Vincent Garcia trains in martial arts as a part of his activities. However, after he developed turf toe and he started to undergo knee pain, Vincent’s performance was affected. Dr. Alex Jimenez, a doctor of chiropractic, helped treat Vincent Garcia’s knee pain along with turf toe, gradually restoring his overall health and well-being. Dr. Alex Jimenez has also helped treat a variety of other sport-related injuries. Chiropractic care utilized corrections and manipulations that were manual to carefully restore the original integrity of the backbone, allowing the human body to heal itself. Vincent Garcia highly recommends Dr. Alex Jimenez as the non-invasive pick for many different accidents and/or conditions, including several sports accidents, among other problems.
Chiro Treatment
We are blessed to present to you�El Paso�s Premier Wellness & Injury Care Clinic.
As El Paso�s Chiropractic Rehabilitation Clinic & Integrated Medicine Center,�we passionately are focused on treating patients after frustrating injuries and chronic pain syndromes. We focus on improving your ability through flexibility, mobility and agility programs tailored for all age groups and disabilities.
We want you to live a life that is fulfilled with more energy, positive attitude, better sleep, less pain, proper body weight and educated on how to maintain this way of life. I have made a life of taking care of every one of my patients.
I assure you, I will only accept the best for you�
If you have enjoyed this video and we have helped you in any way, please feel free to subscribe and recommend�us.
A baker�s cyst can cause pain, swelling, and limit the mobility in the affected knee. In some cases, complications can develop, causing severe problems with the leg. The problem with this type of cyst is that even if it is drained�if the underlying cause isn�t addressed, the cyst can return. Chiropractic can be used to treat baker�s cyst and help relieve the pain that it causes.
What is a Baker�s Cyst?
A Baker�s cyst, also known as a popliteal cyst, is a fluid-filled lump behind the knee. Synovial fluid builds up to form the benign cyst. It starts inside the knee but eventually extruded through the back part of the knee and forms a lump. Many times there is no discomfort or pain from the cyst, although there may be some pressure on the back side of the knee. The pain that is often associated with a Baker�s cyst is usually caused by the underlying problem that causes it. In some cases, a Baker�s cyst can become large enough to inhibit movement which can impact mobility.
What Causes a Baker�s Cyst?
A Baker�s cyst is caused by overproduction of synovial fluid in the knee that leads to the fluid building up and forming a lump. There are several reasons that this can happen, including knee joint inflammation and injury to the knee. A meniscal cartilage tear or another cartilage injury of the knee can cause a cyst to develop. Certain types of arthritis in the knee, such as osteoarthritis and rheumatoid arthritis can cause the excess fluid to accumulate. Knee arthritis, a common condition among older adults, can also cause the development of a Baker�s cyst.
What are the Potential Complications of Baker�s Cyst?
Sometimes the location or size of a Baker�s cyst can cause swelling in the back of the knee. The cyst itself can be as large as a golf ball. This can put pressure on the joint, making it difficult to bend the knee. This pressure can extend through the calf muscle. The patient may experience tenderness and pain after exercising.
In rare cases, a Baker�s cyst can burst, causing the synovial fluid to leak into the calf. This can cause swelling and knee pain that is sharp and can be intense. The patient may notice redness in the calf or experience the sensation of water running down the back of the calf area. Because symptoms of a burst Baker�s cyst can closely resemble a blood clot in the leg, the patient should seek immediate medical attention to rule out a more severe condition.
How is a Baker�s Cyst Treated?
Some no treatment for popliteal cysts and they go away on their own. If a form of arthritis is causing the cyst, treating that problem may resolve the cyst. The same goes for a cyst caused by an injury to the knee. Once the damage is fixed, the cyst typically resolves as well.
If the cyst does not go away or if it is problematic, causing intense pain or limits mobility, the patient may talk to their doctor about getting it drained. The doctor will use a needle, insert it directly into the cyst and drain the fluid. Steroid medications may also be prescribed to reduce inflammation and swelling. In sporadic cases, surgery may be required to remove the cyst.
Chiropractic for Baker�s Cyst
Many patients choose to seek chiropractic care to treat a Baker�s cyst because it is noninvasive and does not use medications that can have unpleasant or harmful side effects. The chiropractor will assess the cyst and conduct diagnostic tests to determine the cause. This will help them decide the best course of treatment. Sometimes an old injury can continue to put stress on the joint, causing a lingering tension pattern. A chiropractor can address this, bringing the body back into alignment, thus alleviating the problem. This will help reduce the pain, inflammation, and swelling. Chiropractic is also an effective treatment for arthritis so if that is the cause of the cyst; regular chiropractic care can help considerably. Often, once the underlying condition is corrected, the cyst goes away on its own.
Arthritis is characterized as the inflammation of one or multiple joints. The most common symptoms of arthritis include pain and discomfort, swelling, inflammation, and stiffness, among others. Arthritis may affect�any joint in the human body, however, it commonly develops in the knee. � Knee arthritis can make everyday�physical activities difficult. The most prevalent types of arthritis are osteoarthritis and rheumatoid arthritis, although there are well over 100 distinct forms of arthritis, affecting children and adults alike. While there is no cure for arthritis, many treatment approaches can help treat the symptoms of knee arthritis.
Anatomy of the Knee
� The knee is the largest and strongest joint in the human body. It is made up of the lower end of the thigh bone,�or femur, the top end of the shin bone, or tibia, and the kneecap, or patella. The ends of the three bones are covered with articular cartilage, a smooth, slippery structure which protects and cushions the bones when bending and straightening the knee.
� Two wedge-shaped parts of cartilage, known as the meniscus, function as shock absorbers between the bones of the knee to help cushion the joint and provide stability. The knee joint is also surrounded by a thin lining known as the synovial membrane. This membrane releases a fluid which lubricates the cartilage and also helps reduce friction in the knee. The significant kinds of arthritis that affect the knee�include osteoarthritis, rheumatoid arthritis, and post-traumatic arthritis.
Osteoarthritis
� Osteoarthritis is the most common type of arthritis which affects the knee joint. This form of arthritis is a degenerative, wear-and-tear health issue which occurs most commonly in people 50 years of age and older, however, it may also develop in younger people.
� In osteoarthritis, the cartilage in the knee joint gradually wears away. As the cartilage wears away, the distance between the bones decreases. This can result in bone rubbing and it can�create painful bone spurs. Osteoarthritis generally develops slowly but the pain may worsen over time.
Rheumatoid Arthritis
� Rheumatoid arthritis is a chronic health issue which affects multiple joints throughout the body, especially the knee joint. RA is also symmetrical, meaning it often affects the same joint on each side of the human body.
� In rheumatoid arthritis, the synovial membrane that covers the knee joint becomes inflamed and swollen, causing knee pain, discomfort, and stiffness. RA is an autoimmune disease, which means that the immune system attacks its own soft tissues. The immune system attacks healthy tissue,�including tendons, ligaments and cartilage, as well as softens the bone.
Post-traumatic Arthritis
� Posttraumatic arthritis is a form of arthritis that develops after damage or injury to the knee. By way of instance, the knee joint may be harmed by a broken bone, or fracture, and result in post-traumatic arthritis years after the initial injury. Meniscal tears and ligament injuries can cause additional wear-and-tear on the knee joint, which over time can lead to arthritis and other problems.
Symptoms of Knee Arthritis
� The most common symptoms of knee arthritis include pain and discomfort, inflammation, swelling, and stiffness. Although sudden onset is probable, the painful symptoms generally�develop gradually over time. Additional symptoms of knee arthritis can be recognized as follows:
The joint may become stiff and swollen, making it difficult to bend and straighten the knee.
Swelling and inflammation may be worse in the morning, or when sitting or resting.
Vigorous activity might cause the pain to flare up.
Loose fragments of cartilage and other soft tissue may interfere with the smooth motion of the joints, causing the knee to lock or stick through motion. It could also creak, click, snap or make a grinding sound, known as crepitus.
Pain can cause a sense of fatigue or buckling from the knee.
Many individuals with arthritis may also describe increased joint pain with rainy weather and climate changes.
Diagnosis for Knee Arthritis
� During the patient’s appointment for diagnosis of knee arthritis, the healthcare professional will talk about the symptoms and medical history, as well as conduct a physical examination. The doctor may also order imaging diagnostic tests, such as X-rays, MRI or blood tests for further diagnosis. During the physical examination, the doctor will search for:
Joint inflammation, swelling, warmth, or redness
Tenderness around the knee joint
Assortment of passive and active movement
Instability of the knee joint
Crepitus, the grating sensation inside the joint, with motion
Pain when weight is placed on the knee
Issues with gait, or manner of walking
Any signs of damage or injury to the muscles, tendons, and ligaments surrounding the knee joint
Involvement of additional joints (an indicator of rheumatoid arthritis)
Imaging Diagnostic Tests
X-rays. These imaging diagnostic tests produce images of compact structures, such as bones. They can help distinguish among various forms of arthritis. X-rays for knee arthritis may demonstrate a portion of the joint distance, changes in the bone as well as the formation of bone spurs, known as osteophytes.
Additional tests. Sometimes, magnetic resonance imaging, or MRI, scans, computed tomography, or CT,�scans, or bone scans are required to ascertain the condition of the bone and soft tissues of the knee.
Blood Tests
� Your doctor may also recommend blood tests to determine which type of arthritis you have. With some kinds of arthritis, such as rheumatoid arthritis, blood tests can help with the proper identification of the disease.
Although the knee joint is one of the strongest and largest joints in the human body, it is often prone to suffering damage or injury, resulting in a variety of conditions. In addition, however, other health issues, such as arthritis, can affect the knee joint. In network for most insurances of El Paso, TX, chiropractic care can help ease painful symptoms associated with knee arthritis, among other health issues. Dr. Alex Jimenez D.C., C.C.S.T. Insight
�
Treatment for Knee Arthritis
Non-surgical Treatment
� Non-surgical treatment approaches are often recommended before considering surgical treatment for knee arthritis. Healthcare professionals may recommend a variety of treatment options, including chiropractic care, physical therapy, and lifestyle modifications, among others.
� Lifestyle modifications. Some lifestyle modifications can help protect the knee joint and impede the progress of arthritis. Minimizing physical activities which aggravate the condition, will put less strain on the knee. Losing weight may also help lessen stress and pressure on the knee joint, resulting in less painful symptoms and increased function.
� Chiropractic care and physical therapy.�Chiropractic care utilizes full body chiropractic adjustments to carefully restore any spinal misalignments, or subluxations, which may�be causing symptoms, including arthritis. The doctor may also recommend physical therapy to create an individualized exercise and physical activity program for each patient’s needs.�Specific exercises will help increase range of motion and endurance, as well as help strengthen the muscles in the lower extremities.
� Assistive devices. Using assistive devices, such as a cane, shock-absorbing shoes or inserts, or a brace or knee sleeve, can decrease painful symptoms. A brace helps with function and stability, and may be particularly useful if the arthritis is based on one side of the knee. There are two types of braces that are often used for knee arthritis: A “unloader” brace shifts weight from the affected section of the knee, while a “support” brace helps support the entire knee load.
� Drugs and/or medications. Several types of medications are useful in treating arthritis of the knee. Since individuals respond differently to medications, your doctor will work closely with you to determine the medications and dosages which are safe and effective for you.
Surgical Treatment
� The healthcare professional may recommend surgical treatment if the patient’s knee arthritis causes severe disability and only if the problem isn’t relieved with non-surgical treatment. Like all surgeries, there are a few risks and complications with surgical treatment for knee arthritis. The�doctor will discuss the possible problems with the patient.
� Arthroscopy. During arthroscopy, physicians use instruments and small incisions to diagnose and treat knee joint problems. Arthroscopic surgery isn’t frequently used in the treatment of arthritis of the knee. In cases where osteoarthritis is accompanied with a degenerative meniscal tear, arthroscopic surgery may be wise to treat the torn meniscus.
� Cartilage grafting. Normal cartilage tissue may be taken from a tissue bank or through a different part of the knee to fill out a hole in the articular cartilage. This process is typically considered only for younger patients.
� Synovectomy. The lining damaged by rheumatoid arthritis is eliminated to reduce swelling and pain.
� Osteotomy. In a knee osteotomy, either the tibia (shinbone) or femur (thighbone) is cut then reshaped to relieve stress and pressure on the knee joint. Knee�osteotomy is utilized when early-stage osteoarthritis has damaged one facet of the knee joint. By changing the weight distribution, this can relieve and enhance the function of the knee.
� Total or partial knee replacement (arthroplasty).�The�doctor will remove the damaged bone and cartilage, then place new plastic or metal surfaces to restore the function of the knee�and its surrounding structures.
� Following any type of surgery for knee�arthritis will involve a period of recovery. Recovery time and rehabilitation will depend on the type of surgery performed. It’s essential to talk with your healthcare professional to determine the best treatment option for your�knee arthritis. The scope of our information is limited to chiropractic and spinal health issues. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at�915-850-0900�.
� Curated by Dr. Alex Jimenez �
�
Additional Topic Discussion: Relieving Knee Pain without Surgery
� Knee pain is a well-known symptom which can occur due to a variety of knee injuries and/or conditions, including�sports injuries. The knee is one of the most complex joints in the human body as it is made-up of the intersection of four bones, four ligaments, various tendons, two menisci, and cartilage. According to the American Academy of Family Physicians, the most common causes of knee pain include patellar subluxation, patellar tendinitis or jumper’s knee, and Osgood-Schlatter disease. Although knee pain is most likely to occur in people over 60 years old, knee pain can also occur in children and adolescents. Knee pain can be treated at home following the RICE methods, however, severe knee injuries may require immediate medical attention, including chiropractic care.
The knee is one of the most complex joints in the human body, consisting of the thigh bone, or femur, the shin bone, or tibia, and the kneecap, or patella, among other soft tissues. Tendons connect the bones to the muscles while ligaments connect the bones of the knee joint. Two wedge-shaped pieces of cartilage, known as the meniscus, provide stability to the knee joint. The purpose of the article below is to demonstrate as well as discuss the anatomy of the knee joint and its surrounding soft tissues.
Abstract
Context: Information regarding the structure, composition, and function of the knee menisci has been scattered across multiple sources and fields. This review contains a concise, detailed description of the knee menisci�including anatomy, etymology, phylogeny, ultrastructure and biochemistry, vascular anatomy and neuroanatomy, biomechanical function, maturation and aging, and imaging modalities.
Evidence Acquisition: A literature search was performed by a review of PubMed and OVID articles published from 1858 to 2011.
Results: This study highlights the structural, compositional, and functional characteristics of the menisci, which may be relevant to clinical presentations, diagnosis, and surgical repairs.
Conclusions: An understanding of the normal anatomy and biomechanics of the menisci is a necessary prerequisite to understanding the pathogenesis of disorders involving the knee.
Keywords:knee, meniscus, anatomy, function
Introduction
Once described as a functionless embryonic remnant,162 the menisci are now known to be vital for the normal function and long-term health of the knee joint.� The menisci increase stability for femorotibial articulation, distribute axial load, absorb shock, and provide lubrication and nutrition to the knee joint.4,91,152,153
Injuries to the menisci are recognized as a cause of significant musculoskeletal morbidity. The unique and complex structure of menisci makes treatment and repair challenging for the patient, surgeon, and physical therapist. Furthermore, long-term damage may lead to degenerative joint changes such as osteophyte formation, articular cartilage degeneration, joint space narrowing, and symptomatic osteoarthritis.36,45,92 Preservation of the menisci depends on maintaining their distinctive composition and organization.
Anatomy of Menisci
Meniscal Etymology
The word meniscus comes from the Greek word m?niskos, meaning �crescent,� diminutive of m?n?, meaning �moon.�
Meniscal Phylogeny and Comparative Anatomy
Hominids exhibit similar anatomic and functional characteristics, including a bicondylar distal femur, intra-articular cruciate ligaments, menisci, and asymmetrical collateral.40,66 These similar morphologic characteristics reflect a shared genetic lineage that can be traced back more than 300 million years.40,66,119
In the primate lineage leading to humans, hominids evolved to bipedal stance approximately 3 to 4 million years ago, and by 1.3 million years ago, the modern patellofemoral joint was established (with a longer lateral patellar facet and matching lateral femoral trochlea).164 Tardieu investigated the transition from occasional bipedalism to permanent bipedalism and observed that primates contain a medial and lateral fibrocartilaginous meniscus, with the medial meniscus being morphologically similar in all primates (crescent shaped with 2 tibial insertions).163 By contrast, the lateral meniscus was observed to be more variable in shape. Unique in Homo sapiens is the presence of 2 tibial insertions�1 anterior and 1 posterior�indicating a habitual practice of full extension movements of the knee joint during the stance and swing phases of bipedal walking.20,134,142,163,168
Embryology and Development
The characteristic shape of the lateral and medial menisci is attained between the 8th and 10th week of gestation.53,60 They arise from a condensation of the intermediate layer of mesenchymal tissue to form attachments to the surrounding joint capsule.31,87,110 The developing menisci are highly cellular and vascular, with the blood supply entering from the periphery and extending through the entire width of the menisci.31 As the fetus continues to develop, there is a gradual decrease in the cellularity of the menisci with a concomitant increase in the collagen content in a circumferential arrangement.30,31 Joint motion and the postnatal stress of weightbearing are important factors in determining the orientation of collagen fibers. By adulthood, only the peripheral 10% to 30% have a blood supply.12,31
Despite these histologic changes, the proportion of tibial plateau covered by the corresponding meniscus is relatively constant throughout fetal development, with the medial and lateral menisci covering approximately 60% and 80% of the surface areas, respectively.31
Gross Anatomy
Gross examination of the knee menisci reveals a smooth, lubricated tissue (Figure 1). They are crescent-shaped wedges of fibrocartilage located on the medial and lateral aspects of the knee joint (Figure 2A). The peripheral, vascular border (also known as the red zone) of each meniscus is thick, convex, and attached to the joint capsule. The innermost border (also known as the white zone) tapers to a thin free edge. The superior surfaces of menisci are concave, enabling effective articulation with their respective convex femoral condyles. The inferior surfaces are flat to accommodate the tibial plateau (Figure 1).28,175
Medial meniscus. The semicircular medial meniscus measures approximately 35 mm in diameter (anterior to posterior) and is significantly broader posteriorly than it is anteriorly.175 The anterior horn is attached to the tibia plateau near the intercondylar fossa anterior to the anterior cruciate ligament (ACL). There is significant variability in the attachment location of the anterior horn of the medial meniscus. The posterior horn is attached to the posterior intercondylar fossa of the tibia between the lateral meniscus and the posterior cruciate ligament (PCL; Figures 1 and and2B).2B). Johnson et al reexamined the tibial insertion sites of the menisci and their topographic relationships to surrounding anatomic landmarks of the knee.82 They found that the anterior and posterior horn insertion sites of the medial meniscus were larger than those of the lateral meniscus. The area of the anterior horn insertion site of the medial meniscus was the largest overall, measuring 61.4 mm2, whereas the posterior horn of the lateral meniscus was the smallest, at 28.5 mm2.82
The tibial portion of the capsular attachment is the coronary ligament. At its midpoint, the medial meniscus is more firmly attached to the femur through a condensation in the joint capsule known as the deep medial collateral ligament.175 The transverse, or �intermeniscal,� ligament is a fibrous band of tissue that connects the anterior horn of the medial meniscus to the anterior horn of the lateral meniscus (Figures 1 and and2A2A).
Lateral meniscus. The lateral meniscus is almost circular, with an approximately uniform width from anterior to posterior (Figures 1 and and2A).2A). It occupies a larger portion (~80%) of the articular surface than the medial meniscus (~60%) and is more mobile.10,31,165 Both horns of the lateral meniscus are attached to the tibia. The insertion of the anterior horn of the lateral meniscus lies anterior to the intercondylar eminence and adjacent to the broad attachment site of the ACL (Figure 2B).9,83 The posterior horn of the lateral meniscus inserts posterior to the lateral tibial spine and just anterior to the insertion of the posterior horn of the medial meniscus (Figure 2B).83 The lateral meniscus is loosely attached to the capsular ligament; however, these fibers do not attach to the lateral collateral ligament. The posterior horn of the lateral meniscus attaches to the inner aspect of the medial femoral condyle via the anterior and posterior meniscofemoral ligaments of Humphrey and Wrisberg, respectively, which originate near the origin of the PCL (Figures 1 and and22).75
Meniscofemoral ligaments. The literature reports significant inconsistencies in the presence and size of meniscofemoral ligaments of the lateral meniscus. There may be none, 1, 2, or 4.? When present, these accessory ligaments transverse from the posterior horn of the lateral meniscus to the lateral aspect of the medial femoral condyle. They insert immediately adjacent to the femoral attachment of the PCL (Figures 1 and and22).
In a series of studies, Harner et al measured the cross-sectional area of the ligaments and found that the meniscofemoral ligament averaged 20% of the size of the PCL (range, 7%-35%).69,70 However, the size of the insertional area alone without knowledge of the insertional angle or collagen density does not indicate their relative strength.115 The function of these ligaments remains unknown; they may pull the posterior horn of the lateral meniscus in an anterior direction to increase the congruity of the meniscotibial fossa and the lateral femoral condyle.75
Ultrastructure and Biochemistry
Extracellular Matrix
The meniscus is a dense extracellular matrix (ECM) composed primarily of water (72%) and collagen (22%), interposed with cells.9,55,56,77 Proteoglycans, noncollagenous proteins, and glycoproteins account for the remaining dry weight.� Meniscal cells synthesize and maintain the ECM, which determines the material properties of the tissue.
The cells of the menisci are referred to as fibrochondrocytes because they appear to be a mixture of fibroblasts and chondrocytes.111,177 The cells in the more superficial layer of the menisci are fusiform or spindle shaped (more fibroblastic), whereas the cells located deeper in the meniscus are ovoid or polygonal (more chondrocytic).55,56,178 Cell morphology does not differ between the peripheral and central locations in the menisci.56
Both cell types contain abundant endoplasmic reticulum and Golgi complex. Mitochondria are only occasionally visualized, suggesting that the major pathway for energy production of fibrochondrocytes in their avascular milieu is probably anaerobic glycolysis.112
Water
In normal, healthy menisci, tissue fluid represents 65% to 70% of the total weight. Most of the water is retained within the tissue in the solvent domains of proteoglycans. The water content of meniscal tissue is higher in the posterior areas than in the central or anterior areas; tissue samples from surface and deeper layers had similar contents.135
Large hydraulic pressures are required to overcome the drag of frictional resistance of forcing fluid flow through meniscal tissue. Thus, interactions between water and the matrix macromolecular framework significantly influence the viscoelastic properties of the tissue.
Collagens
Collagens are primarily responsible for the tensile strength of menisci; they contribute up to 75% of the dry weight of the ECM.77 The ECM is composed primarily of type I collagen (90% dry weight) with variable amounts of types II, III, V, and VI.43,44,80,112,181 The predominance of type I collagen distinguishes the fibrocartilage of menisci from articular (hyaline) cartilage. The collagens are heavily cross-linked by hydroxylpyridinium aldehydes.44
The collagen fiber arrangement is ideal for transferring a vertical compressive load into circumferential �hoop� stresses (Figure 3).57 Type I collagen fibers are oriented circumferentially in the deeper layers of the meniscus, parallel to the peripheral border. These fibers blend the ligamentous connections of the meniscal horns to the tibial articular surface (Figure 3).10,27,49,156 In the most superficial region of the menisci, the type I fibers are oriented in a more radial direction. Radially oriented �tie� fibers are also present in the deep zone and are interspersed or woven between the circumferential fibers to provide structural integrity (Figure 3).# There is lipid debris and calcified bodies in the ECM of human menisci.54 The calcified bodies contain long, slender crystals of phosphorous, calcium, and magnesium on electron-probe roentgenographic analysis.54 The function of these crystals in not completely understood, but it is believed that they may play a role in acute joint inflammation and destructive arthropathies.
Noncollagenous matrix proteins, such as fibronectin, contribute 8% to 13% of the organic dry weight. Fibronectin is involved in many cellular processes, including tissue repair, embryogenesis, blood clotting, and cell migration/adhesion. Elastin forms less than 0.6% of the meniscus dry weight; its ultrastructural localization is not clear. It likely interacts directly with collagen to provide resiliency to the tissue.**
Proteoglycans
Located within a fine meshwork of collagen fibrils, proteoglycans are large, negatively charged hydrophilic molecules, contributing 1% to 2% of dry weight.58 They are formed by a core protein with 1 or more covalently attached glycosaminoglycan chains (Figure 4).122 The size of these molecules is further increased by specific interaction with hyaluronic acid.67,72 The amount of proteoglycans in the meniscus is one-eighth that of articular cartilage,2,3 and there may be considerable variation depending on the site of the sample and the age of the patient.49
By virtue of their specialized structure, high fixed-charge density, and charge-charge repulsion forces, proteoglycans in the ECM are responsible for hydration and provide the tissue with a high capacity to resist compressive loads.� The glycosaminoglycan profile of the normal adult human meniscus consists of chondroitin-6-sulfate (40%), chondroitin-4-sulfate (10% to 20%), dermatan sulfate (20% to 30%), and keratin sulfate (15%; Figure 4).65,77,99,159 The highest glycosaminoglycan concentrations are found in the meniscal horns and the inner half of the menisci in the primary weightbearing areas.58,77
Aggrecan is the major proteoglycan found in the human menisci and is largely responsible for their viscoelastic compressive properties (Figure 5). Smaller proteoglycans, such as decorin, biglycan, and fibromodulin, are found in smaller amounts.124,151 Hexosamine contributes 1% to the dry weight of ECM.57,74 The precise functions of each of these small proteoglycans on the meniscus have yet to be fully elucidated.
Matrix Glycoproteins
Meniscal cartilage contains a range of matrix glycoproteins, the identities and functions of which have yet to be determined. Electrophoresis and subsequent staining of the polyacrylamide gels reveals bands with molecular weights varying from a few kilodaltons to more than 200 kDa.112 These matrix molecules include the link proteins that stabilize proteoglycan�hyaluronic acid aggregates and a 116-kDa protein of unknown function.46 This protein resides in the matrix in the form of disulfide-bonded complex of high molecular weight.46 Immunolocalization studies suggest that it is predominantly located around the collagen bundles in the interterritorial matrix.47
The adhesive glycoproteins constitute a subgroup of the matrix glycoproteins. These macromolecules are partly responsible for binding with other matrix molecules and/or cells. Such intermolecular adhesion molecules are therefore important components in the supramolecular organization of the extracellular molecules of the meniscus.150 Three molecules have been identified within the meniscus: type VI collagen, fibronectin, and thrombospondin.112,118,181
Vascular Anatomy
The meniscus is a relatively avascular structure with a limited peripheral blood supply. The medial, lateral, and middle geniculate arteries (which branch off the popliteal artery) provide the major vascularization to the inferior and superior aspects of each meniscus (Figure 5).9,12,33-35,148 The middle geniculate artery is a small posterior branch that perforates the oblique popliteal ligament at the posteromedial corner of the tibiofemoral joint. A premeniscal capillary network arising from the branches of these arteries originates within the synovial and capsular tissues of the knee along the periphery of the menisci. The peripheral 10% to 30% of the medial meniscus border and 10% to 25% of the lateral meniscus are relatively well vascularized, which has important implications for meniscus healing (Figure 6).12,33,68 Endoligamentous vessels from the anterior and posterior horns travel a short distance into the substance of the menisci and form terminal loops, providing a direct route for nourishment.33 The remaining portion of each meniscus (65% to 75%) receives nourishment from synovial fluid via diffusion or mechanical pumping (ie, joint motion).116,120
Bird and Sweet examined the menisci of animals and humans using scanning electron and light microscopy.23,24 They observed canal-like structures opening deep into the surface of the menisci. These canals may play a role in the transport of fluid within the meniscus and may carry nutrients from the synovial fluid and blood vessels to the avascular sections of the meniscus.23,24 However, further study is needed to elucidate the exact mechanism by which mechanical motion supplies nutrition to the avascular portion of the menisci.
Neuroanatomy
The knee joint is innervated by the posterior articular branch of the posterior tibial nerve and the terminal branches of the obturator and femoral nerves. The lateral portion of the capsule is innervated by the recurrent peroneal branch of the common peroneal nerve. These nerve fibers penetrate the capsule and follow the vascular supply to the peripheral portion of the menisci and the anterior and posterior horns, where most of the nerve fibers are concentrated.52,90 The outer third of the body of the meniscus is more densely innervated than the middle third.183,184 During extremes of flexion and extension of the knee, the meniscal horns are stressed, and the afferent input is likely greatest at these extreme positions.183,184
The mechanoreceptors within the menisci function as transducers, converting the physical stimulus of tension and compression into a specific electrical nerve impulse. Studies of human menisci have identified 3 morphologically distinct mechanoreceptors: Ruffini endings, Pacinian corpuscles, and Golgi tendon organs.�� Type I (Ruffini) mechanoreceptors are low threshold and slowly adapting to the changes in joint deformation and pressure. Type II (Pacinian) mechanoreceptors are low threshold and fast adapting to tension changes.�� Type III (Golgi) are high-threshold mechanoreceptors, which signal when the knee joint approaches the terminal range of motion and are associated with neuromuscular inhibition. These neural elements were found in greater concentration in the meniscal horns, particularly the posterior horn.
The asymmetrical components of the knee act in concert as a type of biological transmission that accepts, transfers, and dissipates loads along the femur, tibia, patella, and femur.41 Ligaments act as an adaptive linkage, with the menisci representing mobile bearings. Several studies have reported that various intra-articular components of the knee are sensate, capable of generating neurosensory signals that reach spinal, cerebellar, and higher central nervous system levels.?? It is believed that these neurosensory signals result in conscious perception and are important for normal knee joint function and maintenance of tissue homeostasis.42
The meniscus is cartilage which provides structural and functional integrity to the knee. The menisci are two pads of fibrocartilaginous tissue which spread out friction in the knee joint when it undergoes tension and torsion between the shin bone, or tibia, and the thigh bone, or femur. The understanding of the anatomy and biomechanics of the knee joint is essential towards the understanding of knee injuries and/or conditions. Dr. Alex Jimenez D.C., C.C.S.T. Insight
�
Biomechanical Function
The biomechanical function of the meniscus is a reflection of the gross and ultrastructural anatomy and of its relationship to the surrounding intra-articular and extra-articular structures. The menisci serve many important biomechanical functions. They contribute to load transmission,�� shock absorption,10,49,94,96,170 stability,51,100,101,109,155 nutrition,23,24,84,141 joint lubrication,102-104,141 and proprioception.5,15,81,88,115,147 They also serve to decrease contact stresses and increase contact area and congruity of the knee.91,172
Meniscal Kinematics
In a study on ligamentous function, Brantigan and Voshell reported the medial meniscus to move an average 2 mm, while the lateral meniscus was markedly more mobile with approximately 10 mm of anterior-posterior displacement during flexion.25 Similarly, DePalma reported that the medial meniscus undergoes 3 mm of anterior-posterior displacement, while the lateral meniscus moves 9 mm during flexion.37 In a study using 5 cadaveric knees, Thompson et al reported the mean medial excursion to be 5.1 mm (average of anterior and posterior horns) and the mean lateral excursion, 11.2 mm, along the tibial articular surface (Figure 7).165 The findings from these studies confirm a significant difference in segmental motion between the medial and lateral menisci. The anterior and posterior horn lateral meniscus ratio is smaller and indicates that the meniscus moves more as a single unit.165 Alternatively, the medial meniscus (as a whole) moves less than the lateral meniscus, displaying a greater anterior to posterior horn differential excursion. Thompson et al found that the area of least meniscal motion is the posterior medial corner, where the meniscus is constrained by its attachment to the tibial plateau by the meniscotibial portion of the posterior oblique ligament, which has been reported to be more prone to injury.143,165 A reduction in the motion of the posterior horn of the medial meniscus is a potential mechanism for meniscal tears, with a resultant �trapping� of the fibrocartilage between the femoral condyle and the tibial plateau during full flexion. The greater differential between anterior and posterior horn excursion may place the medial meniscus at a greater risk of injury.165
The differential of anterior horn to posterior horn motion allows the menisci to assume a decreasing radius with flexion, which correlates to the decreased radius of curvature of the posterior femoral condyles.165 This change of radius allows the meniscus to maintain contact with the articulating surface of both the femur and the tibia throughout flexion.
Load Transmission
The function of the menisci has been clinically inferred by the degenerative changes that accompany its removal. Fairbank described the increased incidence and predictable degenerative changes of the articular surfaces in completely meniscectomized knees.45 Since this early work, numerous studies have confirmed these findings and have further established the important role of the meniscus as a protective, load-bearing structure.
Weightbearing produces axial forces across the knee, which compress the menisci, resulting in �hoop� (circumferential) stresses.170 Hoop stresses are generated as axial forces and converted to tensile stresses along the circumferential collagen fibers of the meniscus (Figure 8). Firm attachments by the anterior and posterior insertional ligaments prevent the meniscus from extruding peripherally during load bearing.94 Studies by Seedhom and Hargreaves reported that 70% of the load in the lateral compartment and 50% of the load in the medial compartment is transmitted through the menisci.153 The menisci transmit 50% of compressive load through the posterior horns in extension, with 85% transmission at 90� flexion.172 Radin et al demonstrated that these loads are well distributed when the menisci are intact.137 However, removal of the medial meniscus results in a 50% to 70% reduction in femoral condyle contact area and a 100% increase in contact stress.4,50,91 Total lateral meniscectomy results in a 40% to 50% decrease in contact area and increases contact stress in the lateral component to 200% to 300% of normal.18,50,76,91 This significantly increases the load per unit area and may contribute to accelerated articular cartilage damage and degeneration.45,85
Shock Absorption
The menisci play a vital role in attenuating the intermittent shock waves generated by impulse loading of the knee with normal gait.94,96,153 Voloshin and Wosk showed that the normal knee has a shock-absorbing capacity about 20% higher than knees that have undergone meniscectomy.170 As the inability of a joint system to absorb shock has been implicated in the development of osteoarthritis, the meniscus would appear to play an important role in maintaining the health of the knee joint.138
Joint Stability
The geometric structure of the menisci provides an important role in maintaining joint congruity and stability.## The superior surface of each meniscus is concave, enabling effective articulation between the convex femoral condyles and flat tibial plateau. When the meniscus is intact, axial loading of the knee has a multidirectional stabilizing function, limiting excess motion in all directions.9
Markolf and colleagues have addressed the effect of meniscectomy on anterior-posterior and rotational knee laxity. Medial meniscectomy in the ACL-intact knee has little effect on anterior-posterior motion, but in the ACL-deficient knee, it results in an increase in anterior-posterior tibial translation of up to 58% at 90o of flexion.109 Shoemaker and Markolf demonstrated that the posterior horn of the medial meniscus is the most important structure resisting an anterior tibial force in the ACL-deficient knee.155 Allen et al showed that the resultant force in the medial meniscus of the ACL-deficient knee increased by 52% in full extension and by 197% at 60� of flexion under a 134-N anterior tibial load.7 The large changes in kinematics due to medial meniscectomy in the ACL-deficient knee confirm the important role of the medial meniscus in knee stability. Recently, Musahl et al reported that the lateral meniscus plays a role in anterior tibial translation during the pivot-shift maneuver.123
Joint Nutrition and Lubrication
The menisci may also play a role in the nutrition and lubrication of the knee joint. The mechanics of this lubrication remains unknown; the menisci may compress synovial fluid into the articular cartilage, which reduces frictional forces during weightbearing.13
There is a system of microcanals within the meniscus located close to the blood vessels, which communicates with the synovial cavity; these may provide fluid transport for nutrition and joint lubrication.23,24
Proprioception
The perception of joint motion and position (proprioception) is mediated by mechanoreceptors that transduce mechanical deformation into electric neural signals. Mechanoreceptors have been identified in the anterior and posterior horns of the menisci.*** Quick-adapting mechanoreceptors, such as Pacinian corpuscles, are thought to mediate the sensation of joint motion, and slow-adapting receptors, such as Ruffini endings and Golgi tendon organs, are believed to mediate the sensation of joint position.140 The identification of these neural elements (located mostly in the middle and outer third of the meniscus) indicates that the menisci are capable of detecting proprioceptive information in the knee joint, thus playing an important afferent role in the sensory feedback mechanism of the knee.61,88,90,158,169
Maturation and Aging of The Meniscus
The microanatomy of the meniscus is complex and certainly demonstrates senescent changes. With advancing age, the meniscus becomes stiffer, loses elasticity, and becomes yellow.78,95 Microscopically, there is a gradual loss of cellular elements with empty spaces and an increase in fibrous tissue in comparison with elastic tissue.74 These cystic areas can initiate a tear, and with a torsional force by the femoral condyle, the superficial layers of the meniscus may shear off from the deep layer at the interface of the cystic degenerative change, producing a horizontal cleavage tear. Shear between these layers may cause pain. The torn meniscus may directly injure the overlying articular cartilage.74,95
Ghosh and Taylor found that collagen concentration increased from birth to 30 years and remained constant until 80 years of age, after which a decline occurred.58 The noncollagenous matrix proteins showed the most profound changes, decreasing from 21.9% � 1.0% (dry weight) in neonates to 8.1% � 0.8% between the ages of 30 to 70 years.80 After 70 years of age, the noncollagenous matrix protein levels increased to 11.6% � 1.3%. Peters and Smillie observed an increase in hexosamine and uronic acid with age.131
McNicol and Roughley studied the variation of meniscal proteoglycans in aging113; small differences in extractability and hydrodynamic size were observed. The proportions of keratin sulfate relative to chondroitin-6-sulfate increased with aging.146
Petersen and Tillmann immunohistochemically investigated human menisci (ranging from 22 weeks of gestation to 80 years), observing the differentiation of blood vessels and lymphatics in 20 human cadavers. At the time of birth, nearly the entire meniscus was vascularized. In the second year of life, an avascular area developed in the inner circumference. In the second decade, blood vessels were present in the peripheral third. After 50 years of age, only the peripheral quarter of the meniscal base was vascularized. The dense connective tissue of the insertion was vascularized but not the fibrocartilage of the insertion. Blood vessels were accompanied by lymphatics in all areas.���
Arnoczky suggested that body weight and knee joint motion may eliminate blood vessels in the inner and middle aspects of the menisci.9 Nutrition of meniscal tissue occurs via perfusion from blood vessels and via diffusion from synovial fluid. A requirement for nutrition via diffusion is the intermittent loading and release on the articular surfaces, stressed by body weight and muscle forces.130 The mechanism is comparable with the nutrition of articular cartilage.22
Magnetic Resonance Imaging of The Meniscus
Magnetic resonance imaging (MRI) is a noninvasive diagnostic tool used in the evaluation, diagnosis, and monitoring of the menisci. MRI is widely accepted as the optimal imaging modality because of superior soft tissue contrast.
On cross-sectional MRI, the normal meniscus appears as a uniform low-signal (dark) triangular structure (Figure 9). A meniscal tear is identified by the presence of an increased intrameniscal signal that extends to the surface of this structure.
Several studies have evaluated the clinical utility of MRI for meniscal tears. In general, MRI is highly sensitive and specific for tears of the meniscus. The sensitivity of MRI in detecting meniscal tears ranges from 70% to 98%, and the specificity, from 74% to 98%.48,62,105,107,117 The MRI of 1014 patients before an arthroscopic examination had an accuracy of 89% for pathology of the medial meniscus and 88% for the lateral meniscus.48 A meta-analysis of 2000 patients with an MRI and arthroscopic examination found 88% sensitivity and 94% accuracy for meniscal tears.105,107
There have been discrepancies between MRI diagnoses and the pathology identified during arthroscopic examination.��� Justice and Quinn reported discrepancies in the diagnosis of 66 of the 561 patients (12%).86 In a study of 92 patients, discrepancies between the MRI and arthroscopic diagnoses were noted in 22 of the 349 (6%) cases.106 Miller conducted a single-blind prospective study comparing clinical examinations and MRI in 57 knee examinations.117 He found no significant difference in sensitivity between the clinical examination and MRI (80.7% and 73.7%, respectively). Shepard et al assessed the accuracy of MRI in detecting clinically significant lesions of the anterior horn of the meniscus in 947 consecutive knee MRI154 and found a 74% false-positive rate. Increased signal intensity in the anterior horn does not necessarily indicate a clinically significant lesion.154
Conclusions
The menisci of the knee joint are crescent-shaped wedges of fibrocartilage that provide increased stability to the femorotibial articulation, distribute axial load, absorb shock, and provide lubrication to the knee joint. Injuries to the menisci are recognized as a cause of significant musculoskeletal morbidity. Preservation of the menisci is highly dependent on maintaining its distinctive composition and organization.
In conclusion, the knee is the largest and most complex�joint in the human body. However, because the knee can commonly become damaged as a result of an injury and/or condition, it’s essential to understand the anatomy of the knee joint in order for patients to receive proper treatment.� The scope of our information is limited to chiropractic and spinal health issues. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at�915-850-0900�.
Curated by Dr. Alex Jimenez
Additional Topic Discussion: Relieving Knee Pain without Surgery
Knee pain is a well-known symptom which can occur due to a variety of knee injuries and/or conditions, including�sports injuries. The knee is one of the most complex joints in the human body as it is made-up of the intersection of four bones, four ligaments, various tendons, two menisci, and cartilage. According to the American Academy of Family Physicians, the most common causes of knee pain include patellar subluxation, patellar tendinitis or jumper’s knee, and Osgood-Schlatter disease. Although knee pain is most likely to occur in people over 60 years old, knee pain can also occur in children and adolescents. Knee pain can be treated at home following the RICE methods, however, severe knee injuries may require immediate medical attention, including chiropractic care.
1. Adams ME, Hukins DWL. The extracellular matrix of the meniscus. In: Mow VC, Arnoczky SP, Jackson DW, editors. eds. Knee Meniscus: Basic and Clinical Foundations. New York, NY: Raven Press; 1992:15-282016
2. Adams ME, McDevitt CA, Ho A, Muir H. Isolation and characterization of high-buoyant-density proteoglycans from semilunar menisci. J Bone Joint Surg Am. 1986;68:55-64 [PubMed]
3. Adams ME, Muir H. The glycosaminoglycans of canine menisci. Biochem J. 1981;197:385-389 [PMC free article][PubMed]
4. Ahmed AM, Burke DL. In-vitro measurement of static pressure distribution in synovial joints: part I. Tibial surface of the knee. J Biomech Eng. 1983;185:290-294 [PubMed]
5. Akgun U, Kogaoglu B, Orhan EK, Baslo MB, Karahan M. Possible reflex pathway between medial meniscus and semi-membranous muscle: an experimental study in rabbits. Knee Surg Sports Traumatol Arthrosc. 2008;16(9):809-814 [PubMed]
6. Alberts B, Johnson A, Lewis J, Raff M, Roberts K, Walter P. Molecular Biology of the Cell. 4th ed. Bethesda, MD: National Center for Biotechnology Information; 2002
7. Allen CR, Wong EK, Livesay GA, Sakane M, Fu FH, Woo SL. Importance of the medial meniscus in the anterior cruciate ligament-deficient knee. J Orthop Res. 2000;18(1):109-115 [PubMed]
8. Arnoczky SP. Building a meniscus: biologic considerations. Clin Orthop Relat Res. 1999;367S:244-253[PubMed]
9. Arnoczky SP. Gross and vascular anatomy of the meniscus and its role in meniscal healing, regeneration and remodeling. In: Mow VC, Arnoczky SP, Jackson DW, editors. , eds. Knee Meniscus: Basic and Clinical Foundations. New York, NY: Raven Press; 1992:1-14
10. Arnoczky SP, Adams ME, DeHaven KE, Eyre DR, Mow VC. The meniscus. In: Woo SL-Y, Buckwalter J, editors. , eds. Injury and Repair of Musculoskeletal Soft Tissues. Park Ridge, IL: American Academy of Orthopaedic Surgeons; 1987:487-537
11. Arnoczky SP, Warren RF. Anatomy of the cruciate ligaments. In: Feagin JA, editor. , ed. The Crucial Ligaments. New York, NY: Churchill Livingstone; 1988:179-195
12. Arnoczky SP, Warren RF. Microvasculature of the human meniscus. Am J Sports Med. 1982;10:90-95[PubMed]
13. Arnoczky SP, Warren RF, Spivak JM. Meniscal repair using exogenous fibrin clot: an experimental study in dogs. J Bone Joint Surg Am. 1988;70:1209-1217 [PubMed]
14. Aspden RM, Yarker YE, Hukins DWL. Collagen orientations in the meniscus of the knee joint. J Anat. 1985;140:371. [PMC free article][PubMed]
15. Assimakopoulos AP, Katonis PG, Agapitos MV, Exarchou EI. The innervations of the human meniscus. Clin Orthop Relat Res. 1992;275:232-236 [PubMed]
16. Atencia LJ, McDevitt CA, Nile WB, Sokoloff L. Cartilage content of an immature dog. Connect Tissue Res. 1989;18:235-242 [PubMed]
17. Athanasiou KA, Sanchez-Adams J. Engineering the Knee Meniscus. San Rafael, CA: Morgan & Claypool Publishers; 2009
18. Baratz ME, Fu FH, Mengato R. Meniscal tears: the effect of meniscectomy and of repair on the intraarticular contact areas and stress in the human knee. A preliminary report. Am J Sports Med. 1986;14:270-275 [PubMed]
19. Barrack RL, Skinner HB, Buckley SL. Proprioception in the anterior cruciate deficient knee. Am J Sports Med. 1989;17:1-6 [PubMed]
21. Beaupre A, Choukroun R, Guidouin R, Carneau R, Gerardin H. Knee menisci: correlation between microstructure and biomechanics. Clin Orthop Relat Res. 1986;208:72-75 [PubMed]
22. Benninghoff A. Form und Bau der Gelenkknorpel in ihren Beziehungen zur Funktion. Erste Mitteilung: Die modellierenden und formerhaltenden Faktoren des Knorpelreliefs. Z Anat Entwickl Gesch. 1925;76:4263
23. Bird MDT, Sweet MBE. Canals of the semilunar meniscus: brief report. J Bone Joint Surg Br. 1988;70:839. [PubMed]
24. Bird MDT, Sweet MBE. A system of canals in semilunar menisci. Ann Rheum Dis. 1987;46:670-673 [PMC free article][PubMed]
25. Brantigan OC, Voshell AF. The mechanics of the ligaments and menisci of the knee joint. J Bone Joint Surg Am. 1941;23:44-66
26. Brindle T, Nyland J, Johnson DL. The meniscus: review of basic principles with application to surgery and rehabilitation. J Athl Train. 2001;32(2):160-169 [PMC free article][PubMed]
27. Bullough PG, Munuera L, Murphy J, et al. The strength of the menisci of the knee as it relates to their fine structure. J Bone Joint Surg Br. 1979;52:564-570 [PubMed]
28. Bullough PG, Vosburgh F, Arnoczky SP, et al. The menisci of the knee. In: Insall JN, editor. , ed. Surgery of the Knee. New York, NY: Churchill Livingstone; 1984:135-149
29. Burr DB, Radin EL. Meniscal function and the importance of meniscal regeneration in preventing late medial compartment osteoarthrosis. Clin Orthop Relat Res. 1982;171:121-126 [PubMed]
30. Carney SL, Muir H. The structure and function of cartilage proteoglycans. Physiol Rev. 1988;68:858-910 [PubMed]
31. Clark CR, Ogden JA. Development of the menisci of the human knee joint. J Bone Joint Surg Am. 1983;65:530 [PubMed]
32. Clark FJ, Horsh KW, Bach SM, Larson GF. Contributions of cutaneous and joint receptors to static knee-position sense in man. J Neurophysiol. 1979;42:877-888 [PubMed]
33. Danzig L, Resnik D, Gonsalves M, Akeson WH. Blood supply to the normal and abnormal meniscus of the human knee. Clin Orthop Relat Res. 1983;172:271-276 [PubMed]
34. Davies D, Edwards D. The vascular and nerve supply of the human meniscus. Am R Coll Surg Engl. 1948;2:142-156
35. Day B, Mackenzie WG, Shim SS, Leung G. The vascular and nerve supply of the human meniscus. Arthroscopy. 1985;1:58-62 [PubMed]
36. DeHaven KE. Meniscectomy versus repair: clinical experience. In: Mow VC, Arnoczky SP, Jackson DW, editors. , eds. Knee Meniscus: Basic and Clinical Foundations. New York, NY: Raven Press; 1992:131-139
37. DePalma AF. Diseases of the Knee. Philadelphia, PA: JB Lippincott Co; 1954
38. De Smet AA, Graf BK. Meniscal tears missed on MR imaging: relationship to meniscal tear patterns and anterior cruciate ligament tears. AJR Am J Roentgenol. 1994;162:905-911 [PubMed]
39. De Smet AA, Norris MA, Yandow DR, et al. MR diagnosis of meniscal tears of the knee: importance of high signal in the meniscus that extends to the surface. AJR Am J Roentgenol. 1993;161:101-107[PubMed]
40. Dye SF. Functional morphologic features of the human knee: an evolutionary perspective. Clin Orthop Relat Res. 2003;410:19-24 [PubMed]
41. Dye SF. The knee as a biologic transmission with an envelope of function: a theory. Clin Orthop Relat Res. 1996;325:10-18 [PubMed]
42. Dye SF, Vaupel GL, Dye CC. Conscious neurosensory mapping of the internal structures of the human knee without intraarticular anesthesia. Am J Sports Med. 1998;26(6):773-777 [PubMed]
43. Eyre DR, Koob TJ, Chun LE. Biochemistry of the meniscus: unique profile of collagen types and site dependent variations in composition. Orthop Trans. 1983;8:56
44. Eyre DR, Wu JJ. Collagen of fibrocartilage: a distinctive molecular phenotype in bovine meniscus. FEBS Lett. 1983;158:265. [PubMed]
45. Fairbank TJ. Knee joint changes after meniscectomy. J Bone Joint Surg Br. 1948;30:664-670[PubMed]
46. Fife RS. Identification of the link proteins and a 116,000-dalton matrix protein in canine meniscus. Arch Biochem Biophys. 1985;240:682. [PubMed]
47. Fife RS, Hook GL, Brandt KD. Topographic localization of a 116,000 dalton protein in cartilage. J Histochem Cytochem. 1985;33:127. [PubMed]
48. Fischer SP, Fox JM, Del Pizzo W, et al. Accuracy of diagnoses from magnetic resonance imaging of the knee: a multi-center analysis of one thousand and fourteen patients. J Bone Joint Surg Am. 1991;73:2-10[PubMed]
49. Fithian DC, Kelly MA, Mow VC. Material properties and structure-function relationships in the menisci. Clin Orthop Relat Res. 1990;252:19-31 [PubMed]
50. Fukubayashi T, Kurosawa H. The contact area and pressure distribution pattern of the knee: a study of normal and osteoarthritic knee joints. Acta Orthop Scand. 1980;51:871-879 [PubMed]
51. Fukubayashi T, Torzilli PA, Sherman MF, Warren RF. An in vivo biomechanical analysis of anterior-posterior motion of the knee, tibial displacement rotation and torque. J Bone Joint Surg Am. 1982;64:258-264 [PubMed]
52. Gardner E. The innervations of the knee joint. Anat Rec. 1948;101:109-130 [PubMed]
53. Gardner E, O�Rahilly R. The early development of the knee joint in staged human embryos. J Anat. 1968;102:289-299 [PMC free article][PubMed]
54. Ghadially FN, LaLonde JMA. Intramatrical lipidic debris and calcified bodes in human semilunar cartilages. J Anat. 1981;132:481. [PMC free article][PubMed]
55. Ghadially FN, LaLonde JMA, Wedge JH. Ultrastructure of normal and torn menisci of the human knee joint. J Anat. 1983;136:773-791 [PMC free article][PubMed]
56. Ghadially FN, Thomas I, Yong N, LaLonde JMA. Ultrastructure of rabbit semilunar cartilage. J Anat. 1978;125:499. [PMC free article][PubMed]
57. Ghosh P, Ingman AM, Taylor TK. Variations in collagen, non-collagenous proteins, and hexosamine in menisci derived from osteoarthritic and rheumatoid arthritic knee joints. J Rheumatol. 1975;2:100-107[PubMed]
58. Ghosh P, Taylor TKF. The knee joint meniscus: a fibrocartilage of some distinction. Clin Orthop Relat Res. 1987;224:52-63 [PubMed]
59. Ghosh P, Taylor TKF, Pettit GD, Horsburgh BA, Bellenger CR. Effect of postoperative immobilization on the regrowth of knee joint semilunar cartilage: an experimental study. J Orthop Res. 1983;1:153.[PubMed]
60. Gray DJ, Gardner E. Pre-natal development of the human knee and superior tibial fibula joints. Am J Anat. 1950;86:235-288 [PubMed]
61. Gray JC. Neural and vascular anatomy of the menisci of the human knee. J Orthop Sports Phys Ther. 1999;29(1):23-30 [PubMed]
62. Gray SD, Kaplan PA, Dussault RG. Imaging of the knee: current status. Orthop Clin North Am. 1997;28:643-658 [PubMed]
63. Greis PE, Bardana DD, Holmstrom MC, Burks RT. Meniscal injury: I. Basic science and evaluation. J Am Acad Orthop Surg. 2002;10:168-176 [PubMed]
64. Gronblad M, Korkala O, Liesi P, Karaharju E. Innervation of synovial membrane and meniscus. Acta Orthop Scand. 1985;56:484-486 [PubMed]
65. Habuchi H, Yamagata T, Iwata H, Suzuki S. The occurrence of a wide variety of dermatan sulfate-chondroitin sulfate copolymers in fibrous cartilage. J Biol Chem. 1973;248:6019-6028 [PubMed]
67. Hardingham TE, Muir H. Binding of oligosaccharides of hyaluronic acid to proteoglycans. Biochem J. 1973;135 (4):905-908 [PMC free article][PubMed]
68. Harner CD, Janaushek MA, Kanamori A, Yagi AKM, Vogrin TM, Woo SL. Biomechanical analysis of a double-bundle posterior cruciate ligament reconstruction. Am J Sports Med. 2000;28:144-151 [PubMed]
69. Harner CD, Kusayama T, Carlin G, et al. Structural and mechanical properties of the human posterior cruciate ligament and meniscofemoral ligaments. In: Transactions of the 40th Annual Meeting of the Orthopaedic Research Society; 1992
70. Harner CD, Livesgay GA, Choi NY, et al. Evaluation of the sizes and shapes of the human anterior and posterior cruciate ligaments: a comparative study. Trans Orthop Res Soc. 1992;17:123
71. Hascall VC. Interaction of cartilage proteoglycans with hyaluronic acid. J Supramol Struct. 1977;7:101-120 [PubMed]
72. Hascall VC, Heineg�rd D. Aggregation of cartilage proteoglycans: I. The role of hyaluronic acid. J Biol Chem. 1974;249(13):4205-4256 [PubMed]
73. Heinegard D, Oldberg A. Structure and biology of cartilage and bone matrix noncollagenous macromolecules. FASEB J. 1989;3:2042-2051 [PubMed]
74. Helfet AJ. Osteoarthritis of the knee and its early arrest. Instr Course Lect. 1971;20:219-230
75. Heller L, Langman J. The meniscofemoral ligaments of the human knee. J Bone Joing Surg Br. 1964;46:307-313 [PubMed]
76. Henning CE, Lynch MA, Clark JR. Vascularity for healing of meniscal repairs. Arthroscopy. 1987;3:13-18 [PubMed]
77. Herwig J, Egner E, Buddecke E. Chemical changes of human knee joint menisci in various stages of degeneration. Ann Rheum Dis. 1984;43:635-640 [PMC free article][PubMed]
78. H�pker WW, Angres G, Klingel K, Komitowksi D, Schuchardt E. Changes of the elastin compartment in the human meniscus. Virchows Arch A Pathol Anat Histopathol. 1986;408:575-592 [PubMed]
79. Humphry GM. A Treatise on the Human Skeleton Including the Joints. Cambridge, UK: Macmillan; 1858:545-546
80. Ingman AM, Ghosh P, Taylor TKF. Variation of collagenous and non-collagenous proteins of human knee joint menisci with age and degeneration. Gerontologia. 1974;20:212-233 [PubMed]
81. Jerosch J, Prymka M, Castro WH. Proprioception of the knee joints with a lesion of the medial meniscus. Acta Orthop Belg. 1996;62(1):41-45 [PubMed]
82. Johnson DL, Swenson TD, Harner CD. Arthroscopic meniscal transplantation: anatomic and technical considerations. Presented at: Nineteenth Annual Meeting of the American Orthopaedic Society for Sports Medicine; July 12-14, 1993; Sun Valley, ID
83. Johnson DL, Swenson TM, Livesay GA, Aizawa H, Fu FH, Harner CD. Insertion-site anatomy of the human menisci: gross, arthroscopic, and topographical anatomy as a basis for meniscal transplantation. Arthroscopy. 1995;11:386-394 [PubMed]
84. Johnson RJ, Pope MH. Functional anatomy of the meniscus. In: Symposium on Reconstruction of the Knee of the American Academy of Orthopaedic Surgeons. St Louis, MO: Mosby; 1978:3
85. Jones RE, Smith EC, Reisch JS. Effects of medial meniscectomy in patients older than forty years. J Bone Joint Surg Am. 1978;60:783-786 [PubMed]
86. Justice WW, Quinn SF. Error patterns in the MR imaging evaluation of the menisci of the knee. Radiology. 1995;196:617-621 [PubMed]
87. Kaplan EB. The embryology of the menisci of the knee joint. Bull Hosp Joint Dis. 1955;6:111-124[PubMed]
88. Karahan M, Kocaoglu B, Cabukoglu C, Akgun U, Nuran R. Effect of partial medial meniscectomy on the proprioceptive function of the knee. Arch Orthop Trauma Surg. 2010;130:427-431 [PubMed]
89. Kempson GE, Tuke MA, Dingle JT, Barrett AJ, Horsfield PH. The effects of proteolytic enzymes on the mechanical properties of adult human articular cartilage. Biochim Biophys Acta. 1976;428(3):741-760[PubMed]
90. Kennedy JC, Alexander IJ, Hayes KC. Nerve supply of the human knee and its functional importance. Am J Sports Med. 1982;10:329-335 [PubMed]
91. Kettelkamp DB, Jacobs AW. Tibiofemoral contact area: determination and implications. J Bone Joint Surg Am. 1972;54:349-356 [PubMed]
92. King D. The function of the semilunar cartilages. J Bone Joint Surg Br. 1936;18:1069-1076
93. Kohn D, Moreno B. Meniscus insertion anatomy as a basis for meniscus replacement: a morphological cadaveric study. Arthroscopy. 1995;11:96-103 [PubMed]
94. Krause WR, Pope MH, Johnson RJ, Wilder DG. Mechanical changes in the knee after meniscectomy. J Bone Joint Surg Am. 1976;58:599-604 [PubMed]
95. Kulkarni VV, Chand K. Pathological anatomy of the aging meniscus. Acta Orthop Scand. 1975;46:135-140 [PubMed]
96. Kurosawa H, Fukubayashi T, Nakajima H. Load-bearing mode of the knee joint: physical behavior of the knee joint with or without menisci. Clin Orthop Relat Res. 1980;149:283-290 [PubMed]
97. LaPrade RF, Burnett QM, II, Veenstra MA, et al. The prevalence of abnormal magnetic resonance imaging findings in asymptomatic knees: with correlation of magnetic resonance imaging to arthroscopic finding in symptomatic knees. Am J Sports Med. 1994;22:739-745 [PubMed]
98. Last RJ. Some anatomical details of the knee joint. J Bone Joint Surg Br. 1948;30:368-688 [PubMed]
99. Lehtonen A, Viljanto J, K�rkk�inen J. The mucopolysaccharides of herniated human intervertebral discs and semilunar cartilages. Acta Chir Scand. 1967;133(4):303-306 [PubMed]
100. Levy IM, Torzilli PA, Warren RF. The effect of lateral meniscectomy on motion of the knee. J Bone Joint Surg Am. 1989;71:401-406 [PubMed]
101. Levy IM, Torzilli PA, Warren RF. The effect of medial meniscectomy on anterior-posterior motion of the knee. J Bone Joint Surg Am. 1982;64:883-888 [PubMed]
102. MacConaill MA. The function of intra-articular fibrocartilages with special reference to the knee and inferior radio-ulnar joints. J Anat. 1932;6:210-227 [PMC free article][PubMed]
103. MacConaill MA. The movements of bones and joints: III. The synovial fluid and its assistants. J Bone Joint Surg Br. 1950;32:244. [PubMed]
104. MacConaill MA. Studies in the mechanics of synovial joints: II. Displacements on articular surfaces and the significance of saddle joints. Ir J Med Sci. 1946;6:223-235 [PubMed]
105. Mackenzie R, Dixon AK, Keene GS, et al. Magnetic resonance imaging of the knee: assessment of effectiveness. Clin Radiol. 1996;41:245-250 [PubMed]
106. Mackenzie R, Keene GS, Lomas DJ, Dixon AK. Errors at knee magnetic resonance imaging: true or false?Br J Radiol. 1995;68:1045-1051 [PubMed]
107. Mackenzie R, Palmer CR, Lomas DJ, et al. Magnetic resonance imaging of the knee: diagnostic performance studies. Clin Radiol. 1996;51:251-257 [PubMed]
108. Markolf KL, Bargar WL, Shoemaker SC, Amstutz HC. The role of joint load in knee instability. J Bone Joint Surg Am. 1981;63:570-585 [PubMed]
109. Markolf KL, Mensch JS, Amstutz HC. Stiffness and laxity of the knee: the contributions of the supporting structures. J Bone Joint Surg Am. 1976;58:583-597 [PubMed]
110. McDermott LJ. Development of the human knee joint. Arch Surg. 1943;46:705-719
111. McDevitt CA, Miller RR, Sprindler KP. The cells and cell matrix interaction of the meniscus. In: Mow VC, Arnoczky SP, Jackson DW, editors. , eds. Knee Meniscus: Basic and Clinical Foundations. New York, NY: Raven Press; 1992:29-36
112. McDevitt CA, Webber RJ. Ultrastructure and biochemistry of meniscal cartilage. Clin Orthop Relat Res. 1990;252:8-18 [PubMed]
113. McNicol D, Roughley PJ. Extraction and characterization of proteoglycan from human meniscus. Biochem J. 1980;185:705. [PMC free article][PubMed]
114. Merkel KHH. The surface of human menisci and its aging alterations during age: a combined scanning and transmission electron microscopic examination (SEM, TEM). Arch Orthop Trauma Surg. 1980;97:185-191 [PubMed]
115. Messner K, Gao J. The menisci of the knee joint: anatomical and functional characteristics, and a rationale for clinical treatment. J Anat. 1998;193:161-178 [PMC free article][PubMed]
116. Meyers E, Zhu W, Mow V. Viscoelastic properties of articular cartilage and meniscus. In: Nimni M, editor. , ed. Collagen: Chemistry, Biology and Biotechnology. Boca Raton, FL: CRC; 1988
117. Miller GK. A prospective study comparing the accuracy of the clinical diagnosis of meniscal tear with magnetic resonance imaging and its effect on clinical outcome. Arthroscopy. 1996;12:406-413 [PubMed]
118. Miller GK, McDevitt CA. The presence of thrombospondin in ligament, meniscus and intervertebral disc. Glycoconjugate J. 1988;5:312
119. Mossman DJ, Sargeant WAS. The footprints of extinct animals. Sci Am. 1983;250:78-79
120. Mow V, Fithian D, Kelly M. Fundamentals of articular cartilage and meniscus biomechanics. In: Ewing JW, editor. , ed. Articular Cartilage and Knee Joint Function: Basic Science and Arthroscopy. New York, NY: Raven Press; 1989:1-18
121. Mow VC, Holmes MH, Lai WM. Fluid transport and mechanical properties or articular cartilage: a review. J Biomech. 1984;17:377. [PubMed]
122. Muir H. The structure and metabolism of mucopolysaccharides (glycosaminoglycans) and the problem of the mucopolysaccharidoses. Am J Med. 1969;47 (5):673-690 [PubMed]
123. Musahl V, Citak M, O�Loughlin PF, Choi D, Bedi A, Pearle AD. The effect of medial versus lateral meniscectomy on the stability of the anterior cruciate ligament-deficient knee. Am J Sports Med. 2010;38(8):1591-1597 [PubMed]
124. Nakano T, Dodd CM, Scott PG. Glycosaminoglycans and proteoglycans from different zones of the porcine knee meniscus. J Orthop Res. 1997;15:213-222 [PubMed]
125. Newton RA. Joint receptor contributions to reflective and kinaesthetic responses. Phys Ther. 1982;62:22-29 [PubMed]
126. O�Connor BL. The histological structure of the dog knee menisci with comments on its possible significance. Am J Anat. 1976;147:407-417 [PubMed]
127. O�Connor BL, McConnaughey JS. The structure and innervation of cat knee menisci, and their relation to a �sensory hypothesis� of meniscal function. Am J Anat. 1978;153:431-442 [PubMed]
128. Oretorp N, Gillquist J, Liljedahl S-O. Long term results of surgery for non-acute anteromedial rotatory instability of the knee. Acta Orthop Scand. 1979;50:329-336 [PubMed]
129. Pagnani MJ, Warren RF, Arnoczky SP, Wickiewicz TL. Anatomy of the knee. In: Nicholas JA, Hershman EB, editors. , eds. The Lower Extremity and Spine in Sports Medicine. 2nd ed. St Louis, MO: Mosby; 1995:581-614
130. Pauwels F. [Developmental effects of the functional adaptation of bone]. Anat Anz. 1976;139:213-220[PubMed]
131. Peters TJ, Smillie IS. Studies on the chemical composition of the menisci of the knee joint with special reference to the horizontal cleavage lesion. Clin Orthop Relat Res. 1972;86:245-252 [PubMed]
132. Petersen W, Tillmann B. Collagenous fibril texture of the human knee joint menisci. Anat Embryol (Berl). 1998;197:317-324 [PubMed]
133. Poynton AR, Javadpour SM, Finegan PJ, O�Brien M. The meniscofemoral ligaments of the knee. J Bone Joint Surg Br. 1997;79:327-330 [PubMed]
134. Preuschoft H, Tardieu C. Biomechanical reasons for divergent morphology of the knee joint and the distal epiphyseal suture in hominoids. Folia Primatol (Basel). 1996;66:82-92 [PubMed]
135. Proctor CS, Schmidt MB, Whipple RR, Kelly MA, Mow VC. Material properties of the normal medial bovine meniscus. J Orthop Res. 1989;7:771-782 [PubMed]
136. Proske U, Schaible H, Schmidt RF. Joint receptors and kinanesthesia. Exp Brain Res. 1988;72:219-224 [PubMed]
137. Radin EL, de Lamotte F, Maquet P. Role of the menisci in the distribution of stress in the knee. Clin Orthop Relat Res. 1984;185:290-294 [PubMed]
138. Radin EL, Rose RM. Role of subchondral bone in the initiation and progression of cartilage damage. Clin Orthop Relat Res. 1986;213:34-40 [PubMed]
139. Raszeja F. Untersuchungen Bber Entstehung und feinen Bau des Kniegelenkmeniskus. Bruns Beitr klin Chir. 1938;167:371-387
140. Reider B, Arcand MA, Diehl LH, et al. Proprioception of the knee before and after anterior cruciate ligament reconstruction. Arthroscopy. 2003;19(1):2-12 [PubMed]
141. Renstrom P, Johnson RJ. Anatomy and biomechanics of the menisci. Clin Sports Med. 1990;9:523-538 [PubMed]
142. Retterer E. De la forme et des connexions que presentment les fibro-cartilages du genou chez quelques singes d�Afrique. Cr Soc Biol. 1907;63:20-25
143. Ricklin P, Ruttimann A, Del Bouno MS. Diagnosis, Differential Diagnosis and Therapy. 2nd ed. Stuttgart, Germany: Verlag Georg Thieme; 1983
144. Rodkey WG. Basic biology of the meniscus and response to injury. In: Price CT, editor. , ed. Instructional Course Lectures 2000. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2000:189-193 [PubMed]
145. Rosenberg LC, Buckwalter JA, Coutts R, Hunziker E, Mow VC. Articular cartilage. In: Woo SLY, Buckwalter JA, editors. , eds. Injury and Repair of the Musculoskeletal Soft Tissues. Park Ridge, IL: American Academy of Orthopaedic Surgeon; 1988:401
146. Roughley PJ. Changes in cartilage proteoglycan structure during aging: origin and effects: a review. Agents Actions. 1986;518:19 [PubMed]
147. Saygi B, Yildirim Y, Berker N, Ofluoglu D, Karadag-Saygi E, Karahan M. Evaluation of neurosensory function of the medial meniscus in humans. Arthroscopy. 2005;21(12):1468-1472 [PubMed]
148. Scapinelli R. Studies on the vasculature of the human knee joint. Acta Anat. 1968;70:305-331[PubMed]
149. Schutte MJ, Dabezius EJ, Zimny ML, Happe LT. Neural anatomy of the human anterior cruciate ligament. J Bone Joint Surg Am. 1987;69:243-247 [PubMed]
150. Scott JE. Supramolecular organization of extracellular matrix glycosaminoglycans, in vitro and in the tissues. FASEB J. 1992;6:2639-2645 [PubMed]
151. Scott PG, Nakano T, Dodd CM. Isolation and characterization of small proteoglycans from different zones of the porcine knee meniscus. Biochim Biophys Acta. 1997;1336:254-262 [PubMed]
152. Seedhom BB. Loadbearing function of the menisci. Physiotherapy. 1976;62(7):223. [PubMed]
153. Seedhom BB, Hargreaves DJ. Transmission of the load in the knee joint with special reference to the role in the menisci: part II. Experimental results, discussion and conclusion. Eng Med. 1979;8:220-228
154. Shepard MF, Hunter DM, Davies MR, Shapiro MS, Seeger LL. The clinical significance of anterior horn meniscal tears diagnosed on magnetic resonance images. Am J Sports Med. 2002;30(2):189-192[PubMed]
155. Shoemaker SC, Markolf KL. The role of the meniscus in the anterior-posterior stability of the loaded anterior cruciate-deficient knee: effects of partial versus total excision. J Bone Joint Surg Am. 1986;68(1):71-79 [PubMed]
156. Skaags DL, Mow VC. Function of the radial tie fibers in the meniscus. Trans Orthop Res Soc. 1990;15:248
157. Skinner HB, Barrack RL. Joint position sense in the normal and pathologic knee joint. J Electromyogr Kinesiol. 1991;1(3):180-190 [PubMed]
159. Solheim K. Glycosaminoglycans, hydroxyproline, calcium, and phosphorus in healing fractures. Acta Univ Lund. 1965;28:1-22
160. Spilker RL, Donzelli PS. A biphasic finite element model of the meniscus for stress-strain analysis. In: Mow VC, Arnoczky SP, Jackson DW, editors. , eds. Knee Meniscus: Basic and Clinical Foundations. New York, NY: Raven Press; 1992:91-106
161. Spilker RL, Donzelli PS, Mow VC. A transversely isotropic biphasic finite element model of the meniscus. J Biomechanics. 1992;25:1027-1045 [PubMed]
162. Sutton JB. Ligaments: Their Nature and Morphology. 2nd ed. London: HK Lewis; 1897
163. Tardieu C. Ontogeny and phylogeny of femoral-tibial characters in humans and hominid fossils: functional influence and genetic determinism. Am J Phys Anthropol. 1999;110:365-377 [PubMed]
164. Tardieu C, Dupont JY. The origin of femoral trochlear dysplasia: comparative anatomy, evolution, and growth of the patellofemoral joint. Rev Chir Orthop Reparatrice Appar Mot. 2001;87:373-383 [PubMed]
165. Thompson WO, Thaete FL, Fu FH, Dye SF. Tibial meniscal dynamics using three-dimensional reconstruction of magnetic resonance imaging. Am J Sports Med. 1991;19:210-216 [PubMed]
166. Tissakht M, Ahmed AM. Tensile stress-strain characteristics of the human meniscal material. J Biomech. 1995;28:411-422 [PubMed]
167. Tobler T. Zur normalen und pathologischen Histologie des Kniegelenkmeniscus. Arch Klin Chir. 1933;177:483-495
168. Vallois H. Etude anatomique de l�articulation du genou chez les primates. Montpelier, France: L�Abeille; 1914
169. Verdonk R, Aagaard H. Function of the normal meniscus and consequences of the meniscal resection. Scand J Med Sci Sports. 1999;9(3):134-140 [PubMed]
170. Voloshin AS, Wosk J. Shock absorption of meniscectomized and painful knees: a comparative in vivo study. J Biomed Eng. 1983;5:157-161 [PubMed]
171. Wagner H-J. Die kollagenfaserarchitecktur der menisken des menschlichen kniegelenkes. Z Mikrosk Anat Forsch. 1976;90:302. [PubMed]
172. Walker PS, Erkman MJ. The role of the meniscus in force transmission across the knee. Clin Orthop Relat Res. 1975;109:184-192 [PubMed]
173. Wan ACT, Felle P. The menisco-femoral ligaments. Clin Anat. 1995;8:323-326 [PubMed]
174. Warren PJ, Olanlokun TK, Cobb AG, Bentley G. Proprioception after knee arthroplasty: the influence of prosthetic design. Clin Orthop Relat Res. 1993;297:182-187 [PubMed]
175. Warren RF, Arnoczky SP, Wickiewiez TL. Anatomy of the knee. In: Nicholas JA, Hershman EB, editors. , eds. The Lower Extremity and Spine in Sports Medicine. St Louis: Mosby; 1986:657-694
176. Watanabe AT, Carter BC, Teitelbaum GP, et al. Common pitfalls in magnetic resonance imaging of the knee. J Bone Joint Surg Am. 1989;71:857-862 [PubMed]
177. Webber RJ, Norby DP, Malemud CJ, Goldberg VM, Moskowitz RW. Characterization of newly synthesized proteoglycans from rabbit menisci in organ culture. Biochem J. 1984;221(3):875-884 [PMC free article][PubMed]
178. Webber RJ, York JL, Vanderschildren JL, Hough AJ. An organ culture model for assaying wound repair of the fibrocartilaginous knee joint meniscus. Am J Sports Med. 1989;17:393-400 [PubMed]
179. Wilson AS, Legg PG, McNeu JC. Studies on the innervations of the medial meniscus in the human knee joint. Anat Rec. 1969;165:485-492 [PubMed]
180. Wirth CJ. The meniscus: structure, morphology and function. Knee. 1996;3:57-58
181. Wu JJ, Eyre DR, Slayter HS. Type VI collagen of the intervertebral disc: biochemical and electron microscopic characterization of the native protein. Biochem J. 1987;248:373. [PMC free article][PubMed]
182. Yasui K. Three dimensional architecture of normal human menisci. J Jpn Ortho Assoc. 1978;52:391
183. Zimny ML. Mechanoreceptors in articular tissues. Am J Anat. 1988;64:883-888
184. Zimny ML, Albright DJ, Dabezies E. Mechanoreceptors in the human medial meniscus. Acta Anat. 1988;133:35-40 [PubMed]
185. Zivanovic S. Menisco-meniscal ligaments of the human knee joint. Anat Anz. 1974;145:35-42[PubMed]
When the weather warms, melting the snow and ice as it ushers in the newness of spring, people are drawn outdoors, and increased activity soon follows. Runners top the list, training for upcoming marathons and races, or to get faster and increase endurance.
While some runners won�t let anything stop them, be it rain, sleet, or snow, most will not venture outside or engage in more rigorous training until the environment is more pleasant. This increased activity, though, can increase a person�s risk of injury, especially if they have been mostly inactive during the winter months. The most prevalent injury is runner�s knee, an umbrella term used to describe a variety of knee injuries including patellofemoral tracking syndrome.
What is Patellar Tracking Disorder?
When the patella, or kneecap, does not remain in place as the leg straightens or bends, it is called patellofemoral tracking syndrome. Many people believe that the kneecap only moves up and down, but that is not accurate. The kneecap is very mobile, rotating and tilting so that there are a variety of contact points between the femur and patella. The most common way that this disorder presents is the kneecap extends too far to the outside of the leg. Less frequent is when the kneecap shifts to the inside. The result is pain (sometimes severe) and limited mobility.
Understanding the syndrome means understanding the mechanics of the knee joint. The thighbone (femur) and lower leg (tibia and fibula) are joined by the knee, a large, complex hinge. A groove runs along the front of the joint, where the thighbone ends. The patella sits in the groove and is held in place by a network on the sides by ligaments and at the top and bottom by tendons. The underside of the kneecap is a layer of cartilage that allows it to move easily, or glide, along with the groove. When there is a problem with any of the parts that make up the knee it can lead to patellofemoral tracking syndrome.
Causes of Patellofemoral Tracking Syndrome
While overuse of the knee is the blanket term that describes the cause of patellofemoral tracking syndrome, it is the result of a combination of several problems. These can include:
Leg ligaments, tendons, or muscles that are too loose or too tight
Structural problems with the knee bones
Weak thigh muscles
The continuous stress put on the knee, such as activities that use a twisting motion to the knee
Repetitive, high-stress activities like running
Repeated movements like squatting, knee bending, or jumping
Improper alignment of the knee bones
Trauma to the knee that forces the kneecap off track, usually to the outside area of the leg
People who are most likely to develop the syndrome are those who experience any of these problems in addition to playing sports or running. Obesity or being overweight, when combined with the above problems can also put a person at risk for the syndrome.
Chiropractic for Patellofemoral Tracking Syndrome
Many people have experienced relief from the pain of patellofemoral tracking syndrome by using chiropractic care. Chiropractic for patellofemoral tracking syndrome is a medication free, non-invasive treatment that quickly and effectively treats the pain and helps to restore mobility. This is usually done by bringing the body back into alignment and performing specific manipulations depending on the unique needs of the patient. Treatment may involve the foot, ankle, spine, and hip in addition to the knee.
The patient may also be advised to make specific dietary adjustments, take special, targeted supplements, and do specific exercises in addition to the chiropractic treatments. Stretching is often recommended, and Kinesio taping is also a standard therapy to aid healing. Chiropractic will not only return the body to its natural balance and alignment, but it will get it to a state where it can begin healing itself.
Sagittal Fluid Sensitive MR slice showing large synovial popliteal (Baker’s) cyst (above top image) and sizeable synovial effusion (above bottom image)
Note multiple patchy dark signal areas on both images, representing fibrinoid inflammatory deposits aka “rice bodies” a characteristic MRI feature of RA
Management Rheumatological Referral & DRM
Conservative management followed by operative care in complicated cases of tendon ruptures and joints dislocations
Supplemental reading:
Diagnosis and Management of Rheumatoid Arthritis – AAFP
Septic arthritis – d/t bacterial or fungal contamination of the joint. SA may cause rapid joint destruction and requires prompt Dx and antibiotic administration
Joints affected: large joints with rich blood supply (knee 50%>hips>shoulders).
Routs of Infection:
1) Hematogenous is m/c
2) Spread from an adjacent site
3) Direct implantation (e.g., trauma, iatrogenically)
Patients at risk: children, diabetics, immunocompromised, pre-existing joint damage/inflammation, e.g., RA, etc.
I.V. drug users are particularly at risk and also may contaminate atypical joints “the S joints” SIJ, SCJ, Symphysis pubis, ACJ, etc.
Clinically: may vary and depends on host immune response and bacterial virulence. May present with rapid onset or exacerbation of pre-existing joint pain, swelling, limitation of ROM. General signs of malaise, fever, fatigue and elevated ESR, CRP, Leucocytosis may be present.
N.B. Diabetics and immunocompromised may present with fewer manifestations and lack of fever d/t declining immune response
Dx: clinical, radiological and laboratory. Arthrocentesis may be necessary for culture, cell count and purulent synovial examination
Management: I.V. antibiotics
Imaging Dx: begins with radiography but in the early stage most likely will be unremarkable. MRI can be sensitive and help with early identification of joint effusion, bone edema, etc. US may be helpful in the superficial joints and children. US helps with needle guidance. Bone scintigraphy may be used occaisonally if MRI is contraindicated
Routes of Joint Contamination
1. Hematogenous (M/C)
2. Spread from the adjacent site
3. Direct inoculation
M/C organism-Staph aureus
N.B Gonococcal infection may be a top differential in some cases
IV drug users: Pseudomonas, candida
Sickle cell: Salmonella
Animal (cats/dogs) bites: Pasteurella
Occasionally fungal contamination may occur
Radiography
Initially non-specific ST/joint effusion, obscuration/distortion of fat planes. Because it takes 30% of compact and 50-75% trabecular bone to be destroyed before seen on x-rays, radiography is insensitive to some of the early changes. MR imaging is the preferred modality
If MRI is not available or contraindicated. Bone scintigraphy with Tc-99 MDT can help
In children, US preferred to avoid ionizing radiation. In children, US can be more sensitive than in adults due to lack of bone maturation
Radiographic Dx
Early findings are unrewarding. Early features may include joint widening d/t effusion. Soft tissue swelling and obscuration/displacement of fat planes
1-2 weeks: periarticular and adjacent osseous changes are manifesting as patchy demineralization, moth-eaten, permeating bone destruction, loss, and indistinctness of the epiphyseal “white cortical line” with an increase in soft tissue swelling. MRI may be helpful with early Dx.
Late features: complete joint destruction and ankyloses
N.B. Septic arthritis may progress rapidly within days and requires early I.V. antibiotic to prevent major joint destruction
T1 & T2 Knee MRI
T1 (above left) and T2 fat-sat sagittal knee MRI slices reveal loss of normal marrow signal on T1 and increase on T2 due to septic edema. Bone sequestrum d/t osteomyelitis progressing into septic arthritis is noted. Marked joint effusion with adjacent soft tissue edema is seen. Dx: OSM and septic arthritis
Imaging may help the Dx of the septic joint. However, the final Dx is based on Hx, physical examination, blood tests and most importantly synovial aspiration (arthrocentesis)
Synovial fluid should be sent for Gram staining, culture, glucose testing, leukocyte count, and differential determination
ESR/CRP may be elevated
Synovial fluid: WBC can be 50,000-60,000/ul, with 80% neutrophils with depleted glucose levels Gram stain: in 75% gram-positive cocci. Gram staining is less sensitive in gonococcal infection with only 25% of cultures +
In 9% of cases, blood cultures are the only source of pathogen identification and should be obtained before antibiotic treatment
Gout: MSU deposition in and around joints and soft tissues. Elevated levels of serum uric acid (UA) (>7mg/dL) caused by overproduction or under-excretion of uric acid
Once UA reached/exceeded 7mg/dL, it will deposit in the peripheral tissues. Primary gout: disturbed metabolism of nucleic acids and purines break down. Secondary gout: increased cell turnover: Psoriasis, leukemia, multiple myeloma, hemolysis, chemotherapy, etc.
Gout presents with 5-characteristic stages:
1)asymptomatic hyperuricemia (years/decades)
acute attacks of gouty arthritis (waxes and wanes and lasts for several years)
Interval phase between attacks
Chronic tophaceous gout
Gouty nephropathy
Clinical Presentation
Depends� on stages
Acute attacks: acute joint pain “first and the worst” even painful to light touch
DDx: septic joint (both may co-exist) bursitis etc.
Gouty arthritis typically presents as monoarthropathy
Chronic tophaceous stage: deposits in joints, ear pinna, ocular structures, and other regions. Nephrolithiasis etc. Men>women. Obesity, diet, and age >50-60.
Radiography: early attacks are unremarkable and may present as non-specific joint effusion
Chronic tophaceous gout radiography: punched out peri-articular, para-articular and intraosseous erosions with overhanging edges. A characteristic rim of sclerosis and internal calcification, soft tissue tophi. Target sites: lower extremity m/c
Rx: allopurinol, colchicine (esp. preventing acute episodes and maintenance)
Synovial Aspiration
Synovial aspiration with polarized microscopy reveal negatively birefringent needle-shaped MSU crystals with large inflammatory PMN presence. DDx: positively birefringent rhomboid-shaped CPPD crystals (above bottom right) seen in Pseudogout and CPPD
Large S.T.
Density and joint effusion punched out osseous erosion with overhanging margins, overall preservation of bone density, internal calcifications Dx: chronic tophaceous gout
MRI Gout Features
Erosions with overhanging margins, a low signal on T1 and high on T2 and fat-suppressed images. Peripheral contrast enhancement of tophaceous deposits d/t granulation tissue
Dx: final Dx; synovial aspiration and polarized microscopy
Pathology: da disease of the articular cartilage. Continuing mechanical stimulation follows by an initial increase in water and cartilage thickness. Gradual loss of proteoglycans and ground substance. Fissuring/splitting. Chondrocytes are damaged and release enzymes into the joint. Cystic progression and further cartilage loss. Subchondral bone is denuded and exposed to mechanical stresses. It becomes hypervascular forming osteophytes. Subchondral cysts and bone thickening/sclerosis develop.
Imaging plays a crucial role in Dx/grading and management
Clinically: pain on walking/rest, crepitus, swelling d/t synovitis, locking/catching d/t osseocartilaginous fragments and gradual functional loss. Knee OA typically presents as mono and oligoarthritis. DDx: morning pain/stiffness is >30-min DDx from inflammatory arthritis
Treatment: in mild to moderate cases-conservative care. Severe OA-total knee arthroplasty
Grade 4: severe JSN, large osteophytes, marked subchondral sclerosis and definite bony deformity
Typical report language will state:
Minor, mild, moderate or severe aka advanced arthrosis
Technique
Radiography: AP weight-bearing knees: note severe JSN of the medial compartment more severely with lateral knee compartment. Osteophytes and marked genu varum deformity and bone deformation
Typically medial femorotibial compartment is affected early and more severely
The patellofemoral compartment is also affected and best visualized on the lateral and Sunrise views
Impressions: severe tri-compartmental knee arthrosis
Recommendations: referral to the orthopedic surgeon
Moderate JSN
B/L AP weight-bearing view (above top image): Moderate JSN primarily of the medial femorotibial compartment. Osteophytosis, subchondral sclerosis and mild bone deformation (genu varum)
May present as asymptomatic chondrocalcinosis, CPPD arthropathy resembling DJD with pan predominance of large subchondral cysts. Often found as isolated PFJ DJD
Pseudogout with an acute attack of knee pain resembling gouty arthritis
Radiography is the 1st step and often reveals the Dx
Arthrocentesis with polarized microscopy may be helpful to DDx between CPPD and Gouty arthritis
Rheumatoid Arthritis
RA: an autoimmune systemic inflammatory disease that targets soft tissues of joints synovium, tendons/ligaments, bursae and extra-articular sites (e.g., eyes, lungs, cardiovascular system)
RA is the m/c inflammatory arthritis, 3% of women and 1% of men. Age: 30-50 F>M 3:1, but may develop at any age. True RA is uncommon in children and should not be confused with Juvenile Idiopathic Arthritis
RA most often affects small joints of the hands and feet as symmetrical arthritis (2nd 3rd MCP, 3rd PIPs, wrists & MTPs, sparing DIPs of fingers and toes)
Radiographically: RA presents with joint effusion leading to hyperemia and marginal erosions and periarticular osteoporosis. In the knee, the lateral compartment is affected more frequently leading to valgus deformity. Uniform aka concentric/symmetrical JSN affects all compartments and remains a key Dx clue
An absence of subchondral sclerosis and osteophytes. Popliteal cyst�(Baker’s cyst) may represent synovial pannus and inflammatory synovitis extending into the popliteal region that may rapture and extend into posterior leg compartment
N.B. Following initial RA joint destruction, it is not unusual to note superimposed 2nd OA
Radiography is the 1st step but early joint involvement may be undetectable by x-rays and can be helped by US and/or MRI.
Final Dx is based on Hx, clinical exam, labs, and radiology
Clinical pearls: patients with RA may present with a single knee being affected
Most patients are likely to have bilateral symmetrical hands/feet RA.
Cervical spine, particularly C1-2 is affected in 75-90% of cases throughout the course of the disease
N.B. Sudden exacerbation of joint pain in RA should not underestimate septic arthritis because patients with pre-existing RA are at higher risk of infectious arthritis. Joint aspiration may help with Dx.
Radiographic DDx
RA (above left) vs. OA (above right)
RA: concentric (uniform) joint space loss, lack of osteophytes and juxta-articular osteopenia.
Clinical Pearls: patients with RA may present radiographically with subchondral sclerosis d/t superimposed DJD. The latter feature should not be interpreted as OA but instead considered as secondary OA
AP Knee Radiograph
Note marked uniform JSN, juxta-articular osteopenia and subchondral cystic changes
Clinical Pearls: subcortical cysts in RA will characteristically lack sclerotic rim noted in OA-associated subcortical cysts.
MRI Sensitivity
MRI is very sensitive and may aid during early Dx of RA.
T2 fat-sat or STIR and T1 + C gad contrast fat-suppressed sequences may be included
MRI Dx of RA: synovial inflammation/effusion, synovial hyperplasia, and pannus formation decreased cartilage thickness, subchondral cysts, and bone erosions
MRI is very sensitive to reveal juxt-articular bone marrow edema, a precursor to erosions
Intra-articular fibrinoid fragments known as “Rice bodies” are characteristic MR sign of RA
Note: T2 fat-sat sagittal MRI revealing large inflammatory joint effusion and pannus synovial proliferation (above arrowheads). No evidence of radiographic or MRI bone erosions present. Dx: RA
STIR MR Slices
Note: STIR MR slices in the axial (above bottom image) and coronal planes (above top image) demonstrate extensive synovitis/effusion (above arrowheads) and multiple erosions in the medial and lateral tibial plateau (above arrows)
Additionally, scattered patchy areas of bone marrow edema are noted (above asterisks) such marrow edema changes are indicative and predictive of future osseous erosions.
Additional features: note thinning and destruction of joint cartilage
IFM's Find A Practitioner tool is the largest referral network in Functional Medicine, created to help patients locate Functional Medicine practitioners anywhere in the world. IFM Certified Practitioners are listed first in the search results, given their extensive education in Functional Medicine