Structural, cellular, and molecular evaluation of bone erosion in experimental models of rheumatoid arthritis: Assessment by μcT, histology, and serum biomarkers

Cheng Chi Chao, Shi Juan Chen, Iannis Adamopoulos, Michael Judo, Agelio Asio, Gulesi Ayanoglu, Edward P. Bowman

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Bone erosion is a clinical endpoint for various diseases including rheumatoid arthritis. In this paper, we used rodent arthritis models with severe bone erosion to examine the structural, cellular, and molecular aspects of the inflammation-driven bone resorption process. Our data show that bone loss is observed only in chronically, severely inflamed joints. The most severely affected anatomic sites were the metatarsal phalangeal joint and tarsal bones of the paw. The magnitude of the inflammation-driven bone erosion was dependent on both the duration of inflammatory response and the severity of the joint swelling response. The application of micro-computed tomography well demonstrated the therapeutic benefit of anti-IL-17A in protection of bones from erosion. Alterations in the cellular profile of the joint occurred prior to any major structural deterioration of the bone. Receptor activator for nuclear factor κB ligand, a potent inducer of osteoclast differentiation and bone resorption, was elevated in animals coincident with severe arthritis initiation. The experimental approaches and concepts outlined in this paper provide a valuable process to evaluate and quantify therapies that modulate rodent arthritis-associated bone-erosion models.

Original languageEnglish (US)
Pages (from-to)642-653
Number of pages12
JournalAutoimmunity
Volume43
Issue number8
DOIs
StatePublished - Dec 2010
Externally publishedYes

Fingerprint

Rheumatoid Arthritis
Histology
Theoretical Models
Biomarkers
Bone and Bones
Joints
Serum
Arthritis
Bone Resorption
Rodentia
Tarsal Bones
Osteitis
Metatarsal Bones
Interleukin-17
Osteoclasts
Cytoplasmic and Nuclear Receptors
Tomography
Ligands
Inflammation
Therapeutics

Keywords

  • adjuvant-induced arthritis
  • anti-IL-17
  • collagen-induced arthritis
  • Micro-computed tomography
  • RANKL

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this

Structural, cellular, and molecular evaluation of bone erosion in experimental models of rheumatoid arthritis : Assessment by μcT, histology, and serum biomarkers. / Chao, Cheng Chi; Chen, Shi Juan; Adamopoulos, Iannis; Judo, Michael; Asio, Agelio; Ayanoglu, Gulesi; Bowman, Edward P.

In: Autoimmunity, Vol. 43, No. 8, 12.2010, p. 642-653.

Research output: Contribution to journalArticle

Chao, Cheng Chi ; Chen, Shi Juan ; Adamopoulos, Iannis ; Judo, Michael ; Asio, Agelio ; Ayanoglu, Gulesi ; Bowman, Edward P. / Structural, cellular, and molecular evaluation of bone erosion in experimental models of rheumatoid arthritis : Assessment by μcT, histology, and serum biomarkers. In: Autoimmunity. 2010 ; Vol. 43, No. 8. pp. 642-653.
@article{486a3583e56048d5a9951d9382f175a0,
title = "Structural, cellular, and molecular evaluation of bone erosion in experimental models of rheumatoid arthritis: Assessment by μcT, histology, and serum biomarkers",
abstract = "Bone erosion is a clinical endpoint for various diseases including rheumatoid arthritis. In this paper, we used rodent arthritis models with severe bone erosion to examine the structural, cellular, and molecular aspects of the inflammation-driven bone resorption process. Our data show that bone loss is observed only in chronically, severely inflamed joints. The most severely affected anatomic sites were the metatarsal phalangeal joint and tarsal bones of the paw. The magnitude of the inflammation-driven bone erosion was dependent on both the duration of inflammatory response and the severity of the joint swelling response. The application of micro-computed tomography well demonstrated the therapeutic benefit of anti-IL-17A in protection of bones from erosion. Alterations in the cellular profile of the joint occurred prior to any major structural deterioration of the bone. Receptor activator for nuclear factor κB ligand, a potent inducer of osteoclast differentiation and bone resorption, was elevated in animals coincident with severe arthritis initiation. The experimental approaches and concepts outlined in this paper provide a valuable process to evaluate and quantify therapies that modulate rodent arthritis-associated bone-erosion models.",
keywords = "adjuvant-induced arthritis, anti-IL-17, collagen-induced arthritis, Micro-computed tomography, RANKL",
author = "Chao, {Cheng Chi} and Chen, {Shi Juan} and Iannis Adamopoulos and Michael Judo and Agelio Asio and Gulesi Ayanoglu and Bowman, {Edward P.}",
year = "2010",
month = "12",
doi = "10.3109/08916931003610992",
language = "English (US)",
volume = "43",
pages = "642--653",
journal = "Autoimmunity",
issn = "0891-6934",
publisher = "Informa Healthcare",
number = "8",

}

TY - JOUR

T1 - Structural, cellular, and molecular evaluation of bone erosion in experimental models of rheumatoid arthritis

T2 - Assessment by μcT, histology, and serum biomarkers

AU - Chao, Cheng Chi

AU - Chen, Shi Juan

AU - Adamopoulos, Iannis

AU - Judo, Michael

AU - Asio, Agelio

AU - Ayanoglu, Gulesi

AU - Bowman, Edward P.

PY - 2010/12

Y1 - 2010/12

N2 - Bone erosion is a clinical endpoint for various diseases including rheumatoid arthritis. In this paper, we used rodent arthritis models with severe bone erosion to examine the structural, cellular, and molecular aspects of the inflammation-driven bone resorption process. Our data show that bone loss is observed only in chronically, severely inflamed joints. The most severely affected anatomic sites were the metatarsal phalangeal joint and tarsal bones of the paw. The magnitude of the inflammation-driven bone erosion was dependent on both the duration of inflammatory response and the severity of the joint swelling response. The application of micro-computed tomography well demonstrated the therapeutic benefit of anti-IL-17A in protection of bones from erosion. Alterations in the cellular profile of the joint occurred prior to any major structural deterioration of the bone. Receptor activator for nuclear factor κB ligand, a potent inducer of osteoclast differentiation and bone resorption, was elevated in animals coincident with severe arthritis initiation. The experimental approaches and concepts outlined in this paper provide a valuable process to evaluate and quantify therapies that modulate rodent arthritis-associated bone-erosion models.

AB - Bone erosion is a clinical endpoint for various diseases including rheumatoid arthritis. In this paper, we used rodent arthritis models with severe bone erosion to examine the structural, cellular, and molecular aspects of the inflammation-driven bone resorption process. Our data show that bone loss is observed only in chronically, severely inflamed joints. The most severely affected anatomic sites were the metatarsal phalangeal joint and tarsal bones of the paw. The magnitude of the inflammation-driven bone erosion was dependent on both the duration of inflammatory response and the severity of the joint swelling response. The application of micro-computed tomography well demonstrated the therapeutic benefit of anti-IL-17A in protection of bones from erosion. Alterations in the cellular profile of the joint occurred prior to any major structural deterioration of the bone. Receptor activator for nuclear factor κB ligand, a potent inducer of osteoclast differentiation and bone resorption, was elevated in animals coincident with severe arthritis initiation. The experimental approaches and concepts outlined in this paper provide a valuable process to evaluate and quantify therapies that modulate rodent arthritis-associated bone-erosion models.

KW - adjuvant-induced arthritis

KW - anti-IL-17

KW - collagen-induced arthritis

KW - Micro-computed tomography

KW - RANKL

UR - http://www.scopus.com/inward/record.url?scp=78149446588&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=78149446588&partnerID=8YFLogxK

U2 - 10.3109/08916931003610992

DO - 10.3109/08916931003610992

M3 - Article

C2 - 20380588

AN - SCOPUS:78149446588

VL - 43

SP - 642

EP - 653

JO - Autoimmunity

JF - Autoimmunity

SN - 0891-6934

IS - 8

ER -