Endochondral Bone Formation and Advanced Enthesitis Are Key Features Of Proteoglycan Induced Spondylitis Mouse Model Of Ankylosing Spondylitis

H Tseng; A Pettit; T Glant; Matthew Brown; G Thomas

Endochondral Bone Formation and Advanced Enthesitis Are Key Features Of Proteoglycan Induced Spondylitis Mouse Model Of Ankylosing Spondylitis

H Tseng, A Pettit, T Glant, Matthew Brown, G Thomas

Research output: Other contribution to conference › Abstract › peer-review

Abstract

Transition from an initial inflammatory phase to the disabling osteoproliferative phase in ankylosing spondylitis (AS) is very poorly understood. Elucidation of the mechanisms underlying this disease progression would identify new therapeutic targets and strategies.

Original language	English
Pages	5-5
Number of pages	1
Publication status	Published - 2013

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@conference{ca9021b478834fb194686152d93a7a4c,

title = "Endochondral Bone Formation and Advanced Enthesitis Are Key Features Of Proteoglycan Induced Spondylitis Mouse Model Of Ankylosing Spondylitis",

abstract = "Transition from an initial inflammatory phase to the disabling osteoproliferative phase in ankylosing spondylitis (AS) is very poorly understood. Elucidation of the mechanisms underlying this disease progression would identify new therapeutic targets and strategies.",

author = "H Tseng and A Pettit and T Glant and Matthew Brown and G Thomas",

year = "2013",

language = "English",

pages = "5--5",

}

TY - CONF

T1 - Endochondral Bone Formation and Advanced Enthesitis Are Key Features Of Proteoglycan Induced Spondylitis Mouse Model Of Ankylosing Spondylitis

AU - Tseng, H

AU - Pettit, A

AU - Glant, T

AU - Brown, Matthew

AU - Thomas, G

PY - 2013

Y1 - 2013

N2 - Transition from an initial inflammatory phase to the disabling osteoproliferative phase in ankylosing spondylitis (AS) is very poorly understood. Elucidation of the mechanisms underlying this disease progression would identify new therapeutic targets and strategies.

AB - Transition from an initial inflammatory phase to the disabling osteoproliferative phase in ankylosing spondylitis (AS) is very poorly understood. Elucidation of the mechanisms underlying this disease progression would identify new therapeutic targets and strategies.

M3 - Abstract

SP - 5

EP - 5

ER -