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An accessory navicular bone is an accessory bone of the foot that occasionally develops abnormally causing a plantar medial enlargement of the navicular. Type III: is the fused accessory navicular to the navicular resulting in large cornuate navicular.
Navicular (boat shaped) is an intermediate tarsal bone on the medial side of the foot.[2] It is located on the medial side of the foot, and articulates proximally with the talus. The presence of accessory navicular 2 or 3 is also a cause of PTT tendinopathy as the insertion of PTT on accessory navicular leads to its proximal insertion (dashed line).
People who have an accessory navicular often are unaware of the condition if it causes no problems.
Pain over the posterior tibialis tendon from a tendinitis and tightness of the tendo-achillis in long standing cases. Routine standing AP and lateral view are enough to look for accessory navicular but in some cases oblique view is also obtained in order to completely define the abnormality of navicular. MRI or CT is indicated (very rare) in order to exclude tumor, fracture of medial tubersity, bone marrow edema.
Recognition of the loss of structural integrity of the longitudinal arch is important because this component of the deformity will not be corrected by surgical treatment if required.
SURGICAL: Depending upon the severity the non operative or conservative treatment should be maintained for at least 4- 6 months before any surgical intervention.
SECOND is Kindler procedure.[5][6] In this the ossicle and navicular prominence is excised as in simple excision but along with the posterior tibial tendon advancement. After surgery 4 week short leg cast, well moulded into the arch with the foot plantigrade is applied. Occasionally, a limited fusion of the cuneiform metatarsal or talonavicular joints also was recommended. This will include use of therapeutic modalities which relieves pain include ultrasonic therapy, TENS, massage, ROM exercises and treatments to strengthen the intrinsic foot muscles and lateral thigh rotators muscles and decrease inflammation. Learn about the shoulder in this month's Physiopedia Plus learn topic with 5 chapters from textbooks such as Magee's Orthopedic Physical Assessment, 2014 & Donatelli's Physical therapy of the shoulder 2012. Figure 2:The axial proton density image with fat saturation shows loss of patellar articular cartilage focally at the median ridge and adjacent medial and lateral facets (long arrows). Figure 3:The sagittal proton density image with fat saturation, obtained near trochlear midline, illustrates the moderate (partial-thickness) articular cartilage loss, with subarticular bone marrow edema (arrow).
Figure 4:On coronal proton density image with fat saturation, mild (partial-thickness) articular cartilage loss is shown also in the medial compartment, femoral aspect (arrow). Osteoarthritis (OA) is a joint disorder that involves degeneration of articular cartilage, with limited inflammation manifested by synovitis, and with changes also at the subchondral bone.
In addition to being very common in humans, and having been identified in skeletal remains from thousands of years ago, OA is also frequent in other mammalian species.
Interestingly, high but not excessive level of activity does not predispose a normal joint to develop OA, but may be considered beneficial, considering that the lack of any vascularity within cartilage makes intermittent loading an important factor promoting cartilage metabolism. Figure 5:Medial compartment OA, with full-thickness articular cartilage loss at both femoral and tibial aspects, exposing the pink vascularized underlying bone (arrow). The central feature of osteoarthritis, breakdown of hyaline articular cartilage, shows a focal involvement usually at the region of highest concentration of transmitted force (5a).
Up to 90% of forces across the knee joint are routinely absorbed by active mechanisms when the knee flexes, mainly through opposing muscles distributing the impact over time and over surface4. Figure 6:This 3D graphic representation demonstrates the densely packed large proteoglycan aggregates "trapped" between the bundles of collagen, both produced by the chondrocytes. When evaluating the MR imaging features of OA, it is beneficial to have a conceptual understanding of the basic components, architecture, and physiology of articular (hyaline) cartilage and adjacent tissues (6a). The aching joint pain of OA is characteristically worsened by weight-bearing activity and relieved by rest.
Just as with MRI findings of intervertebral disc herniations and with meniscal tears at the knee, not all OA lesions detected by MR imaging are associated with clinical symptoms. Extensive literature exists regarding ongoing efforts to develop MR sequences and imaging methods specifically to further optimize cartilage evaluation, with the aim of improving clinical evaluation, as well as to provide replicable and detailed information for use in longitudinal follow-up research studies of the effects of novel surgical or pharmacological therapies8,9. Artifacts influence the MR image of articular cartilage, and need to be recognized to avoid interpretation errors. Figure 7:This sagittal T1-weighted image of normal articular cartilage demonstrates the chemical shift artifact, with subtle mismapping in the x-axis of this image for signal from fat relative to signal from water, with fat shifted slightly to the right on this image, making the cortex next to cartilage at the trochlea (to the left) look artifactually thicker (long arrow), and the cortex posteriorly (to the right) on both the lateral femoral condyle and the patella look artifactually thinner (arrowheads). MRI features characteristic of OA include focal loss of articular (hyaline) cartilage, osteophytes, subchondral marrow lesions, and joint effusion. Figure 9:Images illustrating articular cartilage fissuring (9a), surface fraying and mild loss (9b), moderate loss (partial-thickness) (9c), and severe loss (full-thickness) (9d). Figure 10:A proton density axial image shows a delamination injury (arrow) to cartilage at the cartilage-bone interface at the medial patellar facet, after trauma to the knee.
Cartilage fissuring is characteristically seen on MRI images as linear defects with high signal perpendicular to the cartilage surface, with the high signal attributed to fluid within the fissure or to fluid imbibition in the cartilage along the fissure.
Figure 11:Sagittal proton density image with fat saturation demonstrates a linear low-signal abnormality at the patellar median ridge (11a, arrow), which was seen also on coronal and axial images (not shown), and which was on subsequent arthroscopy shown to represent a cartilage fissure. Subarticular bone marrow lesions: A large number of clinical studies now support the notion that the presence of a subarticular bone marrow lesion makes an OA lesion of cartilage more likely to be associated with the clinical finding of pain. Figure 12:Sagittal T1-weighted (12a) and STIR (12b) images demonstrate well-defined subchondral bone marrow lesions in OA with subchondral cysts and marrow edema at the patellofemoral compartment (arrows), severe (full-thickness) articular cartilage loss, and osteophyte formation.
Figure 13:Sagittal T1-weighted (13a) and STIR (13b) images show a spectrum of less-well defined subarticular marrow lesions in OA, with replacement of marrow fat signal with minimal edema and hemispheric configuration at the posterior femur (arrowhead), mainly low signal at the tibial subchondral lesion (short arrow), and mild bone marrow edema at the trochlear and distal femoral locations (long arrows). Osteophytes: These fibro-cartilage-capped bony outgrowths appear mainly at articular margins in OA, are commonly but not always present in OA, and when present can vary in size between locations and individuals. Figure 14:Coronal T1-weighted image demonstrating marginal osteophytes (arrows) in a patient without articular cartilage loss at the medial and lateral compartments.
Joint effusion: One of the features in MRI studies of OA that has shown a positive correlation with the presence of symptoms is a joint effusion. Meniscal tears, especially extrusion of the meniscus (15a), have shown a strong association with progression of symptomatic OA of the knee9,12,20.
Figure 15:A coronal proton density image with fat saturation in a patient with OA of the medial compartment demonstrates severe loss of femoral articular cartilage (arrow). Terminology for cartilage defects on MR images: Cartilage loss on MR images is often described differently by different radiologists, reflecting a lack of an accepted and easy to use terminology or grading scheme. Trauma: Acute trauma can cause osteochondral injury with features very similar to OA, with focal cartilage loss and sometimes, but not always, also subarticular bone marrow edema. Figure 16:On a sagittal proton density image with fat saturation, obtained after acute injury to the knee in a 14 year-old male, a full-thickness articular cartilage defect 28 mm in length at the lateral femoral condyle is seen to have well-defined angular margins (arrows), with associated subarticular marrow edema. Rheumatoid arthritis: A principally different type of arthritis, erosive inflammatory, RA is associated with bony erosions located at the peripheral bare area of a joint, with bone marrow edema at the erosion if there is active inflammation, or without bone marrow edema if not active. Osteonecrosis: At an earlier stage, osteonecrosis of the knee can be seen as a subarticular bone marrow lesion with normal overlying articular cartilage. Insufficiency fracture of the femoral condyles: A subcortical insufficiency fracture of the medial or lateral femoral condyle or tibial plateau presents as a low signal fracture line immediately deep to the subchondral cortex, with associated often intense bone marrow edema, with intact subchondral cortex and articular cartilage (17a,17b). Figure 17:Coronal (17a) and sagittal (17b) proton density images with fat saturation show subarticular bone marrow edema at the medial tibial plateau, with a low signal insufficiency fracture line (arrow). Traditional OA therapies have consisted of analgesics as needed, exercise programs and physical therapy, sometimes the use of braces, and ergonomic or life style changes; there may be a need for surgery with correction of joint instability or malalignment, and possibly later with prosthetic replacement, especially at weight-bearing joints. Not all cartilage lesions are indications for surgery, but smaller lesions in younger symptomatic individuals may benefit from open surgical drilling or microfracture (arthroscopic use of a pick), both aiming to breach the subchondral cortex at a cartilage lesion reaching into vascularized subchondral bone, thereby causing clot formation and within a few weeks leading to filling of the defect with cartilage.
3 Patellofemoral osteoarthritis coexistent with tibiofemoral osteoarthritis in a meniscectomy population. 10 Short TE MR microscopy: Accurate measurement and zonal differentiation of normal hyaline cartilage. 11 Is intra-articular pathology associated with MCL edema on MR imaging of the non-traumatic knee? 13 Osteoarthritis: MR imaging findings in different stages of disease and correlation with clinical findings.
14 The cartilage black line sign: an unexpected MRI appearance of deep cartilage fissuring in three patients.
15 Osteoarthritis of the knee: correlation of subchondral MR signal abnormalities with histopathologic and radiographic features. 16 Bone marrow edema pattern in osteoarthritic knees: correlation between MR imaging and histologic findings. 17 Bone marrow lesions in people with knee osteoarthritis predict progression of disease and joint replacement: a longitudinal study. 20 Meniscal tear and extrusion are strongly associated with progression of symptomatic knee osteoarthritis as assessed by quantitative MRI.


23 Protective effects of licofelone versus naproxen on cartilage loss in knee osteoarthritis: a first multicentre clinical trial using quantitative MRI. A bone bruise is a traumatic injury one sustains from a forceful impact during sports, accidents or a direct hit. This image (L) shows a knee bone that has been injured, and beside it is a longitudinal cut of the bone which shows the medullary part of the bone (red) that exhibits some broken bone fibers that are bleeding. A bone bruise commonly occurs in the knee bone, involving the long bone of the thigh or femur, but it can also occur in other parts of the body such as the wrist, heel, foot, or hipbone. Depending on the area of bone involvement, there are three kinds of bone bruises, which include a subperiosteal hematoma, an interosseous bruise, and a subchondral bruise.
Subperiosteal hematoma - A bone has a thin covering called the periosteum, and a direct force can cause an injury with bleeding beneath this covering, resulting in a subperiosteal hematoma. Interosseous bruise - On the other hand, high compressive forces that are repetitively inflicted on a bone can cause bleeding inside the bone where the marrow is located, causing a bone bruise called interosseous bruising. Subchondral bruise - Finally, there is the subchondral bruise which occurs between a cartilage and the bone beneath it, causing the cartilage to separate from the bone with bleeding in between. A bone bruise usually results from either a direct and sudden force or from repetitive compressive forces that are not strong enough to break or fracture a bone. Sports injuries - Bone bruises are a common type of sports injuries, especially in those which involve a lot of falling or getting into hard contact with objects or other players. Twisting injuries - This can result in sprained ankles or knees, and these are usually accompanied by bone bruises.
High velocity trauma to a bone - In general, any type of direct impact or high velocity trauma to a bone brought about by an incident such as a car accident, a high fall, or a blunt force can result in a hematoma, a contusion, or a bruise to the bone affected.
A bone bruise may cause minimal damage to a bone which may be detected with magnetic resonance imaging (MRI) but not by plain x-rays. After a traumatic injury, it is best to rule out a fracture by consulting a doctor who may request tests to be done.
Immediately apply an icepack or ice wrapped in thin cloth over the injured area to prevent excessive swelling and pain. One can also take anti-inflammatory medications to reduce severe inflammation and pain, which can last for more than a few weeks to a month. Experts also advise against using tobacco or nicotine, which can delay the healing process, since they constrict blood vessels, thus reducing blood flow to the area. The accssory navicular bone presents as a sesamoid in the posterior tibial tendon, in articulation with the navicular[1] or as an enlargment of the navicular. Here by the leverage of malleolus on the PTT is reduced and therefore stress on the tendon increase. Bilateral films may be indicated as there occurs high incidence of symmetrical abnormalities. Posterior tibial tendon is split and advanced along the medial side of foot to provide support to longitudinal arch. Often is the accessory navicular bone linked to Posterior tibial dysfunction to a pes planus. Patients with Type II accessory navicular are at the risk for disruption either from traction injury or shear forces in the region and and mostly the onset is insidious or post trauma.
F., Voutsinass, ‘Surgical treatment of the symptomatic accessory navicular’, The Journal of Bone and Joint Surgery, 1984, vol. Physiopedia is not a substitute for professional advice or expert medical services from a qualified healthcare provider. The vague region of signal loss at the lateral tibial plateau articular cartilage (arrowhead) is artifactual. It is estimated that as many as half of all those who have osteoarthritic joint changes, by imaging or clinical exam, are not symptomatic or have minimal symptoms.
Studies have shown that long distance middle aged and older runners develop OA with similar but not higher incidence as in the general population6.
Note the slightly yellowish white appearance of the normal adjacent cartilage (asterisk), and the normal cartilage at the lateral femoral condyle and trochlea. Diffuse and smooth loss of cartilage throughout a joint is not characteristic of OA; indeed a cartilage biopsy taken a short distance from a full-thickness lesion may be histologically normal.
In addition, much of articular impact is absorbed by the trabecular bone immediately deep to the cartilage4. In the background note the organization of collagen fibers, with an overall "upside-down U" configuration (Benninghoff's arcades) leading to parallel fibers along the main articular force vector at the deep regions of cartilage, while at the joint surface the fibers are parallel to the surface.
Cartilage is a highly specialized tissue, one of the very few avascular and aneural tissues in the body.
Also common is joint stiffness which is usually worse in the morning, and mild edema and tenderness. Ongoing symptomatology may be absent even when advanced changes of OA are present on imaging exams. Chemical shift artifact, related to mismapping in the frequency-encoded axis at junctions between tissues with fat and water, such as junction of bone marrow and cartilage (due to its high water content), makes the cortex look artifactually thick or thin (7a) on images without fat saturation. The normal ratio of thickness of subchondral bone to articular cartilage is approximately 1:6. Frequently seen with OA and with a probable association are meniscal tears, especially meniscal extrusion, and periligamentous edema at the MCL11. Fissuring (9a) represents disruption at right angle to the cartilage surface, and may extend to partial (arrow) or full thickness of cartilage. The MRI finding of low-signal fissuring (11a,11b) at the patella and midline trochlea, with short well-defined linear signal abnormalities seen on images in more than one plane, has recently been shown to correspond to arthroscopically or arthrographically verified fissures14. An axial proton density image shows similar linear low signal extending from the cartilage surface at the midline trochlea (11b, arrow), compatible with a fissure. While the well-known radiographic feature of subarticular sclerosis can occasionally be seen as low signal on MRI images (9d), the vast majority of subarticular bone marrow lesions in OA do not have low but instead high, or mixed intermediate and high, signal (2a,3a,12a,12b,13a,13b). Osteophytes may form very early or later in OA, and may be a source of pain and loss of function, in the knee specifically related to limitation of joint mobility, but may also be present without causing symptoms, and may even have positive effects by increasing the joint contact surface (12a,12b,14a)17. The incidence of meniscal tear found on MRI examinations in patients with symptomatic OA has been reported in different studies at 52-92%, and it has been found that in advanced OA there are essentially always severe meniscal lesions such as complex tears with deformity or severe destruction13.
The grading schemes created for research evaluations are not always suitable for clinical work. Symptoms are aggravated by either activity (especially walking down stairs) or by prolonged sitting, and are associated with the arthroscopic finding of softened articular cartilage at the patellar facets. If the cartilage defect has well-defined right angle margins (16a), with marrow edema deep to the defect, this suggests a traumatic etiology, and other joint injuries may be present as well.
A corresponding size intra-articular body was present nearby, along midline trochlea (not shown).
RA does not cause osteophyte formation, but is associated with synovitis and often severe synovial thickening (pannus formation).
Surface fraying and mild loss of articular cartilage is also present, compatible with pre-existing mild OA, and there is periligamentous edema at the MCL. However, after maturation this cartilage consists mainly of fibrocartilage with less ability to hold up to stresses over time.
The use of oral glucosamine and chondroitin sulphate, substances primarily derived from shellfish and available as dietary supplements, has been evaluated in several published blinded series, some supporting and others not supporting an association with clinical improvement of OA. This is valuable in the clinical management of patients with OA, facilitating accurate diagnosis, and providing information regarding location and severity of joint pathology. The strong influence of structure on the MR image contrast indicates that MRI is ideally suited to the evaluation of cartilage tissue integrity, and new techniques hold promise for future detection capability related to very early changes of cartilage composition.
This commonly occurs in the knees and ankles of professional basketball or football players. The knees and the ribs are commonly affected, and it is always advisable to wear proper sports gear to avoid these injuries. Twisting a joint causes the involved bones to collide with each other forcefully, leading to a bone bruise. However, the pain involved in a bone bruise tends to be more severe and lasts longer than a soft tissue trauma. When a bone bruise is diagnosed with an MRI, one should rest the involved bone or joint and avoid any type of stress that could impede the healing process. These may include over-the-counter drugs non-steroidal anti-inflammatory drugs (NSAIDS) like ibuprofen (Motrin), diclofenac (Voltaren), or piroxicam (Feldene).
You may experience pain as well as swelling, but you have to take steps to alleviate pain and accelerate the healing.
In some cases, oral or injected steroid medications may be used in combination with immobilization to reduce pain and inflammation.


In this procedure, skin incision is made dorsally to the prominence of accessory navicular.
When the cast is being removed can start building up the ROM to counter atrophy and other physical therapy treatment which include stretching and strengthening exercises.
At the medial trochlear region (arrowhead), the intermediate signal represents pre-femoral fat pad, mimicking articular cartilage. In certain locations, especially the CMC joint of the thumb, the hip and knee joints, OA is known to often cause significant disability. Furthermore, a very sedentary life style is a risk factor for development of OA, with a proposed mechanism attributing this to the lack of muscle strength and coordination4. In addition there is a variable degree of inflammatory reaction, in part caused by breakdown products from cartilage and mediated by the synovium; some of these break-down products can be measured not only in joint fluid but also in the blood of an individual with OA in an active phase. This organization is thought to be reflected in the MR signal from different regions of articular cartilage. Hyaline cartilage always exists in a thin layer, from a fraction of a mm, up to 5-6mm in maximal thickness at the mid-patella which is usually the thickest hyaline cartilage in the body. Other symptoms include a catching or grinding sensation on joint movement, periarticular protuberances (periarticular mucous cysts mainly at the small joints of the fingers, and marginal osteophytes at any joint with OA), and later joint malalignment may develop. When symptoms are present, they are not likely to be generated within the articular cartilage, which is avascular and aneural, instead symptoms are mediated by other joint components including the synovium, joint capsule, and subchondral bone. The size of the resulting focal defects can vary significantly, and the location can vary although certain patterns prevail.
Surface fraying often results in an undulating (9b, arrow) or jagged contour, sometimes with subtle fissuring. This has in histological correlation studies been shown to correspond to marrow fibrosis with interspersed regions of trabecular necrosis, debris and repair features very similar to those of osteonecrosis, with associated variable hyperemic response. More rarely seen mainly with very advanced OA are intra-articular osteophytes, occurring at the articular surface. The synovial inflammation in patients with OA has been shown to contribute to the pathogenesis of OA through formation of various catabolic and pro-inflammatory mediators such as cytokines, prostaglandins and nitric oxide, altering the balance of cartilage matrix degradation and repair.
The cartilage-protective function of an intact meniscus is well known, with significant increases in the incidence of OA of the knee demonstrated in studies of meniscectomy populations3. There is a need to coordinate terminology used with MRI with that used with arthroscopic exams, which is a surface-limited exam while MRI is cross-sectional and does not readily offer a feel for what the surface will look like through an arthroscope. The cartilage is often not structurally permanently damaged, and healing may occur over a sometimes very long period of time, usually with patellar cartilage return to normal, while in some cases there will be progression to cartilage defects, subarticular bone marrow lesions, osteophytes and the features of OA22. The articular cartilage loss in RA is not localized as in OA, but more diffuse and is related to enzymatic action on the cartilage surface; it may progress to an end-stage joint with loss of all articular cartilage. In the last decade, other procedures have become available, if still mostly considered experimental by medical insurance companies.
OA is expected to continue to be a significant medical problem in the future in view of the increased sports activity demands with related injuries and overuse in professionals and also in young individuals involved in sports, the high frequency of obesity in the population, and with a longer life expectancy. MR diagnostic information is therefore likely to increasingly provide an important part of the basis for opportunities for future therapeutic interventions, aiming for more effective therapies for OA.
The swelling may be seen around the soft tissue surrounding the bone, such as the skin and muscles, and may be accompanied by discoloration. However, it is important to take these drugs at the proper dose, preferably with food, to avoid common side effects like gastrointestinal disturbances.
To support and protect a bone near a joint from further trauma, it is advisable to wear a brace, such as a knee brace. The tibialis posterior inserts to the os naviculare.[3] The tibialis posterior muscle also contracts to produce inversion of the foot and assists in the plantar flexion of the foot at the ankle.
Bone is removed to the point where the medial foot has no bony prominence over the navicular, between the head of the talus and first cuneiform. At the medial trochlea further distally, there was a small region of partial-thickness cartilage loss (not shown). Recent studies of OA of the knee have shown that OA involvement of the patellofemoral joint compartment, either isolated or together with medial compartment OA, is associated with more pain and lower function level than when OA is limited to the medial or lateral tibiofemoral compartments2,3. When this load is significantly exceeded, the chondrocytes in cartilage react, with various extent of degradation dominating synthetic activity.
Importantly, cartilage contains no distinct laminar structures, but instead there is a particular functional arrangement of collagen fibril orientation, chondrocyte prevalence, proteoglycans, and water content, with predictable gradual variations from the surface to the deep aspect of cartilage. Another variable feature of OA is the rate of progression of the joint degeneration, which may proceed over months or years, or may remain without progression for many years. Truncation artifact can cause an appearance suggesting sharply defined layers within cartilage; the presence of these layers is not compatible with the histology of articular cartilage. These cartilage abnormalities all involve the articular surface of cartilage, with variation in the depth of involvement. Moderate loss can be difficult to identify correctly, as signal loss at deeper cartilage layers may cause this to look like full-thickness loss (9c, arrow); compare with adjacent normal cartilage (arrowhead). However, care should be taken not to mistake the frequent ill-defined artifactual regions of low-signal in cartilage for low-signal fissuring (4a). Also frequently seen histologically are subchondral cystic change and degenerative microcysts15,16.
Osteophytes are not entirely specific for OA, and a relationship of non-progressing osteophytes to joint instability has been previously suggested.
Use of Grades 1 through 4, without added descriptive terminology, may not be sufficiently clear to all readers of clinical MRI exam reports. These include techniques using autologous cartilage transplants where a plug consisting of bone and cartilage is harvested from an expendable part of the joint and placed into the site of a prior defect, also the use of autologous chondrocyte implantation (ACI) where cartilage cells are harvested at arthroscopy, cultured in the lab, and re-introduced in solution into a cartilage defect, and held in place under a periosteal transplant cover.
When a bone bruise is adjacent to a joint, blood and fluids can spread to the joint, causing it to swell. One model describes OA as a process resulting from imbalance in the mechanical stresses affecting the entire joint, causing articular cartilage matrix degradation to dominate over matrix synthesis, thereby preventing cartilage self-repair and resulting in chondral loss4.
Chondrocytes, like osteocytes in bone, have been found to serve as both mechano-sensors and osmo-sensors, altering their metabolism in response to local physicochemical changes in the microenvironment. The orientation of the collagen fibers (Benninghoff,s arcades) include parallel thick collagen bundles at the surface, oblique orientation at the mid-section, and radial collagen bundles at the deep layers (6a). Changes most frequently progress slowly over years, and longitudinal MR imaging studies have estimated the average yearly loss of cartilage with OA of the knee to 4-6% of total cartilage volume.
Likely due to the arcade-like arrangement of collagen fibers within cartilage (6a), there will be low signal at both the surface and the deep layers of articular cartilage, and variably higher signal in the midzone, related to anisotropy and the effects of magic angle artifact. With traumatic shear injury to cartilage, an injury may occur that does not communicate with the articular cartilage surface, usually with a linear extent of a couple of mm along the cartilage-bone interface, with signal of fluid, described as delamination (9d) at the transition region between cartilage and the stiffer underlying cortical bone. With full-thickness loss, the exposed bony margin is often sharply defined (9d, long arrows), outlined by joint fluid, compared to adjacent partial-thickness loss (K, arrowheads). Subarticular bone marrow lesions occur in both OA patients with and without pain, but with a significantly higher frequency reported in symptomatic patients. More recent research has shown that osteophytes have a close resemblance to healing fracture callus, and that a specific growth factor when introduced into a joint in experimental animals induces osteophyte formation; expression of this growth factor is observed in human osteophytes, suggesting that growth factors may cause precursor cells in the periosteum at a joint margin to produce osteophytes19.
Other proposed models see OA as a systemic metabolic disorder, in which circulating factors linked to altered lipid and glucose metabolism, or dysregulated tissue turnover in many tissues with common mesenchymal origin, may explain the diversity of pathophysiological changes found in generalized OA, including an association with obesity and with vascular disease5. This recent discovery elegantly links extracellular environment events to intracellular signaling cascades.
The presence of collagen fiber cross-linking is strongly associated with function and imparts the characteristic strength and resilience. The loss of signal may vary depending on the orientation of the cartilage region relative to the long axis of the magnetic field. While larger subarticular lesions show stronger association with the presence of pain (but not with the severity of pain), they also in longitudinal studies predicted progression of OA17. Challenges have included attempting to induce the formation of hyaline-like cartilage as opposed to fibrocartilage, with hyaline-type cartilage with cross-linking required for holding up to the stresses of long term use. In addition to the collagen fiber orientation in cartilage, proteoglycans and water concentrations in different regions have been shown to influence cartilage signal variations10.
In a large longitudinal study, absence of bone marrow lesions at baseline or follow-up was associated with a decreased risk of further cartilage loss, and it was also found that although many subarticular bone marrow lesions slowly progress, this was not always the case, and indeed subarticular bone marrow lesions may regress or fully resolve, as in nearly 50% of their cases18. These large proteoglycan molecules are highly negatively charged, and during weight bearing when cartilage is compressed, they are made to move even slightly closer together, further repelling each other, and thereby maintain volume and then re-expand, contributing to the tremendous cartilage resilience manifested by tolerance of high load and high repetition mechanical stresses. In addition, when cartilage is compressed such as in the knee during motion, a minute amount of fluid is squeezed from the surface layers of cartilage onto the contact surfaces, with the lubrication further lowering the friction.



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