Extended Abstract (for invited Faculty only) Osteoarthritis

3.3.2 - Osteoarthritis & Ageing

Presentation Topic
Lecture Time
14:45 - 15:00
Session Type
Special Session
  • B. Von Rechenberg (Birmensdorf, CH)
  • B. Von Rechenberg (Birmensdorf, CH)



“Wear and tear”, structural changes, “inflammaging” as well as thinning of cartilage has been implemented as a reason for cartilage degeneration in aging individuals1-3, but not necessarily always associated with osteoarthritis4. While there is plenty of literature dedicated to osteoarthritis, publications dealing with aging of cartilage are relatively scarce and often from the seventies and eighties.


fig1.jpgfig2.jpgStructural changes in joint congruency were described, such that over time, joint surfaces and congruency change and adapt including thinning of the cartilage surface. Cartilage degeneration and thinning were attributed to a decreasing anabolic response of chondrocytes to damaging stimuli by increasing their matrix synthesis4. Also age dependent decreased lacunar numbers and hypermineralization of osteocyte lacunae (micropetrosis) were found in aging individuals1 as well as senescence of resident cells or changes in methylation in cartilage and subchondral bone cells with shortening of telomers and changes in epigenetics were recorded1,3,5,6.

A close relationship between subchondral bone and overlying hyaline cartilage is outlined in most of these publications, although still not really understood. One of the reasons, why this is the case and these pathways have not been pursued may be the common belief that the calcified cartilage and tidemark separate the hyaline cartilage from the subchondral bone and no connections between these unities exist in the adult individual and, furthermore, that cells within the calcified cartilage zone are compared to hypertrophic chondrocytes in the growth plate. This goes along with the still held belief that in contrast to bone, there is no permanent remodeling of the hyaline cartilage during the adult life time and that chondrocytes only remodel their immediate environment.

Our research with cartilage samples in vitro (Fig.1) and animal experiments in vivo (Fig.2) show that these views need to be revised. Cells in the calcified cartilage zone were viable and not hypertrophic (or even apoptotic). In addition, in vivo results showed that surgical removal of subchondral bone leads to immediate depletion of chondrocytes in the deep cartilage zone and cartilage degeneration, even if autografts were used to fill the bone defect in vicinity of the hyaline cartilage. Cartilage degeneration could be influenced by treatments addressing proliferation and healing capacity in the subchondral bone. These results lead us to the conclusion that only understanding the tight connection between subchondral bone and hyaline cartilage including the physiological remodeling of healthy cartilage will make it possible to influence the life span of joints without osteoarthritis.


1. Loeser RF. Aging processes and the development of osteoarthritis. Curr Opin Rheumatol 2013;25(1):108-13. DOI: 10.1097/BOR.0b013e32835a9428.

2. Bullough PG. The role of joint architecture in the etiology of arthritis. Osteoarthritis Cartilage 2004;12 Suppl A:S2-9. DOI: 10.1016/j.joca.2003.09.010.

3. Hugle T, Geurts J, Nuesch C, Muller-Gerbl M, Valderrabano V. Aging and osteoarthritis: an inevitable encounter? J Aging Res 2012;2012:950192. DOI: 10.1155/2012/950192.

4. Martin JA, Buckwalter JA. Roles of Articular Cartilage Aging and Chondrocyte Senescence in Ostoarthritis. The Iowa Orthopedic Journal 2001;21:1-6.

5. Pippenger BE, Duhr R, Muraro MG, Pagenstert GI, Hugle T, Geurts J. Multicolor flow cytometry-based cellular phenotyping identifies osteoprogenitors and inflammatory cells in the osteoarthritic subchondral bone marrow compartment. Osteoarthritis Cartilage 2015;23(11):1865-9. DOI: 10.1016/j.joca.2015.07.021.

6. Collins JA, Diekman BO, Loeser RF. Targeting aging for disease modification in osteoarthritis. Curr Opin Rheumatol 2018;30(1):101-107. DOI: 10.1097/BOR.0000000000000456.