Molecular treatments for joint pain syndromes in orthopedics like osteoarthritis target the biochemical exchanges at the molecular level. These interactions take place through cell signaling that occurs across membrane receptors on the surface of the cell. Molecular immunobiologics are anabolic growth factors and cytokine proteins (signaling proteins) manufactured by cells that can be used to activate healing pathways and modulate the immune response to joint injury, favoring regeneration and clinical recovery.
Cells operate through signaling molecules in the joint environment that tell them what to do. When there is matrix or cellular damage in a synovial joint like the knee, injured cells release molecules that bind to other cells located in the joint lining, inciting an immune response. These damage proteins that are released by injured cells bind immune cell receptors in the joint and spark an inflammatory response in an attempt to ‘heal’ the damage. Approximately 20% of the cells in the joint lining are immune cells known as macrophages and they direct this process. But where does this come from and why does it happen in the first place?
Most arthritis comes from joint overload due to mechanical alignment in patient’s lower extremities. The bone beneath the cartilage receiving the excess load becomes stiff and loses it’s ‘modulus of elasticity’ as the body lays down extra bone beneath the cartilage to support the overload. This is THE rate-limiting step in the development of osteoarthritis. In other words, osteoarthritis doesn’t occur without subchondral bone stiffening occurring first. The concave tibia receives the load from the convex femur and becomes stiff. Once the subchondral bone in the tibia becomes stiff, the load is reflected back to the convex femur that follows suit with impact and develops stiffness. At that point the two stiff articulations coming into contact with weight bearing cause damage to the cartilage layer covering the ends of the bone in the joint. During this process, matrix molecules and cartilage cell contents are released into the joint fluid as the inflammatory process continues unabated.
Joint overload allows the continued destruction of cartilage matrix and cells in the joint surface and the continued release of matrix and intracellular proteins into the joint fluid that propagates the inflammatory response. Unless the molecular milieu is converted from this catabolic environment where joint destruction is favored due to an ongoing inflammatory response, to an anabolic one favoring healing pathways, joint destruction will persist unabated until the end-stage of the joint is reached and replacement is indicated.
Immunobiologics in orthopedics exploit biochemical healing molecules that can halt the progression of arthritis, particularly when used with off-loading techniques to preserve the joint. Treatments like platelet rich plasma and bone marrow concentrates harness these cellular mechanisms and can eliminate clinical pain syndromes that accompany joint osteoarthritis without surgery and have been proven in the current scientific literature.