Abstract
BackgroundOsteoarthritis is the most widespread joint-affecting disease. Patients with osteoarthritis experience pain and impaired mobility resulting in marked reduction of quality of life. A progressive cartilage loss is responsible of an evolving disease difficult to treat. The characteristic of chronicity determines the need of new active disease modifying drugs. Aim of the present research is to evaluate the role of low doses of native type II collagen in the rat model of osteoarthritis induced by sodium monoiodoacetate (MIA).Methods1, 3 and 10 mg kg-1 porcine native type II collagen were daily per os administered for 13 days starting from the day of MIA intra-articular injection.ResultsOn day 14, collagen-treated rats showed a significant prevention of pain threshold alterations induced by MIA. Evaluation were performed on paws using mechanical noxious (Paw pressure test) or non-noxious (Electronic Von Frey test) stimuli, and a decrease of articular pain was directly measured on the damaged joint (PAM test). The efficacy of collagen in reducing pain was as higher as the dose was lowered. Moreover, a reduced postural unbalance, measured as hind limb weight bearing alterations (Incapacitance test), and a general improvement of motor activity (Animex test) were observed. Finally, the decrease of plasma and urine levels of CTX-II (Cross Linked C-Telopeptide of Type II Collagen), a biomarker of cartilage degradation, suggests a collagen-dependent decrease of structural joint damage.ConclusionsThese results describe the preclinical efficacy of low dosages of native type II collagen as pain reliever by a mechanism that involves a protective effect on cartilage.
Highlights
Osteoarthritis is the most widespread joint-affecting disease
The pharmacological activity of low dosages of type II collagen was evaluated in the rat unilateral osteoarthritis model induced by MIA. 14 days after intra-articular MIA injection the mechanical withdrawal threshold to a noxious stimulus was measured by Paw pressure test (Figure 1)
Osteoarthritis, called degenerative joint disease, is a chronic pathology frequently seen in knee, hip, spine and hand causing pain, stiffness, decreased range of motion, and reduced quality of life for million people throughout the world [5]
Summary
Osteoarthritis is the most widespread joint-affecting disease. Patients with osteoarthritis experience pain and impaired mobility resulting in marked reduction of quality of life. A progressive cartilage loss is responsible of an evolving disease difficult to treat. Aim of the present research is to evaluate the role of low doses of native type II collagen in the rat model of osteoarthritis induced by sodium monoiodoacetate (MIA). Osteoarthritis pathophysiology involves the whole joint in a disease process that includes focal and progressive loss of hyaline articular cartilage. An integrative treatment of osteoarthritis, or rheumatoid arthritis, must consider a supplementation with collagen since it is the most prevalent component of the [16,17]; the autoimmune component of this pathology suggests a mechanism called oral tolerance, the usual response of the gut-associated lymphoid tissue (GALT) to harmless gut antigens inducing local and systemic immunological tolerance [18,19,20]. The knowledge about the relevance of low doses of undenatured collagen in osteoarthritis are more limited [21] and the absence of an immune component in the pathology of osteoarthritis make difficult to assume the oral tolerance as possible mechanism of collagen action
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
