28
views
0
recommends
+1 Recommend
1 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Paratormônio e osteoporose: encontrando o fio da meada. Bases fisiológicas para utilização do PTH no tratamento da osteoporose Translated title: Parathyroid hormone and osteoporosis: solving the puzzle. Physiologic rationale for the therapeutic use of PTH in osteoporosis

      review-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          O paratormônio (PTH) estará disponível em breve em nosso mercado como uma possibilidade terapêutica eficiente para a osteoporose. Esta revisão tem por objetivo apresentar os resultados das pesquisas clínicas e experimentais que justificaram tal fato, assim como procurar esclarecer por quais mecanismos o PTH pode ter ações diferenciadas sobre o esqueleto. Os trabalhos bastante recentes demonstram que existem vias diferentes para a atuação do PTH no osteoblasto, e que isto depende da dose, do tempo de exposição e dos fragmentos de PTH utilizados. Seu uso em dose única diária, por via subcutânea, tem demonstrado resultados surpreendentes em termos de ganho de massa óssea e prevenção de fraturas, superando em muito os resultados obtidos com as terapêuticas anti-reabsortivas. Sua disponibilização trará grandes modificações nos conceitos e atuais formas de tratamento da osteoporose.

          Translated abstract

          Parathyroid hormone (PTH) will be available in a few months for the treatment of osteoporosis. When used as a single daily subcutaneous injection for at least 1 year, it increases bone mass and reduces fracture rate more efficiently than the usual anti-resorptive therapy. Recently published articles show that PTH can act through different intracellular signaling pathways, depending on its concentration, time of exposure and molecular fragments. High concentration and prolonged exposure to amino-terminal PTH fragments stimulate bone resorption. On the other hand, in an intermittent way and in low concentrations, PTH administration increases bone formation. This review aims to present the principal results of clinical and experimental researches on PTH actions, while trying to explain the rationale for its dual effect on bone remodeling.

          Related collections

          Most cited references38

          • Record: found
          • Abstract: found
          • Article: not found

          Effect of parathyroid hormone (1-34) on fractures and bone mineral density in postmenopausal women with osteoporosis.

          Once-daily injections of parathyroid hormone or its amino-terminal fragments increase bone formation and bone mass without causing hypercalcemia, but their effects on fractures are unknown. We randomly assigned 1637 postmenopausal women with prior vertebral fractures to receive 20 or 40 microg of parathyroid hormone (1-34) or placebo, administered subcutaneously by the women daily. We obtained vertebral radiographs at base line and at the end of the study (median duration of observation, 21 months) and performed serial measurements of bone mass by dual-energy x-ray absorptiometry. New vertebral fractures occurred in 14 percent of the women in the placebo group and in 5 percent and 4 percent, respectively, of the women in the 20-microg and 40-microg parathyroid hormone groups; the respective relative risks of fracture in the 20-microg and 40-microg groups, as compared with the placebo group, were 0.35 and 0.31 (95 percent confidence intervals, 0.22 to 0.55 and 0.19 to 0.50). New nonvertebral fragility fractures occurred in 6 percent of the women in the placebo group and in 3 percent of those in each parathyroid hormone group (relative risk, 0.47 and 0.46, respectively [95 percent confidence intervals, 0.25 to 0.88 and 0.25 to 0.861). As compared with placebo, the 20-microg and 40-microg doses of parathyroid hormone increased bone mineral density by 9 and 13 more percentage points in the lumbar spine and by 3 and 6 more percentage points in the femoral neck; the 40-microg dose decreased bone mineral density at the shaft of the radius by 2 more percentage points. Both doses increased total-body bone mineral by 2 to 4 more percentage points than did placebo. Parathyroid hormone had only minor side effects (occasional nausea and headache). Treatment of postmenopausal osteoporosis with parathyroid hormone (1-34) decreases the risk of vertebral and nonvertebral fractures; increases vertebral, femoral, and total-body bone mineral density; and is well tolerated. The 40-microg dose increased bone mineral density more than the 20-microg dose but had similar effects on the risk of fracture and was more likely to have side effects.
            Bookmark
            • Record: found
            • Abstract: not found
            • Article: not found

            Hyperparathyroid and hypoparathyroid disorders.

              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Activated parathyroid hormone/parathyroid hormone-related protein receptor in osteoblastic cells differentially affects cortical and trabecular bone.

              Parathyroid hormone (PTH), an important regulator of calcium homeostasis, targets most of its complex actions in bone to cells of the osteoblast lineage. Furthermore, PTH is known to stimulate osteoclastogenesis indirectly through activation of osteoblastic cells. To assess the role of the PTH/PTH-related protein receptor (PPR) in mediating the diverse actions of PTH on bone in vivo, we generated mice that express, in cells of the osteoblastic lineage, one of the constitutively active receptors described in Jansen's metaphyseal chondrodysplasia. In these transgenic mice, osteoblastic function was increased in the trabecular and endosteal compartments, whereas it was decreased in the periosteum. In trabecular bone of the transgenic mice, there was an increase in osteoblast precursors, as well as in mature osteoblasts. Osteoblastic expression of the constitutively active PPR induced a dramatic increase in osteoclast number in both trabecular and compact bone in transgenic animals. The net effect of these actions was a substantial increase in trabecular bone volume and a decrease in cortical bone thickness of the long bones. These findings, for the first time to our knowledge, identify the PPR as a crucial mediator of both bone-forming and bone-resorbing actions of PTH, and they underline the complexity and heterogeneity of the osteoblast population and/or their regulatory microenvironment.
                Bookmark

                Author and article information

                Journal
                abem
                Arquivos Brasileiros de Endocrinologia & Metabologia
                Arq Bras Endocrinol Metab
                Sociedade Brasileira de Endocrinologia e Metabologia (São Paulo, SP, Brazil )
                1677-9487
                June 2002
                : 46
                : 3
                : 215-220
                Affiliations
                [01] São Paulo SP orgnameUniversidade Federal de São Paulo orgdiv1Disciplina de Endocrinologia mlazaretti@ 123456endocrino.epm.br
                Article
                S0004-27302002000300003 S0004-2730(02)04600303
                10.1590/S0004-27302002000300003
                2cd0c677-0ba9-4798-ae26-8692b24daf10

                This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

                History
                : 03 May 2002
                : 21 March 2002
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 37, Pages: 6
                Product

                SciELO Brazil

                Categories
                Revisões

                Osteoporosis,Treatment,PTH,Parathyroid hormone,Tratamento,Osteoporose,Paratormônio

                Comments

                Comment on this article