTD (50.7%) of P. No differences between AID and ATTD for Ca or P within the same diet were observed. The AID of Arg, Asp, Gly, Ile, Lys, Phe, Thr, and Val were greater (P < 0.05) in low-phytate corn than in normal corn. The AID of all AA in soybean meal were greater (P < 0.05) than in both types of corn, with the exception of Ala, Cys, Leu, and Met. The SID of Lys, Phe, and Thr were higher (P < 0.05) in low-phytate corn than in normal corn. Because low-phytate corn has a higher digestibility of Ca and P, less inorganic Ca and P need to be supplemented to diets containing low-phytate corn than to those containing normal corn, and P excretion may be decreased when low-phytate corn is used in the diet.

Three-year oral clodronate treatment does not impair mineralization of newly formed bone--a histomorphometric study.

Bisphosphonates have been used successfully in the treatment of malignant hypercalcemia and skeletal metastases. Recently, clodronate has been studied in adjuvant settings in primary breast cancer. However, long-term effect of adjuvant clodronate on bone histology has not been reported, whereas bone mineral density studies have been published. The aim of this study was to examine the effect and safety of long-term clodronate treatment on bone quality as measured by histomorphometric techniques from bone biopsies. A total of 299 patients with early stage breast cancer were randomized to receive adjuvant oral clodronate (1.6 g/day) or to a control group for 3 years. All patients had adjuvant treatment: premenopausal women had six cycles of chemotherapy and postmenopausal women had antiestrogen for 3 years. Trabecular bone quality was examined in transiliac bone biopsy specimens by using histomorphometric techniques in 28 clodronate treated and 35 control patients who were disease-free at 3 years and who allowed the biopsy specimen to be obtained. No statistically significant differences were found in the values of osteoid, mineral apposition rate, or mineralization lag time in bone biopsies between the clodronate and the control groups. Postmenopausal women who received two antiresorptive drugs, antiestrogen and clodronate, developed features of secondary hyperparathyroidism with increased eroded surface and osteoclast number. In premenopausal, women clodronate with adjuvant chemotherapy, which induced early menopause and rapid bone loss in most of the patients, seemed to conduct slight depression in bone formation. Three-year oral clodronate treatment does not impair mineralization of newly formed bone: however, clodronate with different adjuvant breast cancer treatments has a diverse impact on bone histomorphometry depending on the type of therapy.

Contribution of raloxifene and calcium and vitamin D3 supplementation to the increase of the degree of mineralization of bone in postmenopausal women.

Raloxifene has been shown to increase bone mineral density and reduce the risk of vertebral fracture in postmenopausal women with osteoporosis. In this study, we report the results of the first prospective longitudinal study to evaluate the mean degree of mineralization of bone (MDMB) in a group of patients enrolled in the Multiple Outcomes of Raloxifene Evaluation trial. Patients were randomly assigned to one of three treatment groups: placebo (n = 24), raloxifene 60 mg/d (RLX60; n = 22), or raloxifene 120 mg/d (RLX120; n = 18). All patients received daily calcium (500 mg) and vitamin D(3) (400-600 IU) supplementation for the duration of the study. Iliac crest biopsies were taken at baseline and after 2 yr of treatment. Quantitative microradiography was used to analyze the biopsy specimens and revealed a statistically significant (P < 0.05) mean percentage increase in total MDMB of 7.0, 5.3, and 5% for RLX60-, RLX120-, and placebo-treated patients, respectively, compared with baseline. Raloxifene treatment was found to shift the distribution of total bone mineral to higher values of MDMB (RLX60, 29%; RLX120, 8%) with greater heterogeneity, compared with placebo. The profile of MDMB observed in biopsies after treatment with placebo and raloxifene, compared with baseline, closely resembles physiological premenopausal bone.

Human, rat and chicken small intestinal Na+ - Cl- -creatine transporter: functional, molecular characterization and localization.

In spite of all the fascinating properties of oral creatine supplementation, the mechanism(s) mediating its intestinal absorption has(have) not been investigated. The purpose of this study was to characterize intestinal creatine transport. [(14)C] creatine uptake was measured in chicken enterocytes and rat ileum, and expression of the creatine transporter CRT was examined in human, rat and chicken small intestine by reverse transcription-polymerase chain reaction, Northern blot, in situ hybridization, immunoblotting and immunohistochemistry. Results show that enterocytes accumulate creatine against its concentration gradient. This accumulation was electrogenic, Na(+)- and Cl(-)-dependent, with a probable stoichiometry of 2 Na(+): 1 Cl(-): 1 creatine, and inhibited by ouabain and iodoacetic acid. The kinetic study revealed a K(m) for creatine of 29 microM. [(14)C] creatine uptake was efficiently antagonized by non-labelled creatine, guanidinopropionic acid and cyclocreatine. More distant structural analogues of creatine, such as GABA, choline, glycine, beta-alanine, taurine and betaine, had no effect on intestinal creatine uptake, indicating a high substrate specificity of the creatine transporter. Consistent with these functional data, messenger RNA for CRT was detected only in the cells lining the intestinal villus. The sequences of partial clones, and of the full-length cDNA clone, isolated from human and rat small intestine were identical to previously cloned CRT cDNAs. Immunological analysis revealed that CRT protein was mainly associated with the apical membrane of the enterocytes. This study reports for the first time that mammalian and avian enterocytes express CRT along the villus, where it mediates high-affinity, Na(+)- and Cl(-)-dependent, apical creatine uptake.

A new bone banking technique to maintain osteoblast viability in frozen human iliac cancellous bone.

The aim of this study was to develop a new cryopreservation technique to maintain the osteoblast viability in frozen iliac bone and to prove cell viability using cell culture techniques. Human iliac cancellous bones were frozen with and without 10% Me(2)SO at -80 degrees C. The tubes were kept in a -80 degrees C freezer for at least 2 days. After the storage period, the frozen bone was thawed by placing the tube in a 37 degrees C water bath. A serial enzymatic digestion technique using 0.2% collagenase was employed to isolate osteoblast-like cells from the bone. The cells that were released were inoculated into tissue culture flasks containing DMEM supplemented with 10% FCS. They were incubated at 37 degrees C in a humidified atmosphere of 95% air and 5% CO(2). Cells of the second passage were plated at a density of 5 x 10(3)cells/cm(2) in a 24-well plate and used for characterization. For characterization, WST-1 assay, determination of alkaline phosphatase, Type I collagen assay, osteocalcin assay, and von Kossa staining were used. The assays were performed at 3, 6, 9, and 12 days after plating the cells. Based on the results of this study, we conclude that the osteoblast-like cells in the frozen bone can survive, only when the bone is frozen with cryoprotectants to prevent injury during freezing and thawing.

Effects of orchidectomy on bone metabolism in beagle dogs.

The effects of orchidectomy on bone metabolism in male beagle dogs were examined using twelve 2-year-old dogs that were orchidectomized. The dogs' bilateral iliac bones, double-labeled with tetracycline and calcein for the histomorphometry, were obtained from three dogs prior to orchidectomy and at 3, 6, 9, and 12 months afterwards. The serum biochemical constituents related to bone metabolism were examined before and every month after orchidectomy. Between 1 and 6 months after orchidectomy, the value of serum testosterone decreased (1 month), while the levels of parathyroid hormone, calcitonin, total calcium, osteocalcin, and alkaline phosphatase activity increased significantly, indicating a high bone turnover. The mean trabecular thickness and the fraction of labeled osteoid surface decreased significantly 3 months after orchidectomy, but other histomorphometric parameters were unchanged. In the period 7-12 months after orchidectomy, the parathyroid hormone level increased ever and above that of the first 6-month period, while the levels of calcitonin, osteocalcin, alkaline phosphatase activity, and phosphorus decreased. The bone volume, mean trabecular thickness, and the fraction of labeled trabecular surface decreased significantly compared with the pre-orchidectomy values. These findings indicate an imbalance in bone metabolism (i.e. bone resorption > bone formation). These results indicate that a loss of bone volume accompanied the fall in sex hormone levels following orchidectomy and suggest that the orchidectomized dog is available as an animal model for studying osteoporosis caused by hypogonadism and the decline of sex functions in men.

Critical size defect in the goat's os ilium. A model to evaluate bone grafts and substitutes.

Bone defects and their treatment are a well known problem in orthopaedic surgery. A critical size defect is a suitable model to study bone replacement materials. This study describes a critical size defect in the goal and the evaluation of three bone fillers (particulate autograft, particulate allograft, and a polyethylene oxide/polybutylene terephthalate copolymer) in this defect. The goat allows for implantation of large implants and has a metabolic rate more comparable with that of humans than small animals. The critical size defect, located in the goat's iliac wing, is easily reproducible and allows qualitative and quantitative evaluation of bone grafts and bone graft substitutes. After 3 months of healing, the unfilled defects showed 13.5% bone in the defect, the autografted defects 36.3%, and the allografted 18.5%. The copolymer gave only 1.5% bone in the defect; this is in contrast to previous reports. The described model allows for the evaluation of bone graft substitutes before introduction into clinical practice.

Strontium distribution and interactions with bone mineral in monkey iliac bone after strontium salt (S 12911) administration.

The analysis of the interaction of strontium (Sr) with bone mineral is of interest because a new agent containing Sr (S 12911) has shown positive effects on bone mass in various animal models of osteoporosis and is currently being developed for preventive and curative treatment of postmenopausal osteoporosis. Iliac bone samples were obtained from 20 male monkeys: 4 untreated control animals, 12 animals sacrificed at the end of a 13-week treatment with high dose levels of S 12911 (750, 275, or 100 mg/kg/day orally), and 4 animals sacrificed 6 weeks after the end of a 13-week treatment with S 12911 (750 or 100 mg/kg/day orally). The distribution of Sr was determined and quantified by X-ray microanalysis. Changes at the crystal level were evaluated by X-ray diffraction and Raman microspectrometry. In the control animals, traces of Sr were found to be homogeneously distributed throughout the bone tissue. In the treated monkeys, Sr could only be detected in calcified matrix. In monkeys sacrificed at the end of the treatment, Sr was found to be dose-dependently incorporated into the mineral substance of the compact and cancellous bone. Sr was heterogeneously distributed with three to four times more Sr in new than in old compact bone, and approximately two and a half times more Sr in new than in old cancellous bone. The bone Sr content dramatically decreased in the animals sacrificed 6 weeks after the end of the treatment. Diffraction showed no significant changes in the characteristics of the crystal lattice. Sr appeared to be easily exchangeable from bone mineral and was slightly linked to mature crystals through ionic substitutions. Even at the highest dose level tested, less than 1 calcium ion out of 10 was substituted by 1 Sr ion in each crystal. In conclusion, taken up by bone, Sr was heterogeneously distributed with a higher concentration in new than in old bone but induced no major modifications of the bone mineral (crystallinity, crystal structure) at the crystal level. As a result, a treatment with S 12911 Sr salt should not induce any alteration of bone mineral.

1,25-dihydroxyvitamin D3-mediated transforming growth factor-beta release is impaired in cultured osteoblasts from patients with multiple pituitary hormone deficiencies.

To evaluate the osteoblastic function in patients with multiple pituitary hormone deficiencies (M-PHD) and with isolated growth hormone deficiency (I-GHD), bone cells were cultured and the effects of 10(-8) M 1,25-dihydroxyvitamin D3 (1,25[OH]2D3) on parameters of cell proliferation, osteoblastic differentiation, and local paracrine regulation were measured. Three days of 1,25(OH)2D3 treatment increased alkaline phosphatase activity and osteocalcin release but inhibited [3H]thymidine incorporation in all cell cultures from patients as well as from controls. In addition, 1,25(OH)2D3 increased the release of both total and active transforming growth factor-beta (TGF-beta) in bone cells from controls by, respectively, 4.9- and 3.2-fold and in bone cells from I-GHD by 5.1- and 1.5-fold, respectively. However, in bone cells from M-PHD, the stimulation of total TGF-beta release was significantly lower (1.3-fold) than in control and I-GHD cells, and active TGF-beta release was not stimulated at all. One year of supplementation with human growth hormone did not improve this deficient TGF-beta release in bone cells from M-PHD. We conclude that cultured bone cells from I-GHD and M-PHD show a normal response to 1,25(OH)2D3 regarding cell proliferation and osteoblastic differentiation, which implicates a normal 1,25(OH)2D3-receptor function. In cells from controls and I-GHD, 1,25(OH)2D3 enhanced both total and active TGF-beta release. However, bone cells from M-PHD showed a deficient TGF-beta response to 1,25(OH)2D3. These results suggest that the regulation of TGF-beta production is a major paracrine factor involved in hypopituitarism.

Local changes in aluminium, calcium and phosphorus content of bone caused by alumina implant.

Thirty rabbits were divided equally into 5 groups randomly. A hole, 6 mm in diameter and 2 mm deep, was bored on each iliac crest. Two pieces of alumina were implanted into the hole of one side, while the opposite side served as control. These rabbits were killed on 10, 20, 40, 60 and 90 days after operation. Calcium, phosphorus and aluminium contents of iliac bone on both sides were determined by Inductively Coupled Plasma--Atomic Emission Spectrometry. The results showed that the aluminium content of the implanted side in each group was higher than that of the control and difference was significant in 10, 40 and 60 day groups (P < 0.05). This shows that the implant releases aluminium into the bone. Moreover, the calcium and phosphorus contents were significantly lower on the implanted side than on the control side in 10 and 20 day groups (P < 0.05-0.001). Apparently, the aluminium released from the implant in the early stage can interfere with the local calcium and phosphorus metabolism and delay the mineralization of the bone.

Comparison of histomorphometric values in iliac trabecular bone of beagle dogs raised under different breeding systems.

In order to clarify individual differences in bone metabolism among colony-raised beagle dogs, histomorphometric values of iliac trabecular bone and values of serum biochemical constituents related to bone were examined in 10 and 17 beagle dogs raised, respectively, under our two breeding systems in which differences in factors such as exercise, ultraviolet rays, and mineral content of the diet affect bone metabolism. At the age of 14 months, all dogs were injected with tetracycline hydrochloride and calcein twice for double bone labeling in order to measure dynamic as well as static parameters by bone histomorphometry and the ilium was later biopsied. The measurement on cancellous bone areas of undecalcified iliac sections was performed with a semiautomatic image analyser. Values of total calcium, phosphorus, alkalinephosphatase activity, parathyroid hormone and calcitonin in serum were also determined. The results showed that there were no significant differences between the two groups in histomorphometric values, except for the osteoid volume (p less than 0.05) and osteoid surface/trabecular surface ratio (p less than 0.01) in females, or in serum biochemical constituents, except for alkalinephosphatase activity (p less than 0.001) in males, indicating there were virtually no individual differences in bone metabolism in normal colony raised beagle dogs.

Concentration of bone elements in osteoporosis.

In aging and in osteoporosis, decreased bone density is associated with decreased bone mass. However, changes in the bone mineral phase remain a matter for investigation. In particular, it is unknown whether bone mineral loss is directly related to reduction in bone mass or associated with changes in the concentration of mineral elements in mineralized bone tissue. In this study, the cortical bone concentration of elements was determined in biopsies of the ilium from 33 subjects (12 controls and 21 individuals with untreated severe osteoporosis). Calcium and phosphorus concentrations were evaluated in cortical and trabecular bone using energy-dispersive x-ray (EDX) microanalysis and inductively coupled plasma optical emission spectrometry (ICPOES). Bone concentrations of Na, K, Mg, Cu, Zn, Fe, Sr, Al, B, and Si were also determined in cortical bone using ICPOES. Additionally, the concentration of F in cortical bone was measured with a specific ion electrode and the concentration of Pb was determined by atomic absorption spectrometry. In mineralized bone tissue there was no significant age-dependent variation in the concentration of Ca, P, or other elements either in controls or in osteoporotic subjects. Moreover, the concentration of elements in bone tissue did not differ in the two groups. These results suggest that the decrease in bone density in osteoporosis is directly related to evolution of the bone mass, without detectable changes in the concentration of elements in bone.

Bone mineral content of the radius: good correlations with physicochemical determinations in iliac crest trabecular bone of normal and osteoporotic subjects.

Specific gravity, porosity index (physical parameters), hydroxyproline, calcium, magnesium, and phosphorus (chemical parameters) were determined in iliac crest trabecular bone of normal and osteoporotic subjects. These physical and chemical parameters were compared to bone mineral contents (BMC) measurements by x-ray photodensitometry of the radius. BMC values correlated negatively with porosity index, specific gravity, and degree of mineralization of trabecular bone matrix, which all increase with osteoporosis. There was a negative correlation between calcium and magnesium contents per net bone volume. "Distal" scans of the radius reflected better the axial skeleton mass than "proximal" scans, and physicochemical data correlated better with bone mineral content values than with bone mineral mass (BMM) values.

Actual concept of osteoporosis in paraplegia.

The osteoporosis which appears in paraplegics below the neurological lesion has been studied in 100 patients with the following parameters: quantitative X-rays, urinary hydroxyproline excretion, kinetic study of calcium metabolism by 45Ca, serum phosphorus and calcium, parathormone and calcitonin radio-immunoassay, quantitative histology, density fractionation of bone and amino-acid composition of fractionated bone analysis. All our results show that the important bone resorption occurring very early in the paraplegia is immediately followed by an increase of the bone repair. This osteoporosis below the neurological lesion in paraplegia represents an unbalance between the synthesis and the resorption of bone which possesses a large degree of activity. Furthermore, we demonstrated that the collagen of this bone is underhydroxylated. Following the quantitative X-rays and intraosseous phlebography results we have considered the aetiopathogenesis of this osteoporosis. It seems that vascular modifications due to the lesion of the autonomic nervous system play an important role and furthermore we believe that immobilisation represents only a minor factor in the aetiology of this osteoporosis.

A tetracycline-based histomorphometric evaluation of bone resorption and bone turnover in hyperthyroidism and hyperparathyroidism.

Increased bone, resorption previously found in hyperthyroidism might be caused by a direct stimulating effect of thyroid hormone(s) on bone cells or by an increased sensitivity to circulating parathyroid hormone. In order to disclose qualitative differences in the response of bone resorbing cells to excess parathyroid hormone and excess thyroid hormone(s), histomorphometric analysis of iliac crest biopsies was performed in 25 hyperparathyroid and 40 hyperthyroid patients after tetracycline double-labelling. The main target cells for parathyroid and thyroid hormones were different. Parathyroid hormone stimulated osteocytic osteolysis and increased osteoclastic resorption surfaces equally in trabecular and cortical bone. The osteoclastic resorption was inactive. Thyroid hormone(s) had no effect on osteocytes but increased the osteoclastic resorption surfaces in trabecular and cortical bone, with a pronounced preponderance in cortical bone. The osteoclastic resorption was active and followed by a significant loss of both cortical and trabecular bone. The findings support the assumption that increased bone resorption in hyperthyroidism is caused by a direct stimulating effect of thyroid hormone(s).