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PubMed2005

Long-term skeletal effects of mandibular symphyseal distraction osteogenesis. An implant study.

The purpose of this study was to investigate the long-term skeletal effects of mandibular symphyseal distraction osteogenesis (MSDO) with a tooth- and bone-borne distraction device, analysed using the metallic implant method. The study sample comprised 20 patients between 15.8 and 25 years of age, with a mean age of 20.01 +/- 2.25 years at the start of treatment. In 12 subjects, titanium implants were inserted in the mandible to analyse mandibular skeletal changes in the short and long term. A custom-made intraoral, tooth- and bone-borne distractor was designed and used. After a latency period of 7 days, the distractor was activated twice daily, by a total amount of 1 mm. Postero-anterior (PA) cephalograms were obtained at the start of distraction and at the end of consolidation (94.95 +/- 5.79 days after surgery) and follow-up periods (21.5 +/- 4.6 months after consolidation). The data were analysed statistically using paired t-tests. The mean amount of screw activation was 8.10 +/- 1.68 mm. The inter-symphyseal and inter-molar implant distances and the bimolar width significantly increased during the consolidation period (P < 0.001) and were maintained at the end of the follow-up. On the other hand, the bicondylar width was markedly decreased (P < 0.05), while no significant skeletal changes were observed in bigonion and biantigonion widths, inter-ramal implant distance, or inter-ramal and implant angles at the end of the consolidation period. The long-term findings of this study indicate that MSDO provides an efficient and stable non-extraction treatment alternative, mainly by increasing the anterior mandibular skeletal and dental arches.

Adolescent↗
PubMed2004

Long-term skeletal effects of recombinant human growth hormone (rhGH) alone and rhGH combined with alendronate in GH-deficient adults: a seven-year follow-up study.

BACKGROUND: GH-deficient patients respond to recombinant human GH (rhGH) replacement therapy by increasing bone mineral density (BMD) at a rate of about 1% a year for at least 4 years. Predictive factors for a beneficial effect on bone are a low bone mass at baseline and gender. Whether the beneficial skeletal effects of GH are sustained in the long term remains to be established. It is also not known whether osteoporotic GH-deficient patients may require additional antiresorptive drugs and whether this treatment would be effective concomitantly with GH replacement. DESIGN: We performed a long-term, controlled study in 30 GH-deficient adults: 15 with osteoporosis and 15 control subjects with low bone mass. All patients were treated with rhGH for at least 4 years; thereafter, 3 years of additional alendronate treatment was given to patients with osteoporosis, while controls continued on GH therapy alone. The GH dose was individualized to maintain an IGF-I within the normal reference range for the duration of the study, and was equal between genders. RESULTS: At the end of 4 years of rhGH replacement therapy, a significant increase in mean lumbar spine BMD was observed in both the osteoporosis group (3.6%) and the control group (7.0%), with no significant difference between groups. Males had a larger increase in BMD than females (P = 0.032). After 4 or 5 years of GH treatment patients with persisting osteoporosis received additional alendronate (10 mg/day) for 3 years. Lumbar spine BMD increased by 8.7% after 3 years (P = 0.001) vs 1.5% (P = NS) in the control group continuing on rhGH replacement alone. The alendronate effect was gender independent (P = 0.59). Mean bone area of the lumbar spine did not change in both groups for the duration of the study. Femoral neck BMD increased significantly in the osteoporosis group (3.5%) and was unchanged in the control group. Five osteoporotic GH-deficient patients had a total of 12 vertebral fractures before start of alendronate. Only one of these patients developed two new vertebral fractures within the first year of treatment with alendronate. CONCLUSION: We observed a significant increase in lumbar spine BMD in the first 4 years of rhGH replacement. The effect of GH on bone was gender dependent, but not BMD dependent. After more than 4 years of GH replacement, BMD seemed to reach a plateau, at least as measured in the 3-4 years thereafter, as no significant increase was present in patients treated with GH alone. By contrast, alendronate rapidly augmented BMD and this effect was maintained for at least 3 years. These increases in BMD were associated with a low incidence of (vertebral) fractures. The long-term use of GH does not preclude a beneficial effect of an additional antiresorptive agent in GH-deficient patients with osteoporosis.

Adult↗
PubMed1998

Skeletal effects of low-dose cyclosporin A in aged male rats: lack of relationship to serum testosterone levels.

The aim of this study was to investigate the skeletal effects of cyclosporin A (CsA) in a dose range relevant to clinical medicine in lumbar vertebral cancellous bone of aged male rats and to correlate these effects with possible changes in serum testosterone levels. Thirty-one 18-month-old male Wistar rats were divided into four weight-matched groups and subcutaneously injected with either 0, 1, 3, or 5 mg of CsA/kg of body weight three times per week After 4 weeks of treatment, all rats were killed after in vivo fluorochrome labeling and the first lumbar vertebrae analyzed by quantitative histomorphometry. Serum was analyzed for total calcium, creatinine, alkaline phosphatase, osteocalcin, parathyroid hormone, total testosterone, and CsA levels. CsA administration resulted in a dose-dependent increase in serum osteocalcin levels and in histomorphometric indices of cancellous bone turnover in the axial skeleton. Furthermore, CsA-treated rats showed a deterioration of vertebral cancellous bone structure with increased discontinuity of the trabecular bone network due to trabecular plate perforations. Serum testosterone levels were not significantly changed by CsA treatment and were uncorrelated to all biochemical or histomorphometric indices of bone turnover. We conclude that the 4-week administration of CsA at doses that are close to those used in transplantation patients induced high turnover osteopenia in the axial skeleton of aged, 18-month-old male rats, and that these effects were likely not mediated by changes in serum testosterone levels.

Aging↗
PubMed1981

The long-term skeletal effects of EHDP in dogs.

Disodium hydroxymethanediphosphonic acid was administered subcutaneously (s.c.) to adult beagle dogs for 1 to 2 years at various dose levels to determine its skeletal effects when given chronically. The effects were followed densitometrically, radiographically and by making histomorphometric measurements in sequential rib biopsies. At low doses (0.1 and 0.5 mg/kg/day s.c.) EHDP caused a time-and-dose dependent reduction in the percentage of bone surfaces with active mineralization, a reduction in mineralization rates, a reduction in resorption spaces but no changes in osteoid seam widths. No treatment related bone fractures were noted at the 0.1 mg/kg/day level, while at 0.5 mg/kg/day, fracture incidence appeared slightly increased. At higher doses (2-10 mg/kg/day), there was also a reduction in the number of resorption spaces, but mineralization activity was totally blocked, osteoid seams became thickened and fracture incidence was markedly increased. In one group of animals, EHDP treatment was discontinued after one year of dosage at 5 mg/kg/day given subcutaneously. In these animals, mineralization activity reappeared within 3 months, but osteoid seams remained thickened until 7 months post-treatment. These data indicate that EHDP can have profound effects on bone remodeling in the dog but that these effects are dose-and-time-dependent and they appear to be reversible.

Animals↗
PubMed2000

Skeletal effects of estrogen deficiency as induced by an aromatase inhibitor in an aged male rat model.

Aromatization of androgens into estrogens may be important for maintenance of the male skeleton. To address this hypothesis, we evaluated the skeletal effects of selective estrogen deficiency as induced by the aromatase inhibitor vorozole (Vor), with or without 17beta-estradiol (E(2)) administration (1.35 microg/day), in aged (12-month-old) male rats. A baseline group was killed at the start of the experiment (Base). The control group (Control), the group treated with vorozole alone (Vor), the group treated with E(2) alone (E(2)), or the group with a combination of both (Vor + E(2)) were killed 15 weeks later. Vorozole significantly increased serum testosterone (T) and reduced serum E(2) compared with Control. Body weight gain and serum insulin-like growth factor-I (IGF-I) were also lower in Vor, whereas significant weight loss and decrease of serum IGF-I occurred as a result of E(2) administration. Bone formation as assessed by serum osteocalcin was unaffected but osteoid surface in the proximal metaphysis of the tibia was increased in Vor-treated rats. Bone resorption as evaluated by urinary deoxypyridinoline excretion was increased in Vor. Biochemical parameters of bone turnover were reduced significantly in all E(2) treated rats. Premature closure of the growth plates and decreased osteoid and mineralizing surfaces were also observed in E(2) and Vor + E(2). Apparent bone density of lumbar vertebrae and femur, as measured by dual-energy X-ray absorptiometry (DXA), was significantly reduced in Vor. Vorozole decreased femoral bone density mainly in the distal femur (trabecular and cortical region). This decrease of bone density was not present in E(2) and Vor + E(2). Similar findings were observed when bone density was assessed by peripheral quantitative computed tomography (pQCT); that is, trabecular density of the distal femur, the proximal tibia, and the distal lumbar vertebra were all lower in Vor. This decrease in density was not observed in all E(2)-treated animals. In conclusion, administration of the aromatase inhibitor, vorozole, to aged male rats induces net trabecular bone loss in both the appendicular and axial skeleton, despite a concomitant increase in serum testosterone. E(2) administration is able to prevent this trabecular bone loss in vorozole-treated animals.

Aging↗
PubMed2001

Mechanisms by which high-dose estrogen therapy produces anabolic skeletal effects in postmenopausal women: role of locally produced growth factors.

Conventional hormone replacement therapy acts primarily by preserving bone, but cannot restore lost bone in women with established osteoporosis. Studies in rodents have shown that high doses of estrogens have anabolic skeletal effects, and recent observations in a group of women treated long term with high doses of estrogen indicated that similar effects occur in humans. This study examines the hypothesis that locally produced growth factors, including transforming growth factor-beta (TGF-beta) and platelet-derived growth factors (PDGFs), are involved in mediating the anabolic effects of high-dose estrogen. Transiliac-crest bone biopsies were taken from ten women, aged 52-67 years (mean 58 years), who had been treated with high-dose estrogen for 15 years. Control samples were obtained from four age-matched postmenopausal women not receiving estrogen therapy. TGF-betas and PDGFs were analyzed for mRNA and protein expression by reverse transcriptase-polymerase chain reaction (RT-PCR) and immunohistochemistry. Results showed both TGF-beta1 and -beta2 mRNA, expressed as a ratio to GAPDH, were increased in the estrogen-treated group with an eightfold increase for TGF-beta1 (0.258 +/- 0.246 [mean +/- SD] vs. 0.032 +/- 0.053 in the control group, p = 0.02) and a twofold increase for TGF-beta2 (p = n.s.). TGF-beta3 analysis showed only negligible amounts in both groups. Protein expression levels for TGF-beta1, -beta2, -betaRI and -RII were higher in the estrogen-treated group than in controls, the most marked effects being seen for TGF-beta1. PDGF-A protein expression was also significantly higher in osteoblasts and osteocytes in women treated with estrogen, whereas PDGF-B showed only modest differences. The percentage of bone surface occupied by osteoclasts, as determined by tartrate-resistant acid phosphatase (TRAP) staining, was significantly reduced in the estrogen-treated group (p = 0.001). These results demonstrate that high-dose estrogen therapy is associated with increased TGF-beta, TGF-betaR, and PDGF synthesis and decreased osteoclast activity, consistent with the hypothesis that these growth factors may mediate the actions of estrogen in bone.

Acid Phosphatase↗
PubMed1982

Skeletal effects of orthovoltage and megavoltage therapy following treatment of nephroblastoma.

A review of 19 patients treated for nephroblastoma between 1945 and 1978 by nephrectomy and radiotherapy with chemotherapy showed a marked improvement in cure rate in recent years. In the decade from 1950 to 1960 there are four survivors. From 1960 to 1970, there are nine survivors from 25 cases and since 1970 there are 19 survivors from 27 cases. Skeletal effects of radiation therapy have been reviewed in 22 patients--seven of whom had orthovoltage and 15 megavoltage therapy. Similar skeletal changes followed both orthovoltage and megavoltage therapy, being more severe after the adolescent growth spurt and when the follow-up was longer. The radiation dose was normally 3000 cGy and skeletal changes followed the lowest dose of 2200 cGY. Scoliosis of the lumbar spine, concave to the side of the tumour, with angulation ranging from less than 5 degrees to 54 degrees developed in 12 patients; all but one showed asymmetry of the body LV2. Kyphosis was present in three patients; anterior beaking of the vertebral body in 10; and 16 patients showed asymmetry of more than one vertebral body. Iliac hypoplasia was present in 19 patients, being unilateral when only the renal bed was irradiated. Analysis of the radiological changes expressed as a total score against the age at follow-up shows that severe changes follow orthovoltage therapy. It is too early to assess the full extent of megavoltage therapy simply because patients have not been followed up for a comparable length of time.

Adolescent↗
PubMed1999

Skeletal effects of zinc deficiency in growing rats.

There is ample evidence that zinc plays an important role in bone metabolism and zinc deficiency has been implicated as a risk factor in the development of osteoporosis. It was the aim of the present study to investigate the skeletal effects of alimentary zinc deficiency in growing rats using quantitative bone histomorphometry. Twenty-four male Sprague Dawley rats with a mean initial body weight of 101 +/- 2 g were allocated in two groups of 12 rats each and had free access to a semi-synthetic, casein-based, zinc-deficient diet (0.76 mg zinc/kg) or to the same diet supplemented with 60 mg zinc per kg. All rats were sacrificed 42 days after the start of the experiment and the right distal femur was removed for bone histomorphometry. Relative to controls (+Zn), the zinc-deficient rats (-Zn) had a significantly lower body weight and about an 80% reduction in plasma and femur zinc concentration. The histomorphometric evaluation of the distal femoral metaphysis showed that zinc deficiency led to a 45% reduction (p < 0.01) in cancellous bone mass and to a deterioration of trabecular bone architecture, with fewer and thinner trabeculae. The osteopenia in -Zn rats was accompanied by significant reductions in osteoid perimeter (-31%, p < 0.05), osteoblast perimeter (-30%, p < 0.05), and osteoclast number (-38%, p < 0.01) relative to +Zn controls. We conclude that zinc deficiency induced low turnover osteopenia in femoral cancellous bone of growing rats. These results support the hypothesis that zinc deficiency during growth may impair the accumulation of maximal bone mass in humans; additionally, they suggest that zinc deficiency may play a role as a risk factor in the pathogenesis of osteoporosis.

Animals↗
PubMed2001

Skeletal effects of systemic treatment with basic fibroblast growth factor.

Systemic treatment of intact and ovariectomized rats with basic fibroblast growth factor (bFGF) has strong bone anabolic effects. These effects include marked increases in osteoblast number and activity along cancellous and endocortical bone surfaces, which result in accumulation of osteoid and augmentation of cancellous and cortical bone mass after only short-term treatment with bFGF. Osteoclast surface is markedly decreased in bFGF-treated rats, but this finding may be secondary to the extensive osteoid surface in these animals. Some undesirable skeletal effects of the growth factor include impaired bone mineralization and formation of structurally inferior woven bone. The lack of a bone anabolic response to bFGF at skeletal sites with fatty marrow and along the periosteal surface of cortical bone is also disappointing. Despite these disadvantages, bFGF stimulates cancellous bone formation to such a great extent that it may eventually be considered for use in patients with severe osteoporosis who are unresponsive to conventional therapies, provided that local delivery of the growth factor to bone can be achieved to avoid systemic side effects.

Journal Article↗
PubMedDate not supplied

The skeletal effects of colony-stimulating factor-1 in toothless (osteopetrotic) rats: persistent metaphyseal sclerosis and the failure to restore subepiphyseal osteoclasts.

Toothless (tl), one of four osteopetrotic mutations in the rat, is characterized by few osteoclasts, undetectable bone resorption, and failure of correction by bone marrow transplantation. We recently reported that CSF-1 treatment improves these skeletal problems but that metaphyseal sclerosis persists. In the present study we demonstrate that optimal reduction of the skeletal sclerosis in tl rats following CSF-1 treatment has lower and upper dosage thresholds and that skeletal sclerosis returns after CSF-1 withdrawal. Osteoclasts increase significantly in tl rats after CSF-1 treatment, but compared to untreated normal littermates, histochemical staining for characteristic enzymes and osteoclast number is reduced and no osteoclasts appear in the subepiphyseal areas of long bones. These data are interpreted to mean that there are dosage limits to the beneficial skeletal effects of CSF-1, that persistent sclerosis is related to the failure to restore subepiphyseal osteoclasts, that osteoclast or progenitor populations may be deficient or differ in their responses to CSF-1, and that the defect in tl rats is not merely lack of a circulating, biologically active form of CSF-1.

Animals↗
PubMed2001

Skeletal effects of developmental lead exposure in rats.

To identify possible direct and indirect mechanisms underlying the effects of lead on skeletal growth, 3 studies were conducted. In the first study, 1 male and 1 female pup/litter (n = 5 litters), were exposed ad libitum to 0, 825, or 2475 ppm lead acetate in the drinking water from gestational day 4 to euthanasia on day 55. Tibial strength was tested by 3-point bending and plasma levels of vitamin D metabolites were measured. A dose-dependent decrease of the load to failure was demonstrated but only in male pups. No differences in plasma levels of vitamin D metabolites were observed. In the second study, conducted to test if hormone treatment would attenuate the lead deficits, male and female pups were exposed to 0 or 2475 ppm lead acetate and then, from 30-60 days of age, received either saline vehicle, L-dopa, testosterone (males only), dihydrotestosterone (DHT, males only), or estradiol (females only). Lead exposure significantly reduced somatic growth, longitudinal bone growth, and bone strength during the pubertal period. Sex steroid replacement did not restore skeletal parameters in lead-exposed rats. L-Dopa increased plasma insulin-like growth factor 1 (IGF(1)) concentrations, rates of bone growth, and bone strength measures in controls while having no effect in lead-exposed pups. The third study was conducted at 100 days of age, when endocrine parameters have been shown to be normalized, to test for effects of lead exposure on bone formation during tibial limb lengthening (distraction osteogenesis, DO). Both DO gap x-ray density and proximal new endosteal bone formation were decreased in the distraction gaps of the lead-treated animals (p < 0.01). In conclusion, lead exposure reduced somatic growth, longitudinal bone growth, and bone strength during the pubertal period, and these effects could not be reversed by a growth hormone (GH) axis stimulator or by sex-appropriate hormones. Finally, lead exposure appears to specifically inhibit osteoblastogenesis in vivo in adult animals.

Animals↗
PubMed2004

The skeletal effects of glucocorticoid excess override those of orchidectomy in mice.

Hypogonadism has been implicated as a contributing factor in glucocorticoid-induced osteoporosis, but evidence for this is limited. Hypogonadism and glucocorticoid excess both cause bone loss, but the cellular mechanisms responsible are distinct. Loss of gonadal steroids causes an increase in bone remodeling by up-regulating osteoblastogenesis and osteoclastogenesis. Glucocorticoid excess, conversely, suppresses remodeling by down-regulating osteoblastogenesis and osteoclastogenesis. Nonetheless, both conditions increase osteoblast apoptosis and decrease osteoclast apoptosis, and both cause bone loss due to an undersupply of osteoblasts relative to the need for cavity repair. To investigate their interactions, we compared the effects of orchidectomy, glucocorticoid excess, or both combined in mice. After 28 d, serum unbound testosterone concentration and seminal vesicle weight were not diminished when prednisolone was administered alone. Vertebral bone mineral density and compression strength decreased to the same extent in animals receiving prednisolone or after orchidectomy, but the changes were not additive. Orchidectomy induced the expected up-regulation of osteoblast and osteoclast progenitors, but these changes were prevented in orchidectomized mice simultaneously receiving glucocorticoids. Likewise, the increase in cancellous osteoid, osteoblasts, osteoclasts, bone formation, and activation frequency caused by orchidectomy were prevented by prednisolone. The prevalence of osteoblast apoptosis increased in the mice receiving prednisolone or after orchidectomy, but the increases were not additive. These data demonstrate that hypogonadism does not occur in or contribute to glucocorticoid-induced osteoporosis and that the adverse skeletal effects of glucocorticoid excess override those of orchidectomy.

Animals↗
PubMed2000

Skeletal effects of parathyroid hormone infusion in ovariectomized rats with or without estrogen repletion.

We employed skeletally matured rats to study changes in biochemical markers of bone turnover, bone mineral density (BMD), and bone biomechanics produced by continuous elevation of parathyroid hormone (PTH) in estrogen-deplete and -replete rodents. Ninety-six 7-month-old virgin female rats were divided randomly into 12 groups (n = 8) and treated as follows. One group was killed on the day of surgery. The remaining groups were either bilaterally ovariectomized (Ovx) or sham-operated and left untreated for 8 weeks, at which point, two groups, one sham and one Ovx, were killed. The remaining nine groups were treated for 2 weeks or 4 weeks. One sham and two Ovx groups received subcutaneous implants of Alzet miniosmotic pumps with vehicle for PTH. Two Ovx groups were given pumps with vehicle as well as a subcutaneous implant of 17beta-estradiol, which delivered 10 microg/kg per day. Two Ovx groups were implanted with rat PTH(1-34) in Alzet miniosmotic pumps, which delivered 30 microg PTH/kg per day. Two Ovx groups were implanted with both estradiol pellets and PTH-loaded pumps. One group of Ovx animals from each treatment was killed after 2 weeks and the other after 4 weeks. Biochemical markers of bone turnover, serum osteocalcin and urinary free pyridinoline, BMD, and mechanical strength of excised bones were measured. As expected, there was a significant increase in N-terminal PTH and serum calcium levels in all PTH infusion groups. Both serum osteocalcin and urinary pyridinoline showed a rapid increase within the first 2 weeks of the PTH infusion and remained elevated at week 4. In estrogen-replete groups, osteocalcin increased by week 2 of PTH infusion but pyridinoline did not increase until week 4. BMD of the distal and proximal femur showed the expected decrease 8 weeks after ovariectomy but did not exhibit any further changes during the 4 weeks of treatment with vehicle. Four weeks of PTH infusion in Ovx animals resulted in BMD loss at the midshaft, distal, and proximal regions of the femur. Estrogen repletion by itself, beginning 8 weeks after ovariectomy, produced no change in BMD at any site when compared with from Ovx vehicle-treated rats. Estrogen repletion in PTH-infused Ovx animals resulted in significant improvements of BMD comparable with sham-operated animals at all three femoral regions. The indentation test at the cancellous bone of the distal femur, three-point bending test at the midshaft femur, and cantilever bending test at the femoral neck showed that the changes in mechanical strength in these sites were consistent to the changes found in BMD. Our results showed that (1) continuously elevated levels of PTH induced additional loss of BMD in estrogen-deficient animals beyond the rapid bone loss phase associated with ovariectomy, (2) estrogen repletion, given by implant, to PTH-infused Ovx animals, reversed these BMD changes increasing BMD to levels comparable with estrogen-sufficient rats, and (3) these changes were reflected in the mechanical strength determined at these sites. These results lend experimental support that hormone replacement therapy may benefit bone health in postmenopausal women with primary hyperparathyroidism (PHPT). In addition, it raises the possibility that a continuous elevation of PTH could exert anabolic effects on skeletal tissue if its catabolic component can be minimized.

Amino Acids↗
PubMed2002

Occlusal and skeletal effects of an oral appliance in the treatment of obstructive sleep apnea.

STUDY OBJECTIVE: s: Oral appliances (OAs) are considered to be a treatment option for patients with obstructive sleep apnea/hypopnea syndrome (OSAHS). Although the effectiveness of these appliances has been evaluated in a number of clinical trials, there are few follow-up studies concerning the dental and skeletal side effects that, theoretically, could be caused by OAs. We sought to examine the long-term skeletal and occlusal effects of a nocturnally worn activator in adult patients treated for OSAHS. DESIGN: We analyzed the dental casts and lateral radiographs of 34 patients (mean age, 52.9 years; SD, 9.6 years; range, 27.1 to 64.6 years) before initiating treatment and after at least 24 months of treatment (mean length of treatment, 29.6 months; range, 24.1 to 43.5 months; SD, 5.1 months). The OA was worn by each patient 6 to 8 h nightly for > 5 days per week. SETTING: Department of Orthodontics, Dental Medical School, Freiburg, Germany. MEASUREMENTS AND RESULTS: Follow-up polysomnography studies confirmed improved breathing parameters with the use of OAs. A statistically significant alteration in the occlusion was found. The anteroposterior position of the molars and the inclination of the upper and lower incisors were changed. No skeletal changes in the position of the mandible were noted. CONCLUSIONS: The data suggest that in addition to control polysomnographic examinations, regular dental follow-up visits are mandatory when lifelong OSAHS treatment with an OA is being considered for patients with obstructive sleep apnea/hypopnea.

Adult↗
PubMed2006

Extra-skeletal effects of bisphosphonates.

Bisphosphonates are pharmacological agents which are currently used both in osteoporosis than in other pathological conditions characterised by an increased bone resorption, such as Paget's disease of bone, malign hypocalcaemia during myeloma, osteolytic bone metastasis and fibrous dysplasia of bone. The most important biological effect of bisphosphonates is the reduction of bone remodelling through the inhibition of osteoclastic activity, but there are many clinical and experimental evidences of extra-skeletal biological effects of bisphosphonates. It has been shown that bisphosphonates exert their effects not only on bone tissue cells, but also on those of the immune system with an "immuno-modulating" effect, influencing the production of pro- and anti-inflammatory cytokines and changing the molecular expression involved in the immune processes and anti-inflammatory response. Although the available data are conflicting, there are several reports concerning the beneficial effects of bisphosphonates in controlling the progression of chronic joint inflammatory diseases, suggesting a wider use for these therapeutic agents in clinical practice.

Animals↗
PubMed2003

Effectiveness of early orthodontic treatment with the Twin-block appliance: a multicenter, randomized, controlled trial. Part 1: Dental and skeletal effects.

This study evaluated the effectiveness of early orthodontic treatment with the Twin-block appliance for the developing Class II Division 1 malocclusion. This multicenter trial was carried out in the United Kingdom. A total of 174 children, aged 8 to 10 years old, with Class II Division 1 malocclusion were randomly allocated to receive treatment with a Twin-block appliance or to an untreated, control group. Data were collected at the start of the study and 15 months later. Results showed that early treatment with Twin-block appliances resulted in reduction of overjet, correction of molar relationships, and reduction in severity of malocclusion. Most of this correction was due to dentoalveolar change, but some was due to favorable skeletal change. Early treatment with the Twin-block appliance is effective in reducing overjet and severity of malocclusion. The small change in the skeletal relationship might not be considered clinically significant.

Age Factors↗
PubMed1995

[The dental and skeletal effects of the jumping-the-bite plate and high-pull headgear combination. A clinical study of treated patients].

While planning treatment of the 30 patients with a dental and skeletal class II anomaly on which this study is based, the primary treatment goals were correction of the dental and skeletal structures and attenuation of vertical growth by means of influencing the maxillary skeletal structures and the resultant mandibular reaction. The desired treatment results were achieved in all patients. Even so, however, the effects on individual patients in respect to skeletal influences were markedly different. It was especially helpful that during therapy simultaneously with exerting influence on the maxillary base plane, the influencing of the occlusal plane occurred in the same direction. Through the additional application of high-pull headgear, maxillary growth was clearly restrained and the inclination of the maxillary base plane inhibited. Even difficult skeletal discrepancies, sagittal as well as vertical, can be treated with the bite-jump appliance in combination with a high-pull headgear. This also makes it possible to achieve protrusive repositioning of the mandible in patients with a pronounced vertical growth pattern without causing on open bite. In retrospective the patients' treatment plans proved to be completely appropriate, however, the fact should not be overlooked that changing the occlusal plane is essential for the realization of a positive therapeutic result.

Activator Appliances↗
PubMed1986

Skeletal effects of carcinoma of the breast and prostate.

Recent research has led to improved understanding of the pathology of skeletal metastases in carcinoma of the breast and prostate. Several humoral mechanisms have been identified which have both primary and secondary consequences on skeletal metabolism and probably depend on the complex interplay of a number of factors derived from tumour tissues. An improved understanding of these interactions may lead to new approaches in the management of these common disorders.

Bone Neoplasms↗