Wednesday, June 27, 2012

What is cartilage?


Structure and Functions

Cartilage shapes the skeleton before bone formation begins in the embryo and persists in certain areas of the human skeleton during adulthood. It supports and protects body parts and acts as a shock absorber for the bones. Cartilage is a specialized nonvascular and nonlymphatic supporting tissue without a nerve supply containing cellular components, extracellular components, and water. The extracellular content consists of a dense matrix of collagen and elastin fibers and a proteoglycan-rich extracellular matrix (ECM). Chondrocytes are specialized cartilage cells. They produce the ECM, become embedded within it, and maintain their ECM under homeostatic conditions. In the adult, cartilage is a tough but flexible tissue present in the skeletal and respiratory system and the ear, where its main function is structural support. The thoracic skeleton has costal cartilages. In the respiratory system, cartilage supports airway shape and ensures its openness. Cartilage keeps the external ear open in order for sound waves to reach the internal ear canal.




There are three kinds of cartilage: hyaline cartilage, fibrocartilage, and elastic cartilage. Each type has different properties that perform a particular function at that unique site and dictate the type and depth of the stresses that it can withstand. The most prevalent of them is hyaline cartilage, which is strong and made of a shiny bluish-white translucent type II collagen. In joints, hyaline cartilage is the articular cartilage that covers the end bones, providing the smooth articular surface of joints and resilience by transferring loads applied to it. Hyaline cartilage prevents possible harmful stress impact to the bone and offers a low-friction bearing surface permitting free joint movement, which is essential for locomotion. It is found in the larynx, ear, nasal septum, and sternum and between the ribs. The nonarticular cartilage includes the elastic cartilage and fibrocartilage. Fibrocartilage contains type I collagen and is found in persistent stress areas such as the meniscus and intervertebral discs. The elastic cartilage includes a network of elastin fibers that gives great flexibility while enabling repeated bending to parts of the nose, ear, epiglottis, and trachea.


The interaction of water with the ECM gives cartilage its biomechanical properties, hence its cushioning function. The water content allows load-dependent deformation of the cartilage tissue while providing nutrition, facilitating lubrication, and producing a low-friction surface against other cartilage or bones.




Disorders and Diseases

Disruption to cartilage homeostasis—as a result of genetic disorders, inflammation, malignancy, or stressful biomechanics to the tissue—compromises this well-organized structure. Therefore, tissue damage might significantly affect a patient’s quality of life, since it is difficult to restore or duplicate cartilage after it has been weakened or worn away. The homeostatic mechanisms of cartilage are essential to sustain a healthy, balanced tissue when disease or injury occurs. Therefore, joint degeneration and pain takes place at the articular cartilage when homeostasis is broken. Breathing problems are present when cartilage of the airways is affected. Cosmetic, hearing, or smelling problems might arise if cartilage of the ear or nose are involved.


Some of the most common cartilage medical conditions are osteoarthritis, costochondritis, achondroplasia, spinal disk herniation, relapsing polychondritis, tumors, and articular cartilage injury. Most of these conditions may not emerge until later in life. Yet, it is possible for young athletes participating in high-demand sports such as basketball, football, or soccer to damage their cartilage and suffer from long-lasting cartilage injuries.


Osteoarthritis (OA) is the noninflammatory degeneration of the articular cartilage. Cartilage around bones becomes thin or completely worn out, producing a bone-to-bone joint, decreasing joint motion, and causing pain. OA is mainly a result of wear and tear, and its treatment might include lifestyle modification, patient education, physical therapy, exercise, or invasive surgery such as arthroplasty. Costochondritis, the inflammation of costal cartilages, causes chest pain. Its treatment includes anti-inflammatory medications, rest, or local heat or ice. Achondroplasia is a genetic disorder in which chondrocyte proliferation is reduced during childhood, causing dwarfism. Presently, there is no treatment for achondroplasia. Cartilage deterioration of the ears, nose, throat, joints, or rib cage is characteristic in relapsing polychondritis. Its etiology is not well known, but it might be an autoimmune disease, in which the body’s immune system targets and destroys its own cartilage tissues within the body. Immunosuppressants are used to treat this condition. During spinal disk herniation, cartilage malfunction causes an asymmetric compression within the intervertebral disk, producing a herniation of its soft content that compresses nearby nerves and results in back pain. Pain medications, rest, physical therapy, or weight control might alleviate symptoms. Surgery is considered only if there is neurological deficit. Tumors formed in cartilage can be either malignant (chondrosarcoma) or benign (chondroma). Surgery is the main treatment, but it is based on the location or severity of the cancer. Articular cartilage injury results either after one direct impact to the knee, from a series of minor injuries over time, or after a pivot on a bent knee causing a meniscus tear. Damage can be mild to severe, and treatment might be nonsurgical or surgical. Recommended conservative measures include exercises to develop muscle strength around the knee, weight loss, shock-absorbing insoles, or hyaluronic acid injections to enhance joint lubrication and reduce biomechanical abrasion.




Perspective and Prospects

The first recorded acknowledgment of cartilage has been traced to Aristotle in the fourth century BCE; in the second century BCE, the medical works of the famous Roman physician Galen briefly described cartilage. In 1543, Andreas Vesalius
included an influential chapter on cartilage on his anatomy book De humani corporis fabrica (On the workings of the human body). Two hundred years later, in 1743, Scottish anatomist and surgeon
William Hunter
stated that “an ulcerated cartilage is a troublesome disease that once destroyed, it is never recovered.”


In the first decade of the twenty-first century, despite novel therapies, medications treating symptoms associated with cartilage damage, or surgical interventions, Dr. Hunter’s 1743 statement still remains valid. No universal method or therapy has been discovered that has the ability to repair or induce new cartilage growth resembling native cartilage in structure and functional load bearing. The vascular phase of any bodily tissue repair mechanism is essential to achieve tissue healing, but cartilage is a nonvascular structure without a blood supply to promote the healing process. Therefore, the repair capacity of cartilage is very limited when it is injured. It is known that cartilage will be restored if direct mechanical injury to the matrix does not damage the cells and they are able to resynthesize new ECM. However, the biomechanical damage of chondrocytes and matrix from trauma will result in only some degree of repair dependent on age, size, and depth of injury or mechanical misalignment of the joint.


Established procedures that can improve clinical symptoms include lavage, shaving and debridement, or marrow stimulation techniques (abrasion arthroplasty and microfracture). A second group of procedures aimed to restore the cartilage surface comprises autologous chondrocyte implantation and osteochondral autograft/allograft transplantation. Knowledge about the cartilage matrix composition, such as the identification of molecular markers in synovial
fluid or serum, can be applied to track changes in cartilage metabolism and to evaluate cartilage damage. Other novel therapies integrate the latest molecular biology methodologies with tissue engineering within transplantation surgery, with the aim of achieving reconstruction of the integrity of the cartilage surface and thus allowing patients to live an unconstrained, pain-free life.




Bibliography


Benedek, T. G. “A History of the Understanding of Cartilage.” Osteoarthritis and Cartilage 14, no. 3 (March, 2006): 203–9.



Bhosale, Abhijit M., et al. “Articular Cartilage: Structure, Injuries, and Review of Management.” British Medical Bulletin 87 (August, 2008): 77–95.



Buchanan, W. W. “William Hunter (1718–1743).” Rheumatology (Oxford) 42, no. 10 (October, 2003): 1260–61.



Dam, Erik B., et al. “Identification of Progressors in Osteoarthritis by Combining Biochemical and MRI-Based Markers.” Arthritis Research and Therapy 11, no. 4 (July, 2009): R115.



Firestein, Gary S., et al., eds. Kelley’s Textbook of Rheumatology. 8th ed. Philadelphia: Elsevier, 2008.



Goldring, M. B., et al. “Cartilage Homeostasis in Health and Rheumatic Diseases.” Arthritis Research and Therapy 11, no. 3 (May, 2009): 224.



International Cartilage Repair Society. "What Is Cartilage?" International Cartilage Repair Society, 2013.



MedlinePlus. "Cartilage Disorders." MedlinePlus, June 7, 2013.



Samuels, J., et al. “Osteoarthritis: A Tale of Three Tissues.” Bulletin for the NYU Hospital for Joint Diseases 66, no. 3 (2008): 244–50.



Seibel, M. J., P. Robin Simon, and John P. Bilezikian, eds. Dynamics of Bone and Cartilage Metabolism. 2d ed. San Diego, Calif.: Academic Press, 2006.



Thorstensson, Carina A., et al. “Help-Seeking Behaviour Among People Living with Chronic Hip or Knee Pain in the Community.” BMC Musculoskeletal Disorders 10 (December, 2009): 153–63.



UCSF Medical Center. "Cartilage Repair." University of California San Francisco, 2013.

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