Calcitonin Treatment Research Articles

Effect of calcitonin on lipid peroxidation in ovariectomized rats

Calcitonin is one of the active substances which is recently used effectively in osteoporosis treatment. In literature there is no information whether calcitonin cause oxidative stress or not. In this study, subcutaneous calcitonin is applied to rats having experimental postmenopausal osteoporosis and the effects of calcitonin on lipid peroxidation and antioxidant system were investigated. Forty-five healthy adult female Swiss albino Wistar rats were used in this study. The rats were divided into three equal groups as control, ovariectomized (Ovx) and ovariectomized+calcitonin (Ovx-CAL). The rats in Ovx and Ovx-CAL were anaesthetized and underwent a bilateral ovariectomy via ventral incision. Ten weeks after ovariectomy, salmon calcitonin (2 IU/kg body weight) was administered via s.c. at a volume of 1 mL per week for 12 weeks to the Ovx-CAL group. At the end of the drug treatment, livers and kidneys of rats were removed and malondialdehyde (MDA) levels and catalase (CAT) activities were determined by biochemical analysis methods. Data were analyzed by one-way ANOVA followed by the post-hoc LSD multiple test. The liver and kidney MDA levels were increased whereas the activity of CAT enzyme was decreased as a result of ovariectomy compared to values in the control group. Similar results were observed in Ovx-CAL group; however, the decline in the CAT activity in the kidney was not significant. In conclusion, we may suggest that calcitonin treatment increases the oxidative stress in osteoporotic rats.

Ultimobranchial gland of freshwater catfish, Heteropneustes fossilis, in response to calcitonin administration

The absence o!!f a hypocalcemic effect of calcitonin (CT) in fishes has been suggested due to exceedingly high plasma levels of CT; the fish may be saturated with respect of circulating CT and therefore unable to respond to exogenously administered CT. Earlier it has been suggested that a hypocalcemic action of injected CT may be obscured by changes in the release of endogenous CT and other calcium regulating hormones. In this study we have used artificial freshwater, calcium-deficient freshwater and calcium-rich freshwater and injected the fish with CT. The aim behind selecting these media were (i) in calcium-deficient medium there would be reduced circulating levels of CT, (ii) in calcium-rich medium there would be diminished secretion of prolactin (this hormone is hypercalcemic in fish), and (iii) by keeping the fish in calcium-rich medium we can test the antihypercalcemic action of CT. Moreover, the present study would reveal the changes in the ultimobranchial gland (UBG) after keeping the fish in all the above three media and/or injecting the fish with CT. Freshwater catfish, Heteropneustes fossilis, were administered intraperitoneally daily with vehicle or 0.5 U/100g body wt of salmon calcitonin (CT) and kept in artificial freshwater, calcium-rich freshwater and calcium-deficient freshwater for 10 days. Blood samples were collected on 1, 3, 5, and 10 days following the treatment and analyzed for serum calcium levels. The ultimobranchial gland (UBG) was also fixed for histological studies on these intervals. In artificial freshwater there was no change in the serum calcium levels of calcitonin-injected fish. The ultimobranchial gland of calcitonin-injected fish exhibited a progressive decrease in the nuclear volume from day 5 onwards. On day 10 vacuolization in the gland was also noticed. In vehicle-injected fish (control) kept in calcium-rich freshwater hypercalcemia has been noticed which persists till the end of the experiment. In calcitonin-treated fish maintained in calcium-rich freshwater there is no change in serum calcium level as compared to vehicle-injected fish. In vehicle-injected fish the UBG depicts decreased staining response and increased nuclear volume at day 5. On day 10 the nuclear volume is further increased and few degenerating cells have been noticed. Calcitonin fails to induce any histological change in the UBG as compared to control. In vehicle-injected fish kept in calcium-deficient freshwater the serum calcium levels decrease from day 1 to day 3. The levels exhibit hypercalcemia on day 10. CT treatment to the fish kept in calcium-deficient freshwater evokes a decrease in the calcium levels on day 1 and day 3. A significant hypercalcemia has been noticed on day 5 and day 10. In vehicle-injected fish kept in calcium-deficient freshwater the UBG reveals a decreased staining response on day 10. In CT-injected fish maintained in calcium-deficient freshwater the UBG depicts an increased nuclear volume and few exhausted cells on day 10. It can be concluded that CT can provoke hypocalcemia only when the fish is kept in medium which reduces the circulating levels of this hormone. The UBG of the fish kept in different calcemic media responded in a manner to indicate that it produces hypocalcemic factor - CT.

Diagnosis and treatment of osteoporotic fractures

Diagnosis and treatment of osteoporotic fractures

Central giant cell lesion of the jaw: Nonsurgical treatment with calcitonin nasal spray

The aim was to evaluate the effectiveness of the long-term administration of intranasal calcitonin spray for the treatment of central giant cell granuloma (CGCG) in a retrospective case study. The medical files of 5 patients (4 male, 1 female; ages 8-66 years) with CGCG of the jaws treated with calcitonin nasal spray 200 U/spray once or twice daily were reviewed for lesion-related parameters, outcome, and adverse effects of therapy. Three lesions were located in the mandibular body and ramus region and 2 in the anterior maxilla. Mean lesion size on radiography was 3.2 x 2.3 cm. The duration of calcitonin treatment was 9-60 months (mean 28 months). All the lesions considerably decreased in size with a high degree of calcification. There were no recurrences. Calcitonin nasal spray appears to be safe and effective for the treatment of CGCG and might be considered an alternative to surgery. Further controlled studies are needed to corroborate these findings.

Influence of calcitonin administration on ultimobranchial and parathyroid glands of pigeon, Columba livia

Pigeons were divided into two numerically equal groups (A and B) containing 30 specimens each. Birds from group A were intraperitoneally injected daily with 0.1 mL/100 g body wt of vehicle (0.1 M acetate buffer, pH 4.3 containing 0.1% gelatin). Specimens from group B were intraperitoneally injected daily with 1 microg/100 g body wt of salmon calcitonin. Six birds were sacrificed from each group 2 h after the last injection on 1st, 3rd, 5th, 10th, and 15th day of the experiment. After collection of blood samples, ultimobranchial and parathyroid glands were fixed for histological studies. In calcitonin-treated C. livia, the plasma calcium levels exhibit a progressive decline from day 1 till day 5. On day 15, the levels become more or less similar to the control value. No change has been noticed on day 1 in the plasma phosphate levels of calcitonin-treated C. livia. The levels decrease progressively from day 3 to day 5; thereafter, it exhibits an elevation so that on day 15, normal plasma phosphate levels is achieved. The ultimobranchial gland of C. livia exhibits no change up to day 5 following calcitonin treatment. The nuclear volume of ultimobranchial cells exhibits a decrease on day 10. This response progresses up to day 15. Few degenerating cells are also discerned following 15 days calcitonin treatment. The parathyroid gland of calcitonin-treated C. livia exhibits no histological alteration up to day 3. The nuclear volume of parathyroidal cells exhibits a progressive increase from day 3 till the close of the experiment (day 15). Moreover, the gland exhibits more compactness on day 10 and day 15. Few degenerating cells are encountered after day 15 following calcitonin treatment.

P.053 Schwannoma of the mandible

The long-term follow-up case of monostotic fibrous dysplasia of the maxilla in a 10-year-old girl is described with her endocrinologic data and therapeutic consequence of calcitonin administration in association with surgical interventions. The fibrous dysplasia tends to become more quiescent or static after skeletal growth ceases, but the causative has been still unknown to date. In this case reported changes of calciotropic hormones in the serum were well corresponding to the ceasing of the tumor growth at the puberty and reflected to the calcitonin administration. Although calcitonin has been applied to the fibrous dysplasia associated with McCune Albright syndrome, no histologic changes have been described after the calcitonin treatment. This report might be the first description of bone remodeling after the calcitonin treatment for the fibrous dysplasia of the maxilla in immature people. Data of this case may provide a clue to the pathogenesis of fibrous dysplasia. Surgical intervention can be performed after the local bone calcification by a calcitonin treatment, because of alleviation of vigorous hemorrhage by the bone remodeling.

Degeneration of Paget’s disease into sarcoma: clinical and therapeutic influencing factors

We analysed a series of 119 patients presenting with Paget's bone disease treated at the Istituto Ortopedico Rizzoli (Bologna Italy) over 35 years (from 1970 to 2006). Among these, we found 18 cases that had degenerated into sarcoma. The first goal of this study was to underline the potential factors of Paget's disease transformation into sarcoma. In detail we considered: age, gender, duration of disease, clinical expression, levels of total alkaline phosphatase and type of therapy. The results highlighted an interesting correlation between therapy and degeneration into sarcoma; more specifically, malignant transformation occurred both in patients who had not received any therapy and those who had received regular calcitonin treatment; otherwise, no sarcoma degeneration occurred in the patients treated with bisphosphonates. These data seem to indicate a preventing effect of bisphosphonates towards the degeneration of Paget's disease into sarcoma.

Calcitonin ??? A Drug of the Past or for the Future?

Postmenopausal osteoporosis results from a continuous imbalance between bone resorption and bone formation, favoring bone resorption. An increasing number of treatments for osteoporosis are in development and on the market. A range of differences and similarities are found between these treatment options, and these need to be carefully evaluated before the initiation of treatment. This article summarizes data from in vitro and animal studies, as well as clinical trials, on the effect of calcitonin on bone turnover. Calcitonin was found to exert its antiresorptive effects via directly reducing osteoclastic resorption, and thus leads to an increase in bone mineral density and bone strength. Furthermore, calcitonin appears to mainly target the most active osteoclasts, and in contrast to most other antiresorptive agents it does not reduce the number of osteoclasts. Finally, in humans, while attenuating resorption, calcitonin treatment does not interfere markedly with bone formation, in contrast to other currently available antiresorptive agents. Thus, we speculate that calcitonin treatment will lead to a continuously positive bone balance in contrast with other antiresorptive agents currently on the market and thereby, in a physiologic manner, result in improved bone quality. Calcitonin is currently only available in injectable and nasal formulations. An oral formulation may, however, improve patient acceptance and compliance. Currently, several different routes are being pursued to identify an optimal oral formulation, of which the technology based on 5-CNAC is the most advanced. There are promising clinical data available for this formulation from both osteoarthritis and osteoporosis clinical trials, although the antifracture efficacy is not yet known.

The Murine Glucagon-Like Peptide-1 Receptor Is Essential for Control of Bone Resorption

Gastrointestinal hormones including gastric inhibitory polypeptide (GIP), glucagon-like peptide (GLP)-1, and GLP-2 are secreted immediately after meal ingestion, and GIP and GLP-2 have been shown to regulate bone turnover. We hypothesize that endogenous GLP-1 may also be important for control of skeletal homeostasis. We investigated the role of GLP-1 in the regulation of bone metabolism using GLP-1 receptor knockout (Glp-1r(-/-)) mice. A combination of bone density and histomorphometry, osteoclast activation studies, biochemical analysis of calcium and PTH, and RNA analysis was used to characterize bone and mineral homeostasis in Glp-1r(-/-) and Glp-1r(+/+) littermate controls. Glp-1r(-/-) mice have cortical osteopenia and bone fragility by bone densitometry as well as increased osteoclastic numbers and bone resorption activity by bone histomorphometry. Although GLP-1 had no direct effect on osteoclasts and osteoblasts, Glp-1r(-/-) mice exhibited higher levels of urinary deoxypyridinoline, a marker of bone resorption, and reduced levels of calcitonin mRNA transcripts in the thyroid. Moreover, calcitonin treatment effectively suppressed urinary levels of deoxypyridinoline in Glp-1r(-/-), mice and the GLP-1 receptor agonist exendin-4 increased calcitonin gene expression in the thyroid of wild-type mice. These findings establish an essential role for endogenous GLP-1 receptor signaling in the control of bone resorption, likely through a calcitonin-dependent pathway.

Calcitonin Promotes Outgrowth of Trophoblast Cells on Endometrial Epithelial Cells: Involvement of Calcium Mobilization and Protein Kinase C Activation

Embryo implantation is a complex process that requires coordinated trophoblast–endometrial interactions. During implantation, trophoblast cells of the attached blastocyst penetrate the luminal epithelium of the endometrium before invasion into the endometrial stroma. Previous studies demonstrated that calcitonin was actively secreted by rat and human endometrial epithelial cells (EEC) during the implantation window and targeted disruption of endometrial calcitonin expression dramatically decreased embryo implantation rates; however, the role and signal transduction of calcitonin in trophoblast–endometrial interactions remained unclear and are therefore examined in this study. BeWo trophoblast and RL95-2 EEC lines were used because they preserve many properties of their respective normal tissues. We co-cultured BeWo trophoblast spheroids with RL95-2 EEC monolayers to mimic the blastocyst–endometrial interaction, and found that most spheroids quickly attached to EEC monolayers and then progressively expanded, with marked displacement of EEC adjacent to the outgrowing trophoblast cells. Interestingly, pretreatment of EEC monolayers with calcitonin before the addition of spheroids significantly enhanced trophoblast expansion on EEC monolayers. Cytosolic calcium (Ca 2+) levels in EEC increased rapidly upon exposure to calcitonin, and blockade of Ca 2+ release by BAPTA-AM effectively prevented the promoting effect of calcitonin on trophoblast expansion on EEC. The Ca 2+-dependent protein kinase C (PKC) was also activated in EEC after calcitonin treatment, and the PKC inhibitors staurosporine and calphostin C could completely abolish calcitonin-induced augmentation of trophoblast expansion on EEC. Our results suggest that calcitonin promotes trophoblastic displacement of EEC through calcium mobilization and PKC activation, thereby facilitating embryo implantation.

Idiopathic infantile hypercalcemia and renal involvement

Idiopathic infantile hypercalcemia is recognized as a rare cause of infantile hypercalcemia. Its renal consequences include nephrocalcinosis with distal tubular dysfunction, nephrolithiasis, and finally renal failure. Herein we report the case of a two-month-old infant presenting with idiopathic infantile hypercalcemia complicated with distal renal tubular acidosis (RTA) and nephrocalcinosis. Despite correction of acidosis and dehydration, the persistant hypercalcemia could only be ameliorated with calcitonin treatment. Early diagnosis and appropriate treatment is life-saving in such cases.

Calcitonin Affects Both Bone and Cartilage

Osteoarthritis (OA) is the most common form of degenerative joint diseases and a major cause of disability and impaired quality of life in the elderly. OA is a complex disease involving both bone and cartilage properties, and may therefore require alternative approaches for treatment. Recent lines of evidence suggest that calcitonin acts on both osteoclasts and chondrocytes. The review summarizes emerging observations from cell biology to preliminary clinical trials, describing possible chondroprotective effects of calcitonin. This review summarizes peer-reviewed articles found using predefined search criteria and published in the PubMed database before June 2007. In addition, abstracts from the OsteoArthritis Research Society International (OARSI) conferences in the time period 2000 to 2006 were included. A range of studies, at the cellular level, in animal models, and in clinical trials, describe positive effects of calcitonin on bone health. Regarding articular cartilage, direct effects of calcitonin on chondrocytes on matrix synthesis, as well as inhibition of cartilage degradation, have been presented. In addition, clinical evidence for a chondroprotective effect of calcitonin is emerging. Several lines of evidence suggest direct anabolic effects of calcitonin on articular chondrocytes, resulting in increased proteoglycan synthesis. The anticatabolic effects of calcitonin may involve induction of cAMP, resulting in attenuation of MMP-mediated cartilage degradation. Presently there is limited availability of chondroprotective agents. Therefore, the current clinical research on calcitonin is highly anticipated, and may prove calcitonin treatment efficacious for the prevention and treatment of OA.

The effect of oral calcitonin on cartilage turnover and surface erosion in an ovariectomized rat model

To investigate whether oral calcitonin treatment influences the increases in type II collagen (CII) degradation and related surface erosions of articular cartilage in ovariectomized rats. Fifty rats were randomly allocated into 1 of the 5 following intervention groups: sham-operated, ovariectomy, ovariectomy plus subcutaneously implanted 17beta-estradiol pellet, ovariectomy plus 2 mg/kg salmon calcitonin plus 50 mg/kg 5CNAC (carrier), or ovariectomy plus 50 mg/kg 5CNAC. Each treatment was administered for 9 weeks after the ovariectomy. Blood samples for biochemical marker analysis were collected from fasting animals at baseline, on day 3, and after 1, 2, 4, 6, and 9 weeks. CII degradation was quantified by specific immunoassay, and the changes in severity scores of articular cartilage erosions were visualized and scored in histologic sections of the knees. Ovariectomy resulted in a marked increase in serum levels of C-telopeptide of type II collagen (CTX-II) (P < 0.001), which could be effectively reversed by 17beta-estradiol supplementation. Oral administration of calcitonin elicited similar decreases in serum levels of CTX-II (P < 0.001). Histologic scoring of cartilage erosion showed significantly less cartilage erosion in calcitonin-treated ovariectomized rats versus control ovariectomized rats that were untreated or treated with 5CNAC alone. (P < 0.01). The in vivo effects of calcitonin in rats suggest that calcitonin is able to counteract CII degradation and the accompanying structural disintegration of articular cartilage promoted by estrogen deficiency. Clinical assessment of the chondroprotective potential of calcitonin in postmenopausal women seems warranted.

Effect of combined humanPTH(1–34) and calcitonin treatment in ovariectomized rats

We examined the combined effects of human parathyroid hormone 1–34 (hPTH) and elcatonin (ECT: a synthetic derivative of eel calcitonin) to prevent loss of bone mass, architecture and strength in ovariectomized (OVX) rats. Fifty-four female rats (aged 13 weeks) were assigned to one of nine groups: Sham (fake surgery performed), OVX, ECT (15 U/kg administered), PTH5, PTH10 and PTH20 (5, 10 or 20 μg/kg administered), and E + PTH5, E + PTH10 and E + PTH20 (15 U/kg of ECT and 5, 10 or 20 μg/kg of hPTH administered). The drug or vehicle was subcutaneously administered three times a week for 12 weeks. The femurs were removed at the completion of the experiment. The right distal femoral metaphysis was used for measuring bone mineral density (BMD), analyzing trabecular bone structure by micro-computed tomography (μCT), and conducting the bone strength test, and the left femur was used for histomorphometric analysis. Trabecular bone volume (BV/TV) and other bone mass parameters were greater in the ECT and PTH groups than in the OVX group. The number of nodes (N.Nd/TV) and trabecular number (Tb.N) were significantly greater in the ECT group, and trabecular thickness (Tb.Th) and trabecular bone pattern factor (TBPf) were significantly greater in the PTH group. These results indicate that these drugs preserve the bone architecture by different means. Analysis by means of μCT revealed that BV/TV, Tb.N, fractal D and N.Nd/TV were significantly greater in the E + PTH groups than in the PTH groups at each concentration. Trabecular separation (Tb.Sp) was significantly lower in the E + PTH5 and E + PTH10 groups than in the respective PTH5 and PTH10 groups. When the maximum load was applied in a compression test on the distal femur, the E + PTH groups had higher values than the PTH groups, however, the three point bending strength of the diaphysis of femur in the E + PTH10 and E + PTH20 groups tended to be low compared to those in the PTH10 and PTH20 groups. These results indicate that combination therapy using PTH and ECT preserves the trabecular microarchitecture better than single-drug therapy using ECT or PTH in OVX rats, however, it is necessary to optimize the calcitonin (CT) dosage and administration in order to achieve the optimal combined effect of PTH and CT.

Calcitonin nasal spray for treatment of central giant cell granuloma: Clinical, radiological, and histological findings and immunohistochemical expression of calcitonin and glucocorticoid receptors

To provide clinical, radiological, and histopathologic analyses of 5 patients with central giant cell granuloma (CGCG) treated with calcitonin nasal spray; to compare the results to 11 well-documented cases in the literature; and to evaluate lesions for immunohistochemical expression of calcitonin receptors (CTR) and glucocorticoid receptors (GCR). Five patients with CGCG were treated with calcitonin nasal spray, 200 to 400 IU/day, for 13 to 64 months. CTR and GCR expression were examined at different treatment times. No lesions showed significant clinical and/or radiological improvement in size. The main benefit was thickening of the cortical plates. All patients eventually underwent curettage and continued calcitonin treatment. Significant radiological improvement was noticed 2 to 4 months postsurgical procedure. Each lesion exhibited a different immunoprofile for CTR and GCR, pretreatment and during treatment. CTR disappeared after long-term calcitonin treatment. GCR exhibited variable changes. Long-term nasal spray calcitonin was ineffective for CGCG management compared with calcitonin injections. It is suggested that lesions with an undesirable response should be evaluated for CTR and GCR expression at different treatment times for maximal benefit of calcitonin treatment.

Calcitonin therapy in central giant cell granuloma of the jaw: a randomized double-blind placebo-controlled study

The successful therapeutic use of calcitonin in patients with a central giant cell granuloma has been shown in several case reports. In a prospective, randomized, double-blinded, placebo-controlled clinical trial, 14 patients with a histologically confirmed central giant cell granuloma and normal calcium and parathyroid hormone serum levels were studied over 2 years. Patients were treated with intranasally administered salmon calcitonin (200 IU/day) or a placebo once a day. The placebo-controlled period was 3 months, after which all patients were treated with calcitonin for 1 year. Treatment response was assessed at the end of the placebo-controlled study phase (3 months), at the end of therapy (15 months’ timepoint with patients being on calcitonin treatment for either 12 or 15 months) and at 6 months’ follow-up. The χ 2-test was used to compare the proportion of patients with a tumour reduction ≥10% of the pretreatment measurement between the 2 populations at the 3 timepoints: no differences were observed between the placebo group and the calcitonin group. At the 6-month follow-up timepoint, tumour volume had decreased by ≥10% in a total of 7 patients with a 37.9% (95% CI 31.3–44.5%) mean volume reduction in this subgroup. Complete remission was not observed.

Phosphodiesterase 4 inhibitor rolipram potentiates the inhibitory effect of calcitonin on osteoclastogenesis

To assess the combination effect of calcitonin and the phosphodiesterase 4 inhibitor rolipram on osteoclastogenesis, adherent cell-depleted bone marrow cells from mouse tibia and femur (ACD-BMCs), which were cultured in the presence of 25 ng/ml colony-stimulating factor 1 (CSF-1) and 100 ng/ml soluble receptor activator of NF-kappaB ligand (sRANKL), were utilized. Calcitonin inhibited formation of tartrate-resistant acid phosphatase-positive multinucleated cells, as mature osteoclasts, by 70% even at 20 pM, whereas rolipram (10 microM) scarcely affected osteoclast formation; in contrast, the combination of both agents led to significant inhibition of multinucleation and pit formation ability of osteoclasts. The combined administration of calcitonin and rolipram attenuated calcitonin receptor mRNA expression in comparison to treatment with either agent alone, whereas expression of RANK and CSF-1 receptor mRNAs was unchanged. Alone, these agents scarcely elevated intracellular cyclic AMP (cAMP) concentration; however, combination treatment with both agents significantly increased cAMP concentration in osteoclast progenitors and osteoclasts. The combination effect was abolished by H-89, an inhibitor of protein kinase A. It appears that rolipram inhibited hydrolysis of cAMP formed by calcitonin in cells and potentiated the inhibitory effect of calcitonin on osteoclastogenesis. The escape phenomenon following calcitonin treatment may also be prevented by concomitant treatment with the phosphodiesterase 4 inhibitor.

A comparison of teriparatide and calcitonin therapy in postmenopausal Asian women with osteoporosis: a 6‐month study

ABSTRACTObjective: The number of hip fractures is expected to double in the next 20 years, with current estimates that Asia will account for 37% of these cases. As bone mineral density (BMD) may be used as a measure of fracture risk, we sought to compare the effects of teriparatide with salmon calcitonin treatment on changes in BMD, biochemical bone markers, and safety in postmenopausal Asian women with osteoporosis.Methodology: A total of 104 patients ( n = 47 teriparatide [20 µg/day subcutaneously] and n = 57 calcitonin [100 IU/day subcutaneously]) were enrolled in Hong Kong, Singapore, Philippines, Malaysia, and Thailand. Calcium (≥ 500 mg/day) and vitamin D (200–400 IU/day) supplements were taken throughout the 6‐month controlled, randomized study.Results: Teriparatide was associated with a 5.03 ± 4.77% increase in lumbar spine BMD ( p < 0.0001, mean ± SD change from baseline), whereas changes in lumbar spine BMD for patients on calcitonin were not statistically significant (mean change of 0.36 ± 4.12%, p = 0.16). Comparison of the two groups indicated that teriparatide treatment improved lumbar spine BMD statistically significantly more than calcitonin ( p < 0.0001). No statistically significant changes were observed for total hip or femoral neck BMD. Serum bone-specific alkaline phosphatase (BSAP) increased by 55.9% (median change from baseline, p < 0.0001) in the teriparatide group, and remained stable with calcitonin (5.0% change, p = 0.24); osteocalcin increased by 156.15% (median change from baseline, p < 0.0001) with teriparatide, and decreased with calcitonin (–15.25%, p = 0.03). Similar rates of adverse events were observed, with nausea and dizziness the most commonly reported for both groups (teriparatide versus calcitonin, 13.0% versus 23.2% p = 0.21, 10.9% versus 21.4% p = 0.19, respectively). There were no clinically relevant changes observed in laboratory parameters.Conclusions: Both treatments were similarly tolerated, however teriparatide was associated with greater increases in lumbar spine BMD and bone formation markers, demonstrating the unique mechanism of action and safety of this treatment for osteoporosis in these Asian women.

Bone Mineral Density Changes in Patients With Prostate Cancer During the First 2 Years of Androgen Suppression

We characterized bone mineral density changes in patients with prostate cancer on androgen deprivation therapy during the first 2 years of uninterrupted therapy, and identified which location most reflects bone mass loss. Using dual energy x-ray absorptiometry, bone mineral density was prospectively assessed in patients with nonmetastatic prostate cancer at the lumbar spine and femoral neck, Ward's triangle, trochanter and total hip. Measurements were performed at baseline and yearly thereafter in patients on ADT, and at baseline and 1 year in controls (age matched patients with prostate cancer, free of biochemical progression after radical prostatectomy). A total of 62 patients were included in the study, 31 in each group. Median age (70 and 69 years, respectively), mean Gleason score and mean baseline serum testosterone did not significantly differ. Patients receiving ADT experienced a significant bone mass loss at 12 months in all locations, ranging from 2.29% to 5.55% (p <0.001). In contrast, bone mineral density did not change significantly (0.64% to 1.68%) in patients not receiving ADT. In the 20 patients on ADT after 24 months, the second year decrease was not as severe, nor was it significant compared to first year values. The major bone mass loss occurred in Ward's triangle, with decreases of 5.55% at 12 months and 7.05% at 24 months. Bone mineral density decreases during the first 24 months of androgen suppression with the most relevant effect occurring in the first year. Ward's triangle is the axial skeletal site that reflects the major bone mass loss. Because the deleterious impact of long-term androgen suppression on bone mineral density is inversely related to fracture risk and indirectly related to survival in patients with prostate cancer, early diagnosis and prevention of bone mass loss are warranted in these patients.

Calcitonin treatment for calcifying tendinitis of the shoulder

In an open, uncontrolled trial, the clinical and radiological responses to calcitonin therapy in the treatment of acute calcifying tendinitis of the shoulder were investigated. A total of 35 patients (38 shoulders) were enrolled. Each patient was injected with 10 U synthetic calcitonin intramuscularly twice a week. The mean number of injections was 6.0 (range, 1–16). At the end of the treatment period, 33 shoulders (87%) were pain-free. In 28 shoulders (74%), the localized pain disappeared within 2 weeks of the start of treatment. In 25 shoulders (66%), the clinical results were rated as good, with complete pain relief and sufficient recovery in the activities of daily living (ADL) and active range of shoulder joint motion (ROM). On the contrary, in 4 shoulders (10%) pain persisted, requiring alternative treatment. In 28 shoulders (74%), the pre-existing calcific deposits were remarkably reduced or had disappeared. Radiologically, the shoulders with fluffy-type deposits had greater pain relief and ROM recovery than those with defined-type deposits. However, there was no correlation between the clinical results and localized region or size of deposits. In 19 cases (50%) where the calcified deposits had completely disappeared, the shoulder had become pain-free, and in all of them except two cases there was complete recovery of ROM. No patient developed clinical complications. These results suggest that calcitonin treatment may be useful for calcifying tendinitis of the shoulder, and that this therapy results in both clinical and radiological improvement in this condition.