Increased bone mass in adult prostacyclin-deficient mice

Nakalekha, Chalida; Yokoyama, Chieko; Miura, Hiroyuki; Alles, Neil; Aoki, Kazuhiro; Ohya, Keiichi; Morita, Ikuo

doi:10.1677/joe-09-0376

Cited by 19 publications

(13 citation statements)

References 41 publications

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“…Similarly, osteocytic cells in vitro were shown to increase COX-2 expression and prostaglandin production in response to diverse mechanical stimuli including fluid flow [103, 104], substrate deformation [105] and hydrostatic pressure [34]. Of the prostaglandins, PGE 2 is the most extensively studied with respect to bone anabolic effects, although prostacyclin (PGI 2 ) has also been reported to have similar actions [106, 107]. Sorting out pathways of prostaglandin signaling between osteocytic and osteoblastic cell populations presents problems, particularly in situ , since both osteoblasts and osteocytes produce prostaglandins.…”

Section: Osteocyte-osteoblast Communicationmentioning

confidence: 99%

Osteocytes: Master Orchestrators of Bone

et al. 2013

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Osteocytes comprise the overwhelming majority of cells in bone and are its only true “permanent” resident cell population. In recent years, conceptual and technological advances on many fronts have helped to clarify the role osteocytes play in skeletal metabolism and the mechanisms they use to perform them. The osteocyte is now recognized as a major orchestrator of skeletal activity, capable of sensing and integrating mechanical and chemical signals from their environment to regulate both bone formation and resorption. Recent studies have established that the mechanisms osteocytes use to sense stimuli and regulate effector cells (e.g. osteoblasts and osteoclasts) are directly coupled to the environment they inhabit – entombed within the mineralized matrix of bone and connected to each other in multicellular networks. Communication within these networks is both direct (via cell-cell contacts at gap junctions) and indirect (via paracrine signaling by secreted signals). Moreover, the movement of paracrine signals is dependent on movement of both solutes and fluid through the space immediately surrounding the osteocytes (i.e. the Lacunar-Canalicular System, LCS). Finally, recent studies have also shown that the regulatory capabilities of osteocytes extend beyond bone to include a role in endocrine control of systemic phosphate metabolism. This review will discuss how a highly productive combination of experimental and theoretical approaches has managed to unearth these unique features of osteocytes and bring to light novel insights into the regulatory mechanisms operating in bone.

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Section: Osteocyte-osteoblast Communicationmentioning

confidence: 99%

Osteocytes: Master Orchestrators of Bone

et al. 2013

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“…Previous work demonstrated that the prostaglandin PGE 2 can either increase bone formation and osteoblastic activity [10] or increase bone resorption [11] depending on experimental conditions. The prostaglandin, PGI 2 or prostacyclin also alters bone formation and bone resorption depending on the experimental model [12,13,14,15,16,17,18,19,20]. Deletion of prostacyclin synthase, the enzyme responsible for prostacyclin synthesis, results in a decrease in bone mineral density in young mice and an increase in bone mineral density in older mice [14].…”

Section: Introductionmentioning

confidence: 99%

Enhanced prostacyclin formation and Wnt signaling in sclerostin deficient osteocytes and bone

Ryan

Craig

Salisbury

et al. 2014

Biochemical and Biophysical Research Communications

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We show that prostacyclin production is increased in bone and osteocytes from sclerostin (Sost) knockout mice which have greatly increased bone mass. The addition of prostacyclin or a prostacyclin analog to bone forming osteoblasts enhances differentiation and matrix mineralization of osteoblasts. The increase in prostacyclin synthesis is linked to increases in β-catenin concentrations and activity as shown by enhanced binding of lymphoid enhancer factor, Lef1, to promoter elements within the prostacyclin synthase promoter. Blockade of Wnt signaling reduces prostacyclin production in osteocytes. Increased prostacyclin production by osteocytes from sclerostin deficient mice could potentially contribute to the increased bone formation seen in this condition.

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“…İLLOPROST Prostasiklin; vasküler endotelyal büyüme faktö-rü salınımını stimule ederek anjiogenezi ve hücresel farklılaşmayı arttıran güçlü bir vazodilatatördür. 86,87 İlloprost ise pulmoner hipertansiyon tedavisinde kullanılan bir prostasiklin analoğudur. 88 Limjeerajarus ve ark.…”

Section: Biodentin(septodont Saint Maur Des Fossés France)unclassified

Vi̇tal Pulpa Tedavi̇leri̇nde Güncel Yaklaşimlar

Gökçek¹,

Bodrumlu²

2015

Atatürk Üniversitesi Diş Hekimliği Fakültesi Dergisi

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ÖZDiş çürükleri pulpal inflamasyona yol açabilen ve ileri dönemlerde diş kaybıyla sonuçlanabilen yaygın bir sağlık problemidir. İnflamasyon nedeniyle pulpa dokusu geri dönüşümlü olarak etkilendiğinde; indirekt pulpa kaplaması, direkt pulpa kaplaması, parsiyel/total pulpatomi gibi vital pulpa tedavi yöntemleri uygulanarak pulpanın canlılığının ve fonksiyonunun devam ettirilmesi sağlanabilmektedir. Dişlerin gelişim süreci boyunca meydana gelen moleküler ve histolojik değişimlerin anlaşılması ile birlikte, son yıllarda gözlenen yenilikler vital pulpa tedavilerinde yeni yaklaşımları gündeme getirmiştir Bu derlemenin amacı; dişlerin vitalitesini korumak için geçmişten günümüze kadar uygulanan vital pulpa tedavi yöntemlerinin ve kullanılan kaplama ajanlarının pulpa dokusu üzerindeki etkilerini değerlendirmektir. Anahtar Kelimeler: Vital pulpa tedavileri, kalsiyum hidroksit, MTA, Biodentin. GİRİŞPulpa, dişin kron ve kök kısmında bulunan, dentin ile çevrelenen, şekil verici, besleyici, duyusal ve koruyucu işlevlere sahip, ektomezenşim kökenli damarlanmış ve sinir ağıyla sarılmış bir bağ dokusudur. 1 Pulpa dokusunun inflamasyonu sonucunda oluşan vazodilatasyon ve artan damar permeabilitesi, pulpal doku basıncının artmasına yol açarak dokunun lokal feed-back mekanizmasını harekete geçirmek-tedir.2 Feed-back mekanizmasına göre inflame pulpada artan interstisyel basınç transkapiller hidrostatik basınç farkını düşürür ve filtrasyona engel olur. Ayrıca lokal ABSTRACTDental caries is a common problem that can cause pulpal inflammation and resultant tooth loss. When pulp tissue is reversibly inflammed, vital pulp therapies like indirect pulp capping, direct pulp capping, partial/total pulpatomy procedures are implemented to preserve vitality and function of the pulp tissue. Recent progress in understanding the molecular and histologic changes during the tooth development is lead to designing new treatment strategies in vital pulp therapies. The aim of this review is to provide an overview of vital pulp therapy from past to present and to assess the efficiency of the pulp capping materials on the pulp tissue. Key Words: Vital pulp therapy, calcium hydroxide, MTA, Biodentine olarak artmış olan interstisyel basınç inflamasyonun görülmediği bitişik dokudaki kapillerin interstisyel sıvıyı absorbe etmesine yardımcı olur ve lenf akışını arttırır. 3Bu iki mekanizma ile doku basıncının artmasına yol açan sıvı, etkilenmiş alanının dışına çıkarılarak doku basıncı düşürülmüş olur.2 Pulpanın inflamasyon sonrası uzun süre kendini koruyabilmesi ve uygun şartlar sağlandığında inflamasyonun gerileyerek pulpal sağlığın tekrar elde edilebilmesi bu mekanizmalar ile açıklanabilmektedir. Pulpa dokusunda tamirin meydana gelebilmesi için vital pulpanın varlığı şarttır

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Increased bone mass in adult prostacyclin-deficient mice

Cited by 19 publications

References 41 publications

Osteocytes: Master Orchestrators of Bone

Osteocytes: Master Orchestrators of Bone

Enhanced prostacyclin formation and Wnt signaling in sclerostin deficient osteocytes and bone

Vi̇tal Pulpa Tedavi̇leri̇nde Güncel Yaklaşimlar

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