Korean researchers find how high blood pressure destroys knee cartilage

Korean researchers have found that high blood pressure can accelerate the progression of osteoarthritis — a discovery that traces how a brain hormone elevated by hypertension travels through the bloodstream to destroy cartilage in the joints.

Blocking the hormone's signaling pathway significantly reduced cartilage damage in experiments.

The Ministry of Science and ICT announced Friday that a joint research team led by Professor Ryu Je-hwang of Chonnam National University and Professor Jeon Jang-soo of Inje University had identified the specific molecular mechanism by which high blood pressure worsens osteoarthritis.

The findings were published in the international academic journal Science.

Osteoarthritis and hypertension are among the most common chronic conditions to co-occur in older adults. While it had long been observed that arthritis tends to be more severe in patients with high blood pressure, the precise mechanism by which a vascular condition like hypertension could affect joints and cartilage had remained unclear.

The research team analyzed data from the Korea National Health and Nutrition Examination Survey and confirmed that people with high blood pressure had a higher prevalence of osteoarthritis. The association with hypertension also grew more pronounced as arthritis severity increased.

Experiments using two different mouse models of hypertension further confirmed that high blood pressure accelerates the progression of osteoarthritis.

The key link the team identified is vasopressin (AVP) — a brain hormone that regulates blood pressure — and its receptor, vasopressin receptor 1A (AVPR1A).

Vasopressin is a neurohormone secreted by the posterior pituitary gland that plays a role in regulating the body's water balance and raising blood pressure.

In a state of hypertension, the concentration of vasopressin in the blood rises. The research team also found that AVPR1A receptors, which are barely detectable in healthy cartilage, increase markedly as joints become damaged or age.

The problem emerged when the two factors met. When vasopressin, elevated by high blood pressure, bound to AVPR1A on cartilage cells, signals that break down cartilage were activated while signals that maintain it were suppressed. The result was accelerated cartilage destruction and worsening osteoarthritis.

Conversely, when the research team genetically removed or functionally inhibited AVPR1A in mice, cartilage damage caused by high blood pressure decreased significantly.

The study is significant for moving beyond the conventional view of osteoarthritis as simply a condition caused by worn-down joints, instead connecting the brain, hormones and joints along a single biological axis.

The team identified a "brain-hormone-joint" pathway in which a blood-pressure-regulating hormone produced in the brain travels through the bloodstream to act on distant joints and promote cartilage destruction.

The findings also point to a new treatment strategy for osteoarthritis. Selectively blocking the signaling between AVP and AVPR1A could potentially be developed into a therapy that directly inhibits cartilage destruction. However, safety and efficacy trials in humans will be required before the approach can be applied to patient treatment.

The research also raises the possibility that blood pressure management in hypertensive patients extends beyond cardiovascular disease prevention to joint health. The findings provide a basis for managing both systemic health and joint disease together in older hypertensive patients with advancing joint damage.

"These results suggest that when treating osteoarthritis patients, clinicians should manage not only the local joint condition but also systemic health factors such as high blood pressure," Professor Ryu said. "We plan to advance follow-up research toward developing a fundamental arthritis treatment that targets the vasopressin signaling system."