By Marc Dellière, Medical Consultant & Trainer – Specialist in Stress, Prevention & Integrative Health
From mechanical wear and tear to biological disease
For a long time, osteoarthritis was perceived as the mechanical result of joint “wear and tear,” tired cartilage, rubbing bones, and pain. Today, scientific literature is converging on a new reality. Osteoarthritis is an active biological disease characterized by low-grade chronic inflammation involving the entire joint, modulated by metabolism and neighboring tissues.
Silent inflammation: a lasting driver
Studies show that in arthritic joints, pro-inflammatory cytokines such as IL-1β, TNF-α, and IL-6 persist continuously. This inflammation, often subtle, is sufficient to alter cartilage metabolism, activate degradation enzymes (MMP, ADAMTS), disrupt matrix synthesis, and weaken chondrocytes. Even when osteoarthritis appears “stable,” the tissue continues to be biologically active.
Cartilage: a living, reactive, and adaptable tissue
Cartilage is not simply an inert shock absorber. It reacts to mechanical stress, oxidative stress, the biological environment, and metabolic status. If the environment becomes unfavorable (inflammation, metabolic imbalance, tissue alterations), degradation accelerates. Osteoarthritis is therefore not just a mechanical problem, but an imbalance in the tissue microenvironment.
The role of adipose tissue and metabolism
Beyond mechanical mechanisms alone, the adipose tissue around the joint, as well as overall metabolism, plays a role. This tissue can release pro-inflammatory mediators, contribute to local inflammation, and influence cartilage degradation. This is why certain forms of osteoarthritis develop even without significant mechanical overload.
Towards functional and preventive management
In light of these findings, the therapeutic strategy can no longer be limited to pain management or waiting for surgery.
The objective must be to:
- preserve tissue,
- slow down inflammatory cascades,
- protect the joint matrix,
- maintain joint function in the long term.
It is no longer just about pain relief: treatment becomes structural, preventive, and functional.
Why is biological support for cartilage becoming central again?
- improve cartilage resistance to stress,
- limit the activation of degradation enzymes,
- support the viscosity of synovial fluid,
- promote better tolerance to movement.
This is not a spectacular immediate effect, but a slow, cumulative process that protects joint capital. It is a strategy that goes beyond symptomatic relief.
For whom is this approach particularly relevant?
It is particularly suitable for:
- patients in the early stages of osteoarthritis,
- post-traumatic osteoarthritis,
- chronic joint pain with moderate inflammation,
- active individuals who want to maintain mobility and function,
- people undergoing rehabilitation or functional care.
The goal is not to “erase” osteoarthritis, but to maintain a functional joint for as long as possible.
Modern osteoarthritis is no longer just an X-ray image or “inevitable wear and tear.” It is tissue under stress, in a modifiable inflammatory environment, subject to adjustable mechanics, on an influenceable metabolic terrain. And everything that is biologically active can and must be biologically supported.
Learn more about Xelflex® for joint health!
Scientific sources :
Knights AJ, Redding SJ, Maerz T. Inflammation in osteoarthritis: the latest progress and ongoing challenges. Curr Opin Rheumatol. 2023.
https://pubmed.ncbi.nlm.nih.gov/36695054/
Sánchez-López E, Coras R, Torres A, et al. Synovial inflammation in osteoarthritis progression. Nat Rev Rheumatol. 2022.
https://pmc.ncbi.nlm.nih.gov/articles/PMC9050956/
Goldring MB, Goldring SR. Inflammation in osteoarthritis. Curr Opin Rheumatol. 2011.
https://pmc.ncbi.nlm.nih.gov/articles/PMC3937875/
Berenbaum F, Eymard F, Houard X. Metabolic regulation of inflammation in osteoarthritis. Arthritis Res Ther. 2017.
https://pubmed.ncbi.nlm.nih.gov/27564539/
Berenbaum F. Osteoarthritis as an inflammatory disease. Osteoarthritis Cartilage. 2013.
https://pubmed.ncbi.nlm.nih.gov/23194896/
Thomson A, Hilkens CMU. Synovial macrophages in osteoarthritis: the key to inflammation and cartilage degradation? Front Immunol. 2021.
https://pmc.ncbi.nlm.nih.gov/articles/PMC8239355/