Two-layered structure of the perichondrium
Morphologically and functionally, the perichondrium is divided into two specialized layers, each performing its share of work to maintain cartilage viability.
- Fibrous (outer) layer. Formed by dense fibrous connective tissue. This is precisely where a dense network of blood vessels runs. Since cartilage tissue itself lacks its own blood supply (is avascular), this outer layer plays the role of the main "feeder", providing adequate trophism for deep structures.
- Cellular (inner) layer. This layer lies directly adjacent to the surface of the cartilage tissue. It lacks large vessels, but is densely populated with cambial elements—young cells ready at any moment to begin the process of division and synthesis.
Chondroblasts and external-type cambium
The main actors of the inner cellular layer of the perichondrium are chondroblasts. These are relatively small, flattened cells possessing the highest synthetic and mitotic activity.
Chondroblasts are capable of active proliferation (division) and intensive synthesis of extracellular matrix components of cartilage. The most important biological feature of the perichondrium is that it represents an external-type cambium. This means that the cambial reserve—the pool of young cells capable of division—is located not inside the tissue itself, but outside its borders, on the surface.
The development of these cells is strictly subject to the cell differon (sequential maturation series):
- Connective tissue stem cells
- Prechondroblasts
- Mature chondroblasts
Mechanisms of appositional growth
The perichondrium provides a specific type of cartilage mass increase—appositional (peripheral) growth. This process is crucial both during the period of embryonic development (embryogenesis) and during the regeneration of injuries in adults.
The essence of the mechanism lies in the deposition of new layers of cartilage from the outside. Chondroblasts of the inner layer of the perichondrium begin to actively secrete and accumulate young extracellular matrix around themselves. Gradually synthesizing the matrix, they literally "wall themselves up" in their own secretions. Having found themselves in such isolation inside the dense extracellular matrix, chondroblasts finally differentiate and transform into mature cartilage cells—chondrocytes. Thus, cartilage thickens due to the addition of mass at the periphery.
Articular cartilages: the price of perfect gliding
There is one crucial functional exception to the general rule of cartilage structure—articular surfaces. The cartilages forming joints are completely devoid of perichondrium.
This absence is not accidental: the presence of a rough, vessel-penetrated fibrous membrane would make smooth and unhindered gliding of articular surfaces against each other impossible. The absence of the perichondrium makes the joint smooth, but entails serious negative consequences. Due to the lack of a cambial cell layer, articular cartilage completely loses its capacity for appositional growth, which catastrophically reduces its regenerative potential during trauma or age-related wear.
Since the perichondrium with its vessels is absent here, tissue nutrition is carried out via diffusion from two independent sources:
- Synovial fluid bathing the joint from the outside.
- Underlying bone tissue supplying nutrients from below.
Briefly: answers to topical questions
Which types of cartilage tissue in the human body lack a perichondrium?
Articular cartilages lack a perichondrium. This is due to the need to maintain a smooth surface for free joint gliding. Due to the absence of this membrane, such cartilages are incapable of appositional growth, which drastically reduces their regenerative capacity, and trophism is provided solely by diffusion.
How does appositional cartilage growth differ from interstitial growth?
Appositional growth provides an increase in cartilage from the outside, whereas interstitial growth provides it from the inside.
| Criterion | Appositional growth | Interstitial growth |
|---|---|---|
| Direction | Deposition of new layers from the outside | Increase in cartilage mass from the inside |
| Effector cells | Perichondrial chondroblasts | Chondrocytes |
| Mechanism | Cells synthesize extracellular matrix, wall themselves up, and become chondrocytes | Cells actively divide and synthesize matrix |
To remember the two layers of the perichondrium, imagine a sandwich: on the outside is a hard crust of bread with vessels (the fibrous layer providing nutrition), and on the inside, right next to the cartilage itself, is a soft cellular filling of active builders (the inner cellular layer with chondroblasts).
Class and exam questions
Why do articular cartilages heal so poorly and slowly after injuries?
Articular cartilages physiologically lack a perichondrium, as its presence would prevent smooth gliding. Due to the absence of an inner cellular layer with chondroblasts, the cartilage is incapable of appositional growth, which drastically reduces its regenerative capacity.
What does the term "external-type cambium" mean?
This term means that the pool of young dividing cells (cambial reserve) is not located inside the cartilage tissue itself, but is situated at its periphery—in the inner layer of the perichondrium.
How does avascular articular cartilage receive nutrients?
Articular cartilage is nourished by diffusion from two different sources: on the outside, it is nourished by joint (synovial) fluid, and on the inside, by vessels of the underlying bone tissue.
How does the transformation of a chondroblast into a chondrocyte occur?
The chondroblast of the inner layer of the perichondrium actively synthesizes extracellular matrix, gradually surrounding itself with it on all sides. Once "walled up" in the matrix, it ceases active growth and becomes a mature chondrocyte.
What else to study on this topic
- Structure and functions of chondroblasts
- Cell differon of cartilage tissue
- Appositional (peripheral) growth of cartilage
- Features of avascular tissue trophism
- Reduction of regenerative potential of articular surfaces
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