The role of megakaryocytes in skeletal homeostasis and rheumatoid arthritis

Melissa Kacena, Mark C. Horowitz

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

PURPOSE OF REVIEW: This review provides an update on the role of megakaryocytes in skeletal homeostasis, and discusses these findings in the context of rheumatoid arthritis. RECENT FINDINGS: Thrombocytosis is a common complication of rheumatoid arthritis, and is presumably caused by an up-regulation in megakaryocytopoiesis. In general, patients with rheumatoid arthritis exhibit localized joint bone erosion with systemic bone loss, and rheumatoid arthritis patients with thrombocytosis tend to have more severe disease. Interestingly, in addition to their role in rheumatoid arthritis with thrombocytosis, it has been demonstrated recently that megakaryocytes play a dual role in regulating skeletal mass by inhibiting bone resorption while simultaneously stimulating bone formation. This seeming contradiction in the putative role of megakaryocytes in skeletal regulation and rheumatoid arthritis is the focus of this review. SUMMARY: In rheumatoid arthritis there are substantial increases in the levels of several pro-inflammatory pleiotropic cytokines. As would be expected, in addition to their role in inflammation, these cytokines play a critical role in the megakaryocytopoiesis seen in patients who develop reactive thrombocytosis, and these cytokines also are known to regulate osteoclastogenesis. Thus, it appears that in rheumatoid arthritis with reactive thrombocytosis, the ability of the cytokines to enhance osteoclastogenesis outweighs the ability of megakaryocytes to inhibit osteoclastogenesis.

Original languageEnglish (US)
Pages (from-to)405-410
Number of pages6
JournalCurrent Opinion in Rheumatology
Volume18
Issue number4
DOIs
StatePublished - Jul 2006
Externally publishedYes

Fingerprint

Megakaryocytes
Rheumatoid Arthritis
Homeostasis
Thrombocytosis
Osteogenesis
Cytokines
Thrombopoiesis
Bone and Bones
Bone Resorption
Up-Regulation
Joints
Inflammation

Keywords

  • Cytokines
  • Fibroblasts
  • Megakaryocytes
  • Osteoblasts
  • Osteoclasts
  • Osteoprotegerin
  • Rheumatoid arthritis
  • Thrombopoietin

ASJC Scopus subject areas

  • Rheumatology
  • Immunology

Cite this

The role of megakaryocytes in skeletal homeostasis and rheumatoid arthritis. / Kacena, Melissa; Horowitz, Mark C.

In: Current Opinion in Rheumatology, Vol. 18, No. 4, 07.2006, p. 405-410.

Research output: Contribution to journalArticle

@article{5e7de920230c4996baca8fd6e584f7dd,
title = "The role of megakaryocytes in skeletal homeostasis and rheumatoid arthritis",
abstract = "PURPOSE OF REVIEW: This review provides an update on the role of megakaryocytes in skeletal homeostasis, and discusses these findings in the context of rheumatoid arthritis. RECENT FINDINGS: Thrombocytosis is a common complication of rheumatoid arthritis, and is presumably caused by an up-regulation in megakaryocytopoiesis. In general, patients with rheumatoid arthritis exhibit localized joint bone erosion with systemic bone loss, and rheumatoid arthritis patients with thrombocytosis tend to have more severe disease. Interestingly, in addition to their role in rheumatoid arthritis with thrombocytosis, it has been demonstrated recently that megakaryocytes play a dual role in regulating skeletal mass by inhibiting bone resorption while simultaneously stimulating bone formation. This seeming contradiction in the putative role of megakaryocytes in skeletal regulation and rheumatoid arthritis is the focus of this review. SUMMARY: In rheumatoid arthritis there are substantial increases in the levels of several pro-inflammatory pleiotropic cytokines. As would be expected, in addition to their role in inflammation, these cytokines play a critical role in the megakaryocytopoiesis seen in patients who develop reactive thrombocytosis, and these cytokines also are known to regulate osteoclastogenesis. Thus, it appears that in rheumatoid arthritis with reactive thrombocytosis, the ability of the cytokines to enhance osteoclastogenesis outweighs the ability of megakaryocytes to inhibit osteoclastogenesis.",
keywords = "Cytokines, Fibroblasts, Megakaryocytes, Osteoblasts, Osteoclasts, Osteoprotegerin, Rheumatoid arthritis, Thrombopoietin",
author = "Melissa Kacena and Horowitz, {Mark C.}",
year = "2006",
month = "7",
doi = "10.1097/01.bor.0000231910.42666.31",
language = "English (US)",
volume = "18",
pages = "405--410",
journal = "Current Opinion in Rheumatology",
issn = "1040-8711",
publisher = "Lippincott Williams and Wilkins",
number = "4",

}

TY - JOUR

T1 - The role of megakaryocytes in skeletal homeostasis and rheumatoid arthritis

AU - Kacena, Melissa

AU - Horowitz, Mark C.

PY - 2006/7

Y1 - 2006/7

N2 - PURPOSE OF REVIEW: This review provides an update on the role of megakaryocytes in skeletal homeostasis, and discusses these findings in the context of rheumatoid arthritis. RECENT FINDINGS: Thrombocytosis is a common complication of rheumatoid arthritis, and is presumably caused by an up-regulation in megakaryocytopoiesis. In general, patients with rheumatoid arthritis exhibit localized joint bone erosion with systemic bone loss, and rheumatoid arthritis patients with thrombocytosis tend to have more severe disease. Interestingly, in addition to their role in rheumatoid arthritis with thrombocytosis, it has been demonstrated recently that megakaryocytes play a dual role in regulating skeletal mass by inhibiting bone resorption while simultaneously stimulating bone formation. This seeming contradiction in the putative role of megakaryocytes in skeletal regulation and rheumatoid arthritis is the focus of this review. SUMMARY: In rheumatoid arthritis there are substantial increases in the levels of several pro-inflammatory pleiotropic cytokines. As would be expected, in addition to their role in inflammation, these cytokines play a critical role in the megakaryocytopoiesis seen in patients who develop reactive thrombocytosis, and these cytokines also are known to regulate osteoclastogenesis. Thus, it appears that in rheumatoid arthritis with reactive thrombocytosis, the ability of the cytokines to enhance osteoclastogenesis outweighs the ability of megakaryocytes to inhibit osteoclastogenesis.

AB - PURPOSE OF REVIEW: This review provides an update on the role of megakaryocytes in skeletal homeostasis, and discusses these findings in the context of rheumatoid arthritis. RECENT FINDINGS: Thrombocytosis is a common complication of rheumatoid arthritis, and is presumably caused by an up-regulation in megakaryocytopoiesis. In general, patients with rheumatoid arthritis exhibit localized joint bone erosion with systemic bone loss, and rheumatoid arthritis patients with thrombocytosis tend to have more severe disease. Interestingly, in addition to their role in rheumatoid arthritis with thrombocytosis, it has been demonstrated recently that megakaryocytes play a dual role in regulating skeletal mass by inhibiting bone resorption while simultaneously stimulating bone formation. This seeming contradiction in the putative role of megakaryocytes in skeletal regulation and rheumatoid arthritis is the focus of this review. SUMMARY: In rheumatoid arthritis there are substantial increases in the levels of several pro-inflammatory pleiotropic cytokines. As would be expected, in addition to their role in inflammation, these cytokines play a critical role in the megakaryocytopoiesis seen in patients who develop reactive thrombocytosis, and these cytokines also are known to regulate osteoclastogenesis. Thus, it appears that in rheumatoid arthritis with reactive thrombocytosis, the ability of the cytokines to enhance osteoclastogenesis outweighs the ability of megakaryocytes to inhibit osteoclastogenesis.

KW - Cytokines

KW - Fibroblasts

KW - Megakaryocytes

KW - Osteoblasts

KW - Osteoclasts

KW - Osteoprotegerin

KW - Rheumatoid arthritis

KW - Thrombopoietin

UR - http://www.scopus.com/inward/record.url?scp=33748065968&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33748065968&partnerID=8YFLogxK

U2 - 10.1097/01.bor.0000231910.42666.31

DO - 10.1097/01.bor.0000231910.42666.31

M3 - Article

C2 - 16763462

AN - SCOPUS:33748065968

VL - 18

SP - 405

EP - 410

JO - Current Opinion in Rheumatology

JF - Current Opinion in Rheumatology

SN - 1040-8711

IS - 4

ER -