Calcitonin as a pharmacological anchorage in orthodontics.

Objective: This study aimed to evaluate the effects of salmon calcitonin administration as a pharmacological anchoring agent in orthodontics and to determine the influence of locally applied calcitonin on serum calcium levels. The secondary aim was to observe the response of dental and periodontal tissues using light microscopy. Methods: Fourteen healthy male adult Wistar rats with an average weight of 250 g had their teeth moved, seven of which received a local injection of salmon calcitonin in the furcation region of the left upper first molar. Concurrently, the remaining seven were used as controls. In the control group, saline solution was injected in the bifurcation region of tooth 26 to subject these animals to the same stress level as those of the experimental group. After 14 days, a 6 mm diameter orthodontic elastic band was inserted between teeth 26 and 27 in all animals to induce the movement of these teeth. The rats were anaesthetised and exsanguinated on day 21. In both groups, tooth movement and serum calcium levels were measured. The jaws were dissected with straight scissors, and tissue blocks containing gingiva, bone and teeth were identified, fixed and demineralised. Then, the pieces were cut into semi-serial slices, stained with hematoxylin, eosin, and Mallory's trichrome, and analysed under an Axiophot light microscope. Results: There was significantly less tooth movement in the experimental group (X̄; 0,150 mm ± 0,037) than in the control group (0,236 mm ± 0,044; P = 0,003), while there was no significant difference in serum calcium levels between the two groups (controlX̄; 9,53 mg/dl ± 1,53; experimental 10,81 mg/dl ± 1,47; P = 0,15). Conclusion: While calcitonin did not completely inhibit osteoclast activity, it promoted orthodontic anchorage, apparently, by local action.

[Calcitonin as an analgesic agent: review of mechanisms of action and clinical applications]. / Calcitonina como agente analgésico: revisão dos mecanismos de ação e das aplicações clínicas.

BACKGROUND AND OBJECTIVES: Calcitonin is a polypeptide hormone regulating the metabolism calcium in the body. For many years calcitonin has been used to maintain and improve bone mineral density and to reduce the fracture rate. Many studies showed that calcitonin had analgesic role in several painful circumstances. This pain-ameliorating effect is irrelevant to its osteoclastic inhibitory effect and mechanisms like altering Na+ channel and serotonin receptor expression or hypothesis including the endorphin-mediated mechanism were used to explain this effect. In this study we performed a thorough review on the role of calcitonin as an analgesic agent in different scenarios and investigated the fact that calcitonin can be a feasible medication to relieve pain. METHOD: Many studies focused on the analgesic effect of calcitonin in several painful circumstances, including acute pains related to vertebral fractures, metastasis, migraine and reflex sympathetic dystrophy as well as neuropathic pains related to spinal injuries or diabetes, and phantom pain. Also, calcitonin was showed to be a useful additive to local anesthesia in the case of controlling postoperative pain or trigeminal neuralgia more effectively. However we faced some contradictory data for conditions like lumbar canal stenosis, complex regional pain syndrome, phantom pain and malignancies. CONCLUSION: This study showed that calcitonin could be helpful analgesic agent in different painful situations. Calcitonin can be considered an eligible treatment for acute pains related to vertebral fractures and a feasible alternative for the treatment of the acute and chronic neuropathic pains where other medications might fail.

Calcitonin as an analgesic agent: review of mechanisms of action and clinical applications / Calcitonina como agente analgésico: revisão dos mecanismos de ação e das aplicações clínicas

Abstract Background and objectives: Calcitonin is a polypeptide hormone regulating the metabolism of calcium in the body. For many years calcitonin has been used to maintain and improve bone mineral density and to reduce the fracture rate. Many studies showed that calcitonin had analgesic role in several painful circumstances. This pain-ameliorating effect is irrelevant to its osteoclastic inhibitory effect and mechanisms like altering Na+ channel and serotonin receptor expression or hypothesis including the endorphin-mediated mechanism were used to explain this effect. In this study we performed a thorough review on the role of calcitonin as an analgesic agent in different scenarios and investigated the fact that calcitonin can be a feasible medication to relieve pain. Method: Many studies focused on the analgesic effect of calcitonin in several painful circumstances, including acute pains related to vertebral fractures, metastasis, migraine and reflex sympathetic dystrophy as well as neuropathic pains related to spinal injuries or diabetes, and phantom pain. Also, calcitonin was showed to be a useful additive to local anesthesia in the case of controlling postoperative pain or trigeminal neuralgia more effectively. However we faced some contradictory data for conditions like lumbar canal stenosis, complex regional pain syndrome, phantom pain and malignancies. Conclusion: This study showed that calcitonin could be helpful analgesic agent in different painful situations. Calcitonin can be considered an eligible treatment for acute pains related to vertebral fractures and a feasible alternative for the treatment of the acute and chronic neuropathic pains where other medications might fail.

Resumo Justificativa e objetivos: A calcitonina é um hormônio polipeptídico que regula o metabolismo do cálcio no organismo. Por muitos anos a calcitonina tem sido usada para manter e melhorar a densidade mineral óssea e reduzir a incidência de fraturas. Muitos estudos mostraram que a calcitonina teve efeito analgésico em várias condições físicas de dor. Esse efeito de melhoria da dor é irrelevante diante de seu efeito inibidor osteoclástico e de mecanismos, tais como a alteração do canal de Na+ e da expressão do receptor de serotonina, inclusive a hipótese do mecanismo mediado pela endorfina, que foram usados para explicar esse efeito. Neste estudo, fizemos uma revisão completa sobre o papel da calcitonina como agente analgésico em diferentes cenários e investigamos o fato de que a calcitonina pode ser uma medicação viável para aliviar a dor. Método: Muitos estudos centraram no efeito analgésico da calcitonina em várias condições de dor, inclusive dores agudas relacionadas a fraturas vertebrais, metástases, enxaqueca e distrofia simpática reflexa, bem como dores neuropáticas relacionadas a lesões medulares ou ao diabetes e dor fantasma. Além disso, a calcitonina mostrou ser um aditivo útil à anestesia local para o controle mais efecaz da dor pós-operatória ou neuralgia do trigêmeo. Porém, nos deparamos com alguns dados contraditórios em condições como estenose do canal lombar, síndrome complexa da dor regional, dor fantasma e malignidades. Conclusão: Este estudo mostrou que a calcitonina pode ser um analgésico útil em diferentes condições de dor. A calcitonina pode ser considerada um tratamento elegível para as dores agudas relacionadas a fraturas vertebrais e uma opção viável para o tratamento das dores neuropáticas agudas e crônicas em que outros medicamentos podem falhar.

STC1 interference on calcitonin family of receptors signaling during osteoblastogenesis via adenylate cyclase inhibition.

Stanniocalcin 1 (STC1) and calcitonin gene-related peptide (CGRP) are involved in bone formation/remodeling. Here we investigate the effects of STC1 on functional heterodimer complex CALCRL/RAMP1, expression and activity during osteoblastogenesis. STC1 did not modify CALCRL and ramp1 gene expression during osteoblastogenesis when compared to controls. However, plasma membrane spatial distribution of CALCRL/RAMP1 was modified in 7-day pre-osteoblasts exposed to either CGRP or STC1, and both peptides induced CALCRL and RAMP1 assembly. CGRP, but not STC1 stimulated cAMP accumulation in 7-day osteoblasts and in CALCRL/RAMP1 transfected HEK293 cells. Furthermore, STC1 inhibited forskolin stimulated cAMP accumulation of HEK293 cells, but not in CALCRL/RAMP1 transfected HEK293 cells. However, STC1 inhibited cAMP accumulation in calcitonin receptor (CTR) HEK293 transfected cells stimulated by calcitonin. In conclusion, STC1 signals through inhibitory G-protein modulates CGRP receptor spatial localization during osteoblastogenesis and may function as a regulatory factor interacting with calcitonin peptide members during bone formation.

Effect of low-level laser therapy and calcitonin on bone repair in castrated rats: a densitometric study.

OBJECTIVE: To investigate the healing of bone defects in male rats treated with salmon calcitonin, low-level laser therapy (LLLT), or both. BACKGROUND: Healing of bone defects still represents a challenge to health professionals in several areas. In this article, the effect of calcitonin in combination with LLLT on bone repair was studied. Densitometry was used as a valuable tool for the measurement of bone regeneration. METHODS: Sixty male Wistar rats underwent bilateral castration surgery before the creation of a surgical bone defect. The animals were randomly divided into four groups: control, treated with calcitonin (Ca), treated with LLLT (La), and treated with calcitonin and LLLT (CaLa). Groups Ca and CaLa received 2 IU/kg of synthetic salmon calcitonin intramuscularly three times a week. Groups La and CaLa received laser therapy using a gallium-aluminum-arsenide laser (10 mW, 20 J/cm(2), wavelength 830 nm). Control animals were submitted to sham irradiation. The animals were sacrificed 7, 14, and 21 days after surgery, and bone defects were analyzed using densitometry. RESULTS: The CaLa group had a higher degree of bone regeneration 14 and 21 days after surgery. CONCLUSIONS: The La and CaLa had significantly higher bone mineral density than the control and Ca groups.

Homeopathic treatment for bone regeneration: experimental study.

AIM AND METHOD: The objective of this research was to study the effect of homeopathic treatment with Plumbum metallicum (Plumbum met.) on mandibular bone repair in rats. MATERIALS AND METHODS: We analyzed the mandibles of 60 male rats, approximately 3-month-old, randomly divided into three groups of 20 animals each: control, treated with calcitonin, and treated with a homeopathic medicine. A circumscribed bone defect measuring 4mm in diameter was made in the mandible and covered with a polytetrafluorethylene (PTFE) barrier. The group treated with calcitonin received 2IU/kg intramuscularly three times a week; the group treated with Plumbum met. 30c received three drops in water every day. The animals were sacrificed after 7, 14, 21 and 28 days. The mandibles were removed and submitted to histologic and histomorphometric analyses. RESULTS: Data were analyzed statistically by two-way ANOVA and by the Tukey test. The interaction effect (ANOVA, F df(6; 48)=4.64; p=0.001<0.05) indicated that the relationship between treatments was not the same at each time of sacrifice. Although statistical analysis of the histomorphometric data showed a similar results for the treated and control groups. But histological analysis showed complete filling of the surgical defect throughout its extent was only for the group treated with Plumbum met. CONCLUSION: The study demonstrated that for repair of surgical defects in rat mandibles Plumbum met. 30c and control did not differ significantly in histomorphometric terms.

Calcitonin in bone-guided regeneration of mandibles in ovariectomized rats: densitometric, histologic and histomorphometric analysis.

The aim of the present study was to investigate bone promotion in surgical defects created in the mandible of normal and ovariectomized female rats using calcitonin associated with a polytetrafluoroethylene barrier. The 100 female rats were divided into four groups: control (C), control treated with calcitonin (CM), ovariectomized control (OV) and ovariectomized treated with calcitonin (OVM). A circumscribed bone defect 4mm in diameter was created in the region of the mandibular angle, and covered with the barrier. Groups CM and OVM received 2 IU/kg of synthetic salmon calcitonin intramuscularly three times a week. The animals were killed 3, 7, 14, 21 and 28 days after surgery. The bone defects were submitted to densitometric, histologic and histomorphometric analysis. Groups C and CM showed higher levels of bone formation after 7 days compared to the OV and OVM groups. A significant difference was observed between groups C and OV at 3-14 days. The OV group presented slower bone regeneration of the surgical bone defect created in the mandibular angle than group C. Synthetic salmon calcitonin accelerated regeneration of the bone defect in the mandibles of OVM animals similarly to group C, and also increased the formation of new bone during the regeneration process in CM.

Somatostatinergic modulation of firing pattern and calcium-activated potassium currents in medium spiny neostriatal neurons.

Somatostatin is synthesized and released by aspiny GABAergic interneurons of the neostriatum, some of them identified as low threshold spike generating neurons (LTS-interneurons). These neurons make synaptic contacts with spiny neostriatal projection neurons. However, very few somatostatin actions on projection neurons have been described. The present work reports that somatostatin modulates the Ca(2+) activated K(+) currents (K(Ca) currents) expressed by projection cells. These actions contribute in designing the firing pattern of the spiny projection neuron; which is the output of the neostriatum. Small conductance (SK) and large conductance (BK) K(Ca) currents represent between 30% and 50% of the sustained outward current in spiny cells. Somatostatin reduces SK-type K(+) currents and at the same time enhances BK-type K(+) currents. This dual effect enhances the fast component of the after hyperpolarizing potential while reducing the slow component. Somatostatin then modifies the firing pattern of spiny neurons which changed from a tonic regular pattern to an interrupted "stuttering"-like pattern. Semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) tissue expression analysis of dorsal striatal somatostatinergic receptors (SSTR) mRNA revealed that all five SSTR mRNAs are present. However, single cell RT-PCR profiling suggests that the most probable receptor in charge of this modulation is the SSTR2 receptor. Interestingly, aspiny interneurons may exhibit a "stuttering"-like firing pattern. Therefore, somatostatin actions appear to be the entrainment of projection neurons to the rhythms generated by some interneurons. Somatostatin is then capable of modifying the processing and output of the neostriatum.

Effect of estrogen replacement and calcitonin therapies on bone around titanium implants placed in ovariectomized rats: a histometric study.

PURPOSE: The aim of the present study was to evaluate whether hormone replacement therapy (HRT) and calcitonin (CT) administration could influence bone healing around implants placed in ovariectomized (OVX) rats. MATERIALS AND METHODS: One screw-type titanium implant was placed bilaterally in OVX rats. The animals were assigned to one of the following groups: group 1 (n = 15), sham surgeries; group 2 (n = 15), OVX rats; group 3 (n = 14), OVX rats administered CT 4 days/week (16 IU/kg); group 4 (n = 14), OVX rats administered 17beta estradiol daily (20 microg/kg). After 60 days, the animals were sacrificed and undecalcified sections obtained. Bone-to-implant contact (BIC) and bone area (BA) around the implants were determined separately for the cortical (zone A) and cancellous (zone B) bone areas. RESULTS: In zone A, intergroup analysis did not reveal a significant difference regarding BIC. In contrast, the HRT group (group 4) presented greater BA than groups 2 and 3 (P < .05). Data from zone B revealed that HRT eliminated the negative effect of the ovariectomy on BIC and BA (P < .05), while CT had no effect (P > .05). DISCUSSION: It was the first study to evaluate and demonstrate the impact of HRT and CT on bone around titanium implants in an estrogen-deficient model. CONCLUSION: Within the limits of the present study, it may be concluded that HRT may prevent the influence that estrogen deficiency exerts on bone healing around titanium implants.

Effect of calcitonin on bone formation around titanium implant. A histometric study in rabbits.

Bone healing around titanium implants has already been evaluated; however, the effect of drugs such as calcitonin during the period of bone maturation around titanium implants has not yet been investigated. The purpose of this study was to evaluate the effects of calcitonin administration on the late period of bone healing following titanium implant insertion. Twenty-seven adult New Zealand rabbits received one implant in each femur. Thirteen animals were randomly selected as the test group (2 IU/kg--calcitonin) and fourteen animals served as control (saline). The animals were sacrificed 6, 8, 12 and 18 weeks after surgery. Endosteal/periosteal bone length (EB/PB), endosteal/periosteal bone area (EBA/PBA) and total cortical length (TCL) around the implants were analyzed. After 6, 8, 12 and 18 weeks, a positive time effect was strongly observed (P < 0.05). Considering the treatment factor, there was a positive effect of calcitonin on EBA and EB variables at 12 weeks and TCL at 18 weeks. In conclusion, the administration of salmon calcitonin to healthy animals may improve bone mass at the later stages of bone healing following titanium implant insertion.

Effect of combined treatment with calcitonin on bone densitometry of patients with treated hypothyroidism

INTRODUCTION: Thyroid hormones (TH) may affect bone metabolism and turnover, inducing a loss of bone mass among hyperthyroid and in hypothyroid patients under hormone replacement treatment. Thyroid dysfunction leads to changes in the dynamics of parathyroid hormone (PTH) and calcitonin (CT) secretion. OBJECTIVE: The objective of the study was to determine the usefulness of CT as adjuvant therapy in the prevention of bone loss during the treatment of hypothyroidism. MATERIAL AND METHODS: We studied 16 female patients with recently diagnosed primary hypothyroidism, divided into two groups: group G1 (n=8) submitted to treatment with thyroxine (L-T4), and Group 2 (n=8) that, in addition to being treated with L-T4, received a nasal CT spray. All patients were submitted to determination of TSH, free T4, bone mineral densitometry (BMD) and total bone calcium (TBC) at the time of diagnosis, after 6 to 9 months of treatment, and after 12 months of treatment. RESULTS: No statistical significant differences were detected in either group between the total BMD values obtained for the femur and lumbar spine before and after treatment. However, group G1 presented a statistical significant TBC loss after 12 months of treatment compared to initial values. In contrast, no TBC loss was observed in the group treated with LT-4 in combination with CT, a fact that may suggest that CT was responsible for the lower bone reabsorption during treatment of hypothyroidism.

Regulation of cell cyclic AMP in medullary thick ascending limb of Henle in a rat model of chronic renal failure.

Chronic renal failure (CRF) is accompanied by adaptive changes in electrolyte reabsorption in the thick ascending limb of Henle of surviving nephrons. To study the cellular mechanism of this adaptation, we measured intracellular cAMP in micro-dissected medullary thick ascending limb (mTAL) segments in rats with CRF. mTAL exhibited in CRF an increase of basal cAMP from 25.6 +/- 10.0 in controls to 65.8 +/- 11.3 fmol mm-1 tubule in CRF (P < 0.05). Vasopressin and calcitonin stimulated mTAL adenylate-cyclase in a dose-dependent manner in controls but failed to stimulate in CRF. Likewise, maximal stimulation with 10(-3) M 3-isobutyl-1-methylxanthine (IBMX) plus 10(-5) M forskolin increased cAMP in controls to 63.0 +/- 16.0 but not in CRF, where maximal stimulated values remained at 63.1 +/- 18.8 fmol mm-1 tubule (P NS). Alpha2-adrenoreceptor activation with clonidine at concentrations ranging from 10(-8) to 10(-6) M diminished cAMP production by 37% in CRF (P < 0.05), whereas no differences were found in controls. Thus, the basal intracellular cAMP is increased in rat mTAL in CRF. The finding that neither forskolin nor vasopressin were able to further augment intracellular cAMP would suggest that stimulatory pathways of the adenylate-cyclase system are activated in the basal state. However, mTAL cells in CRF seem to retain the response of normal epithelium to inhibitory pathways such as the one mediated by alpha2-adrenoreceptors.

A study of calcitonin effect on synaptosomal membrane enzymes.

Calcitonin is a hormone peptide produced by the thyroid gland, whose best described role is to prevent bone reabsorption. It also participates in other biological functions, even at central nervous system level. We studied the effect of added calcitonin on ATPase and acetylcholinesterase activities in synaptosomal membranes isolated from rat cerebral cortex. Calcitonin at 10(-7) - 10(-5)M concentration decreased 20-40% Na+, K(+)-ATPase and 15-25% K(+)-p-nitrophenylphosphatase activities, and at 10(-6)-10(-5)M reduced 20-30% Mg(2+)-p-nitrophenylphosphatase activity. However, this peptide failed to modify Mg(2+) - and Ca(2+)-ATPase or acetylcholinesterase activities. Results suggest that the sodium pump may be a target for calcitonin effects at neuronal level. Thus, calcitonin inhibition of sodium/potassium transport through synaptic membranes supports a regulatory role of this peptide on neurotransmission.

Avaliaçäo da resistência óssea com e sem a administraçäo prévia de calcitonina de salmäo em ratos com desnutriçäo protéica / Evaluation of osseous resistance with and without previous adminsitration of salmon calcitonin in rats with proteic malnutrition

Foi realizado trabalho experimental com ratos da raça Wistar para avaliar a influência da calcitonina de salmao e da desnutriçao protéica, isoladas e associadas, na resistência mecânica e na rigidez do tecido ósseo. Os ratos foram divididos em quatro grupos: dieta normal, dieta normal mais calcitonina, desnutridos, desnutridos mais calcitonina. Após duas semanas, foram submetidos a fratura manual da tíbia direita e, ao término de seis semanas, sacrificados. Foram avaliados os parâmetros mecânicos de resistência e rigidez óssea das tíbias fraturadas e nao fraturadas (controle) dos quatro grupos. Concluiu-se que: a administraçao de calcitonina reduziu a resistência máxima das tíbias-controle do grupo com dieta normal; a resistência e rigidez das tíbias fraturadas (processo de consolidaçao) e controle (processo de remodelaçao) foram prejudicadas pela desnutriçao protéica; no grupo desnutrido, a administraçao de calcitonina nao compensou a diminuiçao da resistência e da regidez das tíbias, mas reduziu a ocorrência de pseudartrose.

Effect of parathyroid hormone and calcitonin on cholinergic markers in rat parathyroid gland.

The effect of parathyroid hormone (PTH) and calcitonin on 3H-choline uptake and on 3H-acetylcholine synthesis by rat parathyroid glands were examined. Incubation of tissue for 120 min with PTH or calcitonin resulted in an inverted bell-shaped, dose-dependent inhibition of 3H-choline uptake, with a maximal effect at 10(-9) M concentration. The effect of PTH on parathyroid choline uptake was blunted by preincubation with the PTH antagonist NLe(8-18)-PTH (3-34) amide. PTH brought about a dose-dependent inhibition of 3H-choline conversion to 3H-acetylcholine, with significant effects at 10(-8) M concentration or higher. This inhibitory effect of PTH on 3H-acetylcholine synthesis was blocked by co-incubation with the PTH antagonist NLe(8-18)-PTH (3-34) amide. Only at a 10(-7) M concentration calcitonin was effective to impair the in vitro conversion of radioactive choline into 3H-acetylcholine by parathyroid fragments. The results indicate that, in vitro, PTH, and to a less extent, calcitonin, inhibit cholinergic activity in rat parathyroid glands.

Cortical astroglial conditioned medium induces in vitro radial-like forms.

Cerebral cortex and striatal cell dissociates obtained from rat fetuses (E 17) were subcultured and enriched in astroglial cells before being grown in regional (cerebral cortex, striatum) astroglial conditioned media (CM) or defined basal medium. Incidence of radial-like astroglia (vimentin+ or glial fibrillary acid protein, GFAP+) and length of processes in cortical cell subcultures showed a greater increase when exposed to cerebral cortex CM than to striatal CM or basal medium. Stellate (GFAP+) forms prevailed in subcultures grown in basal medium while striatal cells exposed to CM of either origin remained undifferentiated. Additionally, cultures were treated with various concentrations of cAMP (0.25 and 0.5 mM) and calcitonin gene related peptide (CGRP) (0.1, 0.5, and 1.0 microM). Under these conditions CM-exposed cultures (with predominant "radial-like" forms) did not increase stellate glial numbers, while fetal calf serum (FCS)-exposed cultures (morphologically undifferentiated) underwent significant degrees of stellate transformation. When CM-exposed cultures were shifted to FCS supplemented basal medium for 24-48 hr and then to basal medium alone prior to treatment, cAMP and CGRP were effective in transforming flat astroglia into stellate morphology. Results are indicative of the existence of astroglial diffusible factors affecting the in vitro expression of astroglial morphotypes from the cerebral cortex. Previous exposure to CM interferes with cytoskeletal astrocytic changes induced by cAMP and CGRP. It is speculated that astroglial factors could act in vivo to maintain the expression of radial-like cells during early developmental stages of the cerebral cortex, but it would not be effective in E 17 striatum.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of parathyroid hormone and calcitonin on acetylcholine release in rat sympathetic superior cervical ganglion.

The effects of parathyroid hormone (PTH) and calcitonin on acetylcholine release by rat superior cervical ganglion (SCG) were evaluated in vitro. SCG labeled with [3H]choline were exposed to four 5 min-long pulses of 40 mM K+, 35 min apart. PTH increased, and calcitonin inhibited, in a dose-dependent way, K(+)-elicited [3H]acetylcholine release, with apparent effective doses 50 of about 10(-9) M. The effect of PTH was inhibited by co-incubation with the PTH receptor antagonist NLe [8-18]-PTH (3-34) amide. Incubation of SCG for 120 min with PTH or calcitonin resulted in dose-dependent augmentation or inhibition of K(+)-induced increase of high affinity [3H]choline uptake, respectively, with a maximal effect at 10(-8) M concentration (PTH) and 10(-9) M concentration (calcitonin) and declining at higher concentrations. The increase in SCG [3H]choline uptake induced by PTH was blunted by preincubation with the PTH antagonist NLe [8-18]-PTH (3-34) amide. At 10(-7) M concentrations, PTH increased significantly the in vitro conversion of [3H]choline to [3H]acetylcholine, an effect inhibited by PTH receptor antagonist. Calcitonin did not modify SCG [3H]acetylcholine synthesis by rat SCG. The results indicate that, in vitro, PTH increases, and calcitonin inhibits, acetylcholine release in rat SCG.

Effect of calcitonin on alveolar wound healing.

The effect of calcitonin (CT) on alveolar wound healing was studied with histomorphometric methods. Wistar rats weighing 80-90 g were submitted to extraction of the three mandibular molars. Half of them were injected intraperitoneally with daily therapeutic doses of CT. The control group received no further treatment. All the rats were killed 14 days after the onset of the experiment. Bone healing was impaired in CT treated animals and involved a more intense bone remodeling activity. Bone resorptive areas were present both on the profiles of the newly formed bone and on the alveolar ridge surface. These results suggest that CT would accelerate the process of bone healing.