A cartilaginous joint is a connection between two bones where cartilage serves as the primary linking tissue, allowing little to no movement. Unlike the freely movable joints in your knees and shoulders, cartilaginous joints are built for stability, shock absorption, and in some cases, growth. They fall into two distinct subtypes with very different roles in the body, and they show up in places you might not expect, from a newborn’s skull base to the discs between your vertebrae.
Where Cartilaginous Joints Fit Among Joint Types
Joints are classified by the tissue holding the bones together. Fibrous joints use dense connective tissue (think the sutures in your skull). Synovial joints have a fluid-filled capsule that lets bones glide freely (your knee, hip, and elbow). Cartilaginous joints sit in the middle: the bones are linked by cartilage, and the joint allows only slight movement or none at all. In functional terms, cartilaginous joints are classified as amphiarthroses, meaning they permit limited motion, which distinguishes them from both the immovable fibrous joints and the freely movable synovial ones.1Europe PMC. Anatomy, Joints
The two subtypes of cartilaginous joints differ in the kind of cartilage involved and in what they do for the skeleton. Primary cartilaginous joints, called synchondroses, are held together by hyaline cartilage. Secondary cartilaginous joints, called symphyses, are joined by a pad of fibrocartilage. That difference in cartilage type is not just a histological curiosity; it determines whether the joint is temporary or permanent, how much give it has, and what goes wrong when it fails.
Synchondroses, the Temporary Joints
A synchondrosis connects bones with hyaline cartilage, the smooth, glassy type of cartilage you find on the ends of bones inside a synovial joint. The defining feature of most synchondroses is that they are designed to disappear. The cartilage gradually turns into bone through a process called endochondral ossification, and once that is complete, the joint is gone and the two bones have fused into one.
The most familiar example is the growth plate (also called the physis or epiphyseal plate) in the long bones of children and adolescents. This thin disc of hyaline cartilage sits between the shaft and the end of a bone like the femur or tibia. Chondrocytes within the plate go through stages of proliferation, enlargement, and death, and as they die, bone-forming cells move in and replace the cartilage with solid bone. That cycle is what makes bones grow longer. Once a person finishes growing, the growth plate closes entirely and is replaced by a thin line of bone.2PubMed Central. The growth plate: a physiologic overview
Growth plates are not the only synchondroses. The cranial base in a newborn contains several synchondroses between the bones of the skull floor. These joints act as growth centers that help shape the skull and face during infancy and childhood. Research in primates shows that cranial synchondroses have organized zones of proliferating and enlarging cartilage cells, a hallmark of active growth.3PubMed. Cranial synchondroses of primates at birth When they close prematurely, as happens in certain genetic conditions, the skull base can end up shorter than normal and facial proportions change.
Synchondroses are not unique to mammals, either. In alligators, a cartilaginous layer between the vertebral body and the neural arch (the neurocentral synchondrosis) fuses through the same endochondral ossification process seen in human growth plates. Histological examination of alligator vertebrae shows the joint has a bipolar organization of cartilage cells, and fusion proceeds as bone gradually invades the cartilage from both sides.4PubMed. Histology-based morphology of the neurocentral synchondrosis in Alligator mississippiensis (Archosauria, Crocodylia) The basic blueprint of a temporary cartilage joint that eventually ossifies is ancient and widespread across vertebrates.
Symphyses, the Permanent Joints
A symphysis uses fibrocartilage instead of hyaline cartilage. Fibrocartilage is tougher and more flexible, packed with dense collagen fibers that give it the ability to resist compression and absorb shock. Unlike synchondroses, symphyses are generally permanent; they are not meant to ossify and disappear. Their job is to connect bones that need to stay slightly mobile throughout life.
The intervertebral discs are the most numerous symphyses in the body. Each disc is a fibrocartilaginous pad connecting two vertebral bodies, distributing the forces of body weight and movement across the spine. These discs operate in an extremely low-oxygen environment and have almost no blood supply, relying instead on diffusion of nutrients from surrounding tissues.5Orthopaedics and Trauma. Chapter 6 – Intervertebral Disc That avascular design is efficient but also explains why disc injuries heal so slowly and why disc degeneration is so common with age.
The pubic symphysis is another well-known example. It sits at the front of the pelvis, joining the left and right pubic bones with a wedge of fibrocartilage. Under normal circumstances it allows only a few millimeters of movement. The manubriosternal joint, where the upper portion of the breastbone meets the body of the sternum, is also classified as a symphysis, though debate exists about whether it should be called a synchondrosis in younger people before the fibrocartilage fully develops.
How Cartilage Handles Load Without a Blood Supply
One of the more remarkable aspects of cartilaginous joints is that the cartilage tissue itself lacks blood vessels. Articular cartilage in synovial joints gets nutrients mainly by diffusion from the surrounding synovial fluid, and researchers have studied whether the mechanical pumping action of walking helps push nutrients deeper into the tissue. Experiments using human cartilage plugs showed that for small molecules like glucose and oxygen, the main nutrients cartilage cells need, cyclic loading did not significantly speed up delivery compared with simple diffusion. For larger molecules like serum albumin, however, the pumping effect increased the transport rate substantially.6PubMed Central. Influence of cyclic loading on the nutrition of articular cartilage
Cartilage is also a surprisingly effective shock absorber. Under impact compression, articular cartilage absorbs energy per unit volume at roughly four times the rate of the subchondral bone beneath it.7PubMed. Shock absorbing ability of articular cartilage and subchondral bone under impact compression The superficial and middle layers of cartilage play a particularly critical protective role. When those upper layers are damaged or thinned, the stiffness of the remaining cartilage drops by about 40%, and the energy absorbed by the underlying bone jumps by roughly a third, putting that bone at much higher risk of injury.8PubMed. Shock absorbing ability in healthy and damaged cartilage-bone under high-rate compression This is part of why cartilage damage can cascade into deeper problems over time.
The Pubic Symphysis During Pregnancy
The pubic symphysis undergoes dramatic changes during pregnancy. Hormones, particularly relaxin, remodel the fibrocartilaginous disc and surrounding ligaments to make the pelvis more flexible for delivery. A systematic review of the adult pubic symphysis found that circulating relaxin induces resorption along the edges of the joint and structural changes in the fibrocartilage, widening the joint and increasing its mobility.9PubMed Central. The adult human pubic symphysis: a systematic review
Relaxin levels are highest in the first trimester and again near delivery. The combination of loosened ligaments and the compressive force of the baby’s weight can sometimes lead to excessive separation of the pubic symphysis, a painful condition that occasionally requires treatment.10PubMed Central. Role of relaxin in diastasis of the pubic symphysis peripartum For most people, the joint returns to near-normal width after delivery, but in some cases lingering instability or pain persists for months.
This hormonal remodeling is a feature specific to symphyses. The fibrocartilage design allows the joint to widen and then recover, which hyaline cartilage in a synchondrosis would not tolerate. It is one of the clearest illustrations of why the two subtypes of cartilaginous joints exist: synchondroses are rigid and temporary, symphyses are flexible and adaptive.
Pubic Fusion Across Primates
The flexibility of the pubic symphysis is not universal across species. A study examining pubic symphysis fusion across 68 primate species found that the joint fuses completely in at least 40 of them, spanning all major branches of the primate order.11PubMed Central. Variation in Pubic Symphysis Fusion Across Primates: Implications for Obstetric Adaptation This fusion occurred in both wild and captive animals, ruling out captivity-related pathology as an explanation. Humans are among the species where the pubic symphysis normally remains unfused throughout life, a trait that may be related to the demands of bipedal locomotion and childbirth. The fact that most primates eventually fuse this joint suggests that retaining a flexible symphysis into adulthood is the derived condition, not the default one.
What Happens to Cartilaginous Joints as You Age
Synchondroses and symphyses age in different ways, but both change significantly over a lifetime.
Synchondroses are supposed to close, so their disappearance is normal. The timing matters, though. Growth plates in long bones typically close in the late teens or early twenties, and the cranial base synchondroses close at various ages during childhood. Premature closure, driven by overactive signaling through a receptor called FGFR3, is seen in conditions like achondroplasia (the most common form of dwarfism). In both human cases and mouse models, premature synchondrosis closure in the spine and cranial base was associated with increased bone formation around the joint, effectively welding the bones together too early and limiting growth.12PubMed Central. FGFR3 promotes synchondrosis closure and fusion of ossification centers through the MAPK pathway
Symphyses, by contrast, are meant to last, but they degrade. The manubriosternal joint shows age-related thinning and loss of hydration in its fibrocartilage, along with disorganization of collagen fibers and focal lesions consistent with a degenerative process.13PubMed. Manubriosternal joint: synchondrosis or symphysis? Analysis of morphology and aging in humans The intervertebral discs go through similar degenerative changes, losing water content and becoming stiffer and more prone to herniation with age. The pubic symphysis surface erodes and remodels progressively, which is actually useful in forensic anthropology as one method of estimating age at death from skeletal remains.
Growth Plate Injuries in Children
Because growth plates are still made of cartilage, they are structurally weaker than the surrounding bone. In children and adolescents, a fracture that would break through solid bone in an adult often runs through the growth plate instead. Injury to the growth plate can stimulate abnormal bone repair, potentially leading to a bony bridge forming across the plate, limb length differences, or angular deformity of the bone.14Orthopaedics and Trauma. Growth plate injuries and management
The severity depends on how much of the plate is damaged and where. Injuries that cross through the proliferating zone of the growth plate are more likely to disrupt future growth than injuries that stay in the bone on one side. Lower extremity growth plate injuries are especially consequential because even small differences in leg length can affect gait and joint loading over years.15PubMed Central. Growth Plate Injuries of the Lower Extremity: Case Examples and Lessons Learned Treatment often involves monitoring growth over time to catch problems early, and in some cases surgical intervention to correct or prevent deformity.
Genetic Disorders That Target the Growth Plate
Several genetic conditions specifically disrupt the cartilage in growth plates, leading to abnormal skeletal development and short stature. Defects in genes that control the organization and function of the growth plate affect the process by which cartilage is replaced by bone, and even subtle disruptions can have outsized effects on height and limb proportions.16PubMed Central. Growth plate extracellular matrix defects and short stature in children
Multiple epiphyseal dysplasia (MED) is one such condition. It causes mild dwarfism and early-onset arthritis, and it can result from mutations in the gene for matrilin-3, a protein in the cartilage matrix. In mouse models of this disease, the mutant protein gets stuck inside cartilage cells instead of being secreted properly, triggering a stress response. Over time, fewer cartilage cells proliferate and more die at the wrong time and place within the growth plate, which is what disrupts bone lengthening and produces the characteristic short-limbed proportions.17Human Molecular Genetics. Decreased chondrocyte proliferation and dysregulated apoptosis in the cartilage growth plate are key features of a murine model of epiphyseal dysplasia caused by a matn3 mutation
Seeing Cartilaginous Joints on Imaging
Cartilage does not show up on standard X-rays, which is why cartilaginous joints can be tricky to evaluate. An X-ray will show the bones on either side of the joint and the space between them, but the cartilage itself is invisible. MRI changed that. It can characterize soft tissues noninvasively and has become the primary tool for evaluating cartilage throughout the body.18PubMed Central. MRI EVALUATION OF KNEE CARTILAGE
For articular cartilage in the knee, MRI techniques have become increasingly sophisticated. Standard sequences can detect structural defects like cracks and thinning, while newer compositional techniques can pick up changes in the collagen network and water content of cartilage before any visible damage has appeared.19PubMed Central. Articular cartilage in the knee: current MR imaging techniques and applications in clinical practice and research This early detection capability matters for symphyses and growth plates alike, since catching degeneration or injury before cartilage is structurally compromised opens a wider window for treatment.
Why Cartilage Repair Remains Difficult
The same properties that make cartilaginous joints effective, their avascular design, low cell density, and reliance on diffusion, also make them extremely hard to repair when damaged. Without a blood supply, the inflammatory and healing cascade that fixes most tissues never fully engages in cartilage. This is why a torn meniscus or a degenerated intervertebral disc can linger for years.
Tissue engineering was expected to solve this problem relatively early. Cartilage seemed like a straightforward target: it has only one cell type, no blood vessels, and a relatively simple structure. In practice, building replacement cartilage that matches the mechanical properties and durability of the original has proven far more challenging than anticipated. As of 2024, only one cell-based cartilage repair product is approved for marketing in the United States, and none are indicated for severe osteoarthritis or rheumatoid arthritis.20Nature Reviews Rheumatology. Recent advancements in cartilage tissue engineering innovation and translation Research into new cell sources, scaffold materials, and scaffold-free approaches continues to show promise, but the gap between laboratory success and clinical products available to patients remains substantial.21PubMed Central. The role of tissue engineering in articular cartilage repair and regeneration
The difficulty of cartilage repair underscores something about cartilaginous joints that is easy to overlook: they work remarkably well for decades under constant mechanical stress, but they were not built with a backup plan. The intervertebral discs absorb thousands of loading cycles a day for an entire lifetime. Growth plates coordinate millimeter-precise bone lengthening across years of childhood. The pubic symphysis remodels on demand during pregnancy and then reassembles itself. When these joints work, they are among the most elegant structures in the skeleton. When they fail, medicine is still catching up with how to fix them.