Articular cartilage Q&A discussion 24

**Dr. Smith**: Let's start with the basics, Dr. Patel. Can you tell me about the different types of cartilage?

**Dr. Patel**: Sure! Cartilage comes in five forms. The most commonly known is **hyaline or articular cartilage**, which covers the ends of bones in joints. Then we have **fibroelastic cartilage**, found in the meniscus, **fibrocartilage**, present where tendons or ligaments insert into bone, **elastic cartilage** in places like the trachea, and finally, **physeal cartilage** or the growth plate, important during bone growth.

**Dr. Smith**: So, focusing on **articular cartilage**, what's its main function in the joints?

**Dr. Patel**: Articular cartilage reduces friction between bones and helps distribute load during movement. It’s especially efficient due to its high water content, which stress-shields the matrix components. This makes it a great shock absorber while also being highly resilient.

**Dr. Smith**: Interesting! How about its composition? What are the primary components of this cartilage?

**Dr. Patel**: Articular cartilage is mostly extracellular matrix, comprising **water, collagen**, and **proteoglycans**. In fact, water makes up about 65-80% of its mass. Type II collagen accounts for 90-95% of its total collagen content, and **chondrocytes** are the primary cells responsible for producing this collagen and proteoglycans.

**Dr. Smith**: You mentioned water content. How does this change with age and disease?

**Dr. Patel**: That’s a good point. With normal aging, the water content decreases. But in conditions like **osteoarthritis (OA)**, water content actually increases. This leads to higher permeability, decreased cartilage strength, and a reduced Young’s modulus, meaning the cartilage becomes less elastic.

**Dr. Smith**: Fascinating. What about the collagen and proteoglycan balance? How do these change with osteoarthritis?

**Dr. Patel**: In early-stage OA, proteoglycan content increases, but it decreases in late stages. As for collagen, type II remains predominant, but with OA, there’s disorganization due to increased collagenase activity. This disorganization contributes to the cartilage's breakdown.

**Dr. Smith**: Moving on to the structure of articular cartilage, could you walk us through the different layers?

**Dr. Patel**: Absolutely. Articular cartilage has three distinct zones plus the **tidemark**:

1. **Superficial zone**: The collagen here is aligned parallel to the joint, with flattened chondrocytes and the highest collagen concentration.

2. **Intermediate zone**: Collagen fibers are organized randomly or obliquely, and it’s the thickest zone.

3. **Deep zone**: Collagen fibers are perpendicular to the joint, and this zone has the highest proteoglycan concentration.

Lastly, the **tidemark** separates the true articular cartilage from the calcified cartilage beneath.

**Dr. Smith**: I see. So, the tidemark is a key structure here. What role does it play in cartilage health?

**Dr. Patel**: The tidemark is crucial because it divides the uncalcified and calcified cartilage. It’s also a marker of where nutrient sources for chondrocytes change, with synovial fluid nourishing the upper layers and subchondral bone supporting the lower layers.

**Dr. Smith**: Speaking of nourishment, cartilage is avascular, right? How does it sustain itself?

**Dr. Patel**: Yes, cartilage lacks its own blood supply. Instead, it relies on **synovial fluid** for nutrients at the surface and the **subchondral bone** at the base. Most of its energy comes from glycolysis.

**Dr. Smith**: What about mechanical stress? How does cartilage respond to loading?

**Dr. Patel**: Cartilage thrives under moderate, cyclic mechanical stress—this stimulates matrix synthesis. However, excess stress or static load can lead to cartilage breakdown and chondrocyte death, primarily through apoptosis.

**Dr. Smith**: That makes sense. Now, aging and osteoarthritis seem to have overlapping but distinct effects on cartilage. How can we differentiate between the two?

**Dr. Patel**: Great question. With **aging**, cartilage shows a decrease in water content, increased collagen crosslinking, and fewer chondrocytes. In contrast, with **osteoarthritis**, water content increases, collagen disorganizes, and chondrocytes cluster, particularly in late-stage OA. Both processes, however, lead to reduced elasticity and cartilage stiffness over time.

**Dr. Smith**: And what happens when the cartilage is injured? How does it attempt to heal?

**Dr. Patel**: The healing response depends on the depth of the injury. Superficial lacerations don’t heal well because cartilage is avascular. But if the injury penetrates through the **tidemark** into the subchondral bone, fibrocartilage forms, which is less resilient than the original hyaline cartilage. This is why injuries that cross the tidemark are more likely to result in arthritis over time.

**Dr. Smith**: That’s a good overview. Lastly, what’s the role of growth factors in maintaining or healing cartilage?

**Dr. Patel**: Various growth factors play essential roles. For example, **TGF-β** promotes proteoglycan synthesis and suppresses inflammatory responses. **IGF-1** is key for cartilage matrix synthesis, and **b-FGF** stimulates DNA synthesis in chondrocytes. However, excessive TGF-β can lead to osteophyte formation, which is problematic in joint diseases.

**Dr. Smith**: It’s clear that maintaining a balance in these factors is vital for healthy cartilage function. Thanks for breaking this down, Dr. Patel!

**Dr. Patel**: My pleasure, Dr. Smith!

Reference 

https://www.orthobullets.com/basic-science/9017/articular-cartilage