Osteoarthritis as an organ disease

from the cradle to the grave

Richard M. Aspden (Corresponding Author), Fiona Saunders

Research output: Contribution to journalArticle

1 Citation (Scopus)
6 Downloads (Pure)

Abstract

Considered for decades as a cartilage disease, recent studies of osteoarthritis (OA) take us back to the concepts discussed at the naming of the disorder as “bone-joint-inflammation”. By describing the joint as an organ, can OA be called an organ disease – similar to heart disease? Is there a systemic (which system?) involvement? Would this help with diagnosis or therapy? Hyperplasia of the joint tissues is one of the most notable early features of the disease: articular cartilage thickens, chondrocytes proliferate and increase matrix biosynthesis, but not its incorporation; the subchondral bone densifies but is hypomineralised and there is an increase in bone marrow fat content. Associations between OA and hypertension, hypercholesterolaemia and blood glucose suggest systemic and metabolic components are involved. The source of pain is still unknown but here is evidence for peripheral and central sensitisation. Joint deformity is difficult to quantify, but statistical shape modelling provides a tool to use as an imaging biomarker. A genome-wide association study meta-analysis has identified novel genes associated with hip shape with many genes related to tissue growth and development. There are associations between hip shapes and age of first walking as well as with obesity through adulthood. These life-course events and a recapitulation in old age of developmental processes suggest that the cradle may affect our path to the grave. These observations suggest that tissue regeneration approaches, treating only the cartilage in OA joints, may only be of limited benefit.
Original languageEnglish
Pages (from-to)74-87
Number of pages14
JournalEuropean Cells & Materials
Volume37
DOIs
Publication statusPublished - 30 Jan 2019

Fingerprint

Osteoarthritis
Cartilage
Joints
Bone
Genes
Tissue
Hip
Tissue regeneration
Cartilage Diseases
Biosynthesis
Central Nervous System Sensitization
Biomarkers
Osteitis
Oils and fats
Genome-Wide Association Study
Glucose
Blood Glucose
Articular Cartilage
Chondrocytes
Hypercholesterolemia

Keywords

  • osteoarthritis
  • joint
  • systemic disease
  • metabolic disease
  • aetiology
  • growth
  • hyperplasia
  • development
  • Growth
  • Hyperplasia
  • Joint
  • Aetiology
  • Metabolic disease
  • Systemic disease
  • Development
  • Osteoarthritis
  • SUBCHONDRAL BONE PLATE
  • FEMORAL-HEAD
  • CRUCIATE LIGAMENT INTEGRITY
  • ILIAC CREST BONE
  • HIP SHAPE
  • SINGLE IMPACT LOAD
  • OLIGOMERIC MATRIX PROTEIN
  • HUMAN ARTICULAR-CARTILAGE
  • BODY-MASS INDEX
  • KNEE OSTEOARTHRITIS

ASJC Scopus subject areas

  • Bioengineering
  • Biochemistry
  • Biomedical Engineering
  • Cell Biology
  • Biomaterials

Cite this

@article{17db94e4b7a64fbbadba0f335c6836c1,
title = "Osteoarthritis as an organ disease: from the cradle to the grave",
abstract = "Considered for decades as a cartilage disease, recent studies of osteoarthritis (OA) take us back to the concepts discussed at the naming of the disorder as “bone-joint-inflammation”. By describing the joint as an organ, can OA be called an organ disease – similar to heart disease? Is there a systemic (which system?) involvement? Would this help with diagnosis or therapy? Hyperplasia of the joint tissues is one of the most notable early features of the disease: articular cartilage thickens, chondrocytes proliferate and increase matrix biosynthesis, but not its incorporation; the subchondral bone densifies but is hypomineralised and there is an increase in bone marrow fat content. Associations between OA and hypertension, hypercholesterolaemia and blood glucose suggest systemic and metabolic components are involved. The source of pain is still unknown but here is evidence for peripheral and central sensitisation. Joint deformity is difficult to quantify, but statistical shape modelling provides a tool to use as an imaging biomarker. A genome-wide association study meta-analysis has identified novel genes associated with hip shape with many genes related to tissue growth and development. There are associations between hip shapes and age of first walking as well as with obesity through adulthood. These life-course events and a recapitulation in old age of developmental processes suggest that the cradle may affect our path to the grave. These observations suggest that tissue regeneration approaches, treating only the cartilage in OA joints, may only be of limited benefit.",
keywords = "osteoarthritis, joint, systemic disease, metabolic disease, aetiology, growth, hyperplasia, development, Growth, Hyperplasia, Joint, Aetiology, Metabolic disease, Systemic disease, Development, Osteoarthritis, SUBCHONDRAL BONE PLATE, FEMORAL-HEAD, CRUCIATE LIGAMENT INTEGRITY, ILIAC CREST BONE, HIP SHAPE, SINGLE IMPACT LOAD, OLIGOMERIC MATRIX PROTEIN, HUMAN ARTICULAR-CARTILAGE, BODY-MASS INDEX, KNEE OSTEOARTHRITIS",
author = "Aspden, {Richard M.} and Fiona Saunders",
note = "We thank all the members, past and present, of the Orthopaedics Research Group whose work forms our contribution to the quest for a solution to this most disabling disease. We also wish to thank all our surgical colleagues in NHS Grampian who have kindly allowed us to use tissue donated by their patients and provided many stimulating clinical insights. We are grateful to the Medical Research Council, the Arthritis Research Campaign, the Engineering and Physical Sciences Research Council, the Sir Halley Stewart Trust and The Health Foundation for funding research related to this work. We acknowledge grant funding from TMRI Ltd. for some of the SSM studies.",
year = "2019",
month = "1",
day = "30",
doi = "10.22203/eCM.v037a06",
language = "English",
volume = "37",
pages = "74--87",
journal = "European Cells & Materials",
issn = "1473-2262",
publisher = "Swiss Society for Biomaterials",

}

TY - JOUR

T1 - Osteoarthritis as an organ disease

T2 - from the cradle to the grave

AU - Aspden, Richard M.

AU - Saunders, Fiona

N1 - We thank all the members, past and present, of the Orthopaedics Research Group whose work forms our contribution to the quest for a solution to this most disabling disease. We also wish to thank all our surgical colleagues in NHS Grampian who have kindly allowed us to use tissue donated by their patients and provided many stimulating clinical insights. We are grateful to the Medical Research Council, the Arthritis Research Campaign, the Engineering and Physical Sciences Research Council, the Sir Halley Stewart Trust and The Health Foundation for funding research related to this work. We acknowledge grant funding from TMRI Ltd. for some of the SSM studies.

PY - 2019/1/30

Y1 - 2019/1/30

N2 - Considered for decades as a cartilage disease, recent studies of osteoarthritis (OA) take us back to the concepts discussed at the naming of the disorder as “bone-joint-inflammation”. By describing the joint as an organ, can OA be called an organ disease – similar to heart disease? Is there a systemic (which system?) involvement? Would this help with diagnosis or therapy? Hyperplasia of the joint tissues is one of the most notable early features of the disease: articular cartilage thickens, chondrocytes proliferate and increase matrix biosynthesis, but not its incorporation; the subchondral bone densifies but is hypomineralised and there is an increase in bone marrow fat content. Associations between OA and hypertension, hypercholesterolaemia and blood glucose suggest systemic and metabolic components are involved. The source of pain is still unknown but here is evidence for peripheral and central sensitisation. Joint deformity is difficult to quantify, but statistical shape modelling provides a tool to use as an imaging biomarker. A genome-wide association study meta-analysis has identified novel genes associated with hip shape with many genes related to tissue growth and development. There are associations between hip shapes and age of first walking as well as with obesity through adulthood. These life-course events and a recapitulation in old age of developmental processes suggest that the cradle may affect our path to the grave. These observations suggest that tissue regeneration approaches, treating only the cartilage in OA joints, may only be of limited benefit.

AB - Considered for decades as a cartilage disease, recent studies of osteoarthritis (OA) take us back to the concepts discussed at the naming of the disorder as “bone-joint-inflammation”. By describing the joint as an organ, can OA be called an organ disease – similar to heart disease? Is there a systemic (which system?) involvement? Would this help with diagnosis or therapy? Hyperplasia of the joint tissues is one of the most notable early features of the disease: articular cartilage thickens, chondrocytes proliferate and increase matrix biosynthesis, but not its incorporation; the subchondral bone densifies but is hypomineralised and there is an increase in bone marrow fat content. Associations between OA and hypertension, hypercholesterolaemia and blood glucose suggest systemic and metabolic components are involved. The source of pain is still unknown but here is evidence for peripheral and central sensitisation. Joint deformity is difficult to quantify, but statistical shape modelling provides a tool to use as an imaging biomarker. A genome-wide association study meta-analysis has identified novel genes associated with hip shape with many genes related to tissue growth and development. There are associations between hip shapes and age of first walking as well as with obesity through adulthood. These life-course events and a recapitulation in old age of developmental processes suggest that the cradle may affect our path to the grave. These observations suggest that tissue regeneration approaches, treating only the cartilage in OA joints, may only be of limited benefit.

KW - osteoarthritis

KW - joint

KW - systemic disease

KW - metabolic disease

KW - aetiology

KW - growth

KW - hyperplasia

KW - development

KW - Growth

KW - Hyperplasia

KW - Joint

KW - Aetiology

KW - Metabolic disease

KW - Systemic disease

KW - Development

KW - Osteoarthritis

KW - SUBCHONDRAL BONE PLATE

KW - FEMORAL-HEAD

KW - CRUCIATE LIGAMENT INTEGRITY

KW - ILIAC CREST BONE

KW - HIP SHAPE

KW - SINGLE IMPACT LOAD

KW - OLIGOMERIC MATRIX PROTEIN

KW - HUMAN ARTICULAR-CARTILAGE

KW - BODY-MASS INDEX

KW - KNEE OSTEOARTHRITIS

UR - http://www.scopus.com/inward/record.url?scp=85060792551&partnerID=8YFLogxK

U2 - 10.22203/eCM.v037a06

DO - 10.22203/eCM.v037a06

M3 - Article

VL - 37

SP - 74

EP - 87

JO - European Cells & Materials

JF - European Cells & Materials

SN - 1473-2262

ER -