Since the 1970s, scientific researchers have been studying collagen hydrolysate Fortigel®, the main ingredient in CH-Alpha and its effects on cartilage metabolism. Recent laboratory findings, practical medical experience, and clinical studies have confirmed that Fortigel accumulates in joints and supports cartilage regeneration.¹ It is this unique effect on cartilage metabolism that offers physicians a breakthrough approach to promoting joint health.

Collagen is the most frequently occurring protein in mammals. Its biosynthesis occurs through a number of intracellular intermediates. The typical fibrils of collagen are formed in the extracellular space; these are cross-linked by covalent bonds and provide the collagen with its characteristic tensile strength. Fortigel is produced by enzymatic hydrolysis of collagenous tissue from raw material.

Production of Fortigel

The Potential of CH-Alpha in Cartilage Regeneration

Joint cartilage consists of collagen, proteoglycans, and select proteins in an extracellular matrix (ECM), or framework, responsible for strength and elasticity.¹ The ECM is composed primarily of water, collagen (which provides strength and cushioning), and proteoglycans (which ensure compression strength). Maintaining normal collagen levels in bone, cartilage, tendons, ligaments, and joint tissues is vital to maintaining joint health. When the natural regeneration process can’t keep up with daily wear and tear, overexertion, or extra weight, joint cartilage can break down.

As cartilage is lost, there is less cushioning, fissuring, and development of osteophytes, resulting in increased stiffness and loss of flexibility and a gradual increase in discomfort.

Unlike nearly every other tissue in the human body, cartilage does not contain blood vessels or nerves, which makes it slow to heal or grow.² However, cartilage is an active, growing tissue that needs continuous regeneration to provide the protection and strength joints require to perform without stiffness and maintain their flexibility.

CH-Alpha is the only product with a U.S. patent for cartilage regeneration. It is also the only product proven to stimulate specialized cells called chondrocytes, which are responsible for the metabolic maintenance of the ECM.¹ Chondrocytes control the rate of cartilage regeneration in joints and detect changes in the composition of the cartilage. They respond to these changes by growing more cartilage. Studies have shown that CH-Alpha increases the concentration of collagen and proteoglycans through this stimulatory effect on chondrocytes.

Cartilage Metabolism

Joint cartilage consists of chondrocytes and an extracellular matrix (ECM), the latter being of particular physiological significance.¹ The ECM of joint cartilage comprises two classes of macromolecules: collagen (type II collagen fibrils) forms the structure of the ECM and provides it with its tensile and sheer strength; and proteoglycans (such as aggrecans), which are responsible for the compressive strength and elasticity of the tissue.

Cartilage, like bone, is subject to continuous regeneration during which anabolic and catabolic processes are in equilibrium.^1,2 Any imbalance in this equilibrium between matrix degeneration and regeneration results in a decrease in the components of the ECM, such as type II collagen, and ultimately leads to loss of cartilage. Apart from the lysosomal proteases (cathepsins), which have a direct pericellular effect within the cartilage cell, there are numerous matrix metalloproteases (such as collagenase, stromelysin, and aggrecanase), which, at neutral pH, can degrade all the cartilage building blocks. According to current scientific understanding, the activity of these components is controlled by the cytokine interleukin-1 (IL-1).

Chondrocytes and the ECM, composed of proteoglycans and collagen, maintain equilibrium in cartilage metabolism1

If the activity of some matrix metalloproteases begins to degrade cartilage building blocks, other components can initiate a response to an imbalance in the ECM.² For example, a tissue inhibitor of the matrix metalloproteases and a plasminogen activator inhibitor are responsible for inhibiting the catabolic enzymes, thus slowing cartilage degradation. Certain polypeptide mediators, in the form of growth factors, stimulate anabolic processes in cartilage, thus contributing, to a limited extent, to new cartilage formation. This group of mediators includes the insulin-like growth factor-1 and the transforming growth factor-ß, both of which stimulate proteoglycan synthesis. Recent results have shown that collagen fragments, such as those contained in CH-Alpha, can also function as mediators that stimulate the synthesis of cartilage matrix.¹

References:

1. Oesser S, Seifert J. Stimulation of type II collagen biosynthesis and secretion in bovine chondrocytes cultured with degraded collagen. Cell Tissue Res. 2003;311:393-399.
2. Buckwalter JA, Mankin HJ. Articular cartilage. Part I: Tissue design and chondrocyte-matrix interactions. J Bone Joint Surg. 1997;79:600-611.