Email Us Subscribe. Home » Prolotherapy News » How do ligaments heal: Non-surgical repair of ligament injury. How do ligaments heal: Non-surgical repair of ligament injury In this article we will explore how ligaments heal and how you may be able to accelerate that healing.
This article is currently being updated. What are we seeing in this image? An explanation of an ankle sprain What you probably do not need to know about an ankle sprain is the exact number in the millions of people that seeking medical care for it. A complete rupture or disintegration of a ligament will most likely require surgery.
Do you have a graded sprain? In your information search or diagnosis who may have been identified as having: Grade I sprain. Your ligament, in a hyperextension type motion has become stretched out and may have torn a little. But you can walk on it or have little range of motion difficulties. Grade II sprain is a bit worse version of Grade I. This may be characteristic of a more severe discoloration in the joint.
More tear, more bleeding, and more black and blue. There is also a little more restriction of movement and putting weight on it hurts a little more. Grade III is a completely torn or ruptured ligament. If this has happened to you and you have a walking boot on or your shoulder is now in a sling, this will in many cases require surgical care and you should consult with the orthopedist about a surgical date. We also understand that some of you reading this article have already gone down this route and are trying to avoid a surgery.
The typical treatment guidelines If you have reached this point in this article it is likely that you have a more complex problem because the simple remedies have not worked for you. They either do not heal well or they become stiff and inflexible RICE generally involves resting or immobilizing an injured joint. You had a ligament sprain, you twisted your ankle or knee or low back in a bad way.
Phase 1: The swelling is the acute inflammatory phase. The discoloration may represent an internal bleeding, a tear in the ligament and surrounding tissue. Your body is sending healing factors and fluid to the site of the injury. This is why you may be recommended to resting the injured joint. A tweak of the ankle could result in an overstretched ligament that becomes tender, swollen and stiff, but the ankle should still be stable enough to support the weight of walking.
Recovery from a torn ligament may take several weeks, and should be done under the supervision of a health care provider. A strain is the overstretching or tearing of a muscle or tendon, which are the fibers that connect the muscles to the bones. They can occur from a single incident or from repetitive movements over the long term. Muscle spasms, weakness, cramping and immobility, as well as pain, bruising and swelling are symptomatic of a strain.
Like sprains, strains vary in severity. It could take a few weeks for the symptoms of a mild-to-moderate strain to subside. Tears are the ripping of fibrous tissue that can occur in the ligaments, muscles or tendons from similar activities that cause fibers to overstretch, but the diagnosis is more serious and muscle and tendon tears could take multiple months to heal.
Non-surgical rehabilitation is often sufficient. However, some tears may require surgery to repair, such as those to the anterior cruciate ligament, or ACL.
This process can actually continue for up to 2 years. Your programme should also take into account any underlying causative factors to prevent recurrence. Firstly, inflammation and swelling is normal after an injury and takes longer to resolve than most people expect.
There are things you can do each stage to speed up healing, help your body create a better repair and prevent recurrence. A physiotherapist will be able to advise you on the right treatment and exercises to carry out at the right time. As an essential healthcare clinic, we continue to remain open as normal. Under the new lockdown, you are allowed to make and attend any medical appointments should you need them. We are here to help, so please call us on if you have any questions or would like to see a physiotherapist.
We are open from 8am to 8pm, Monday to Saturday, offering both face to face and video appointments. When tension is applied, ligaments deform, or elongate, in a non-linear fashion through the recruitment of crimped collagen fibers. As the tension placed on the ligament increases, the collagen fibers progressively un-crimp, or elongate, until all fibers are nearly linear.
See Figure 1. As the fibers become increasingly linear, the ligament structure becomes increasingly stiff. Varying degrees of ligament stiffness are necessary for various loads and various ranges of joint motion.
Ligaments can lose their ability to retain their original shape when stretched or elongated past a certain point for a prolonged period of time. When this occurs, the ligament becomes lax and unable to properly support the joint, leading to instability, pain, and eventual osteoarthritis of the joint.
When an applied load causes all fibers to become nearly linear, the ligament continues to absorb energy until tensile failure or disruption of the tissue. Just as overstretched ligaments cause joint instability, ligament disruptions, or tears, will also create joint instability.
In attempt to prevent overstretching and disruption, ligaments utilize their viscoelastic properties to exhibit both creep and relaxation behaviors.
Creep and load relaxation behaviors help to prevent fatigue failure of the tissue when ligaments are loaded in tension.
Creep is defined as the deformation, or elongation, of a ligament over time under a constant load or stress. Load relaxation refers to a decrease in stress of the tissue over time when the ligament is subjected to a constant elongation.
When ligaments are exposed to loading over an extended period of time, they increase in mass, stiffness, and load to failure. When these discontinuities, also known as disruptions or tears, occur, the body responds by attempting to heal the injury through a specialized sequence of overlapping, but distinct cellular events. The acute inflammatory phase begins within in minutes of injury and continues over the next hours. During this phase, blood collects at the site of injury and platelet cells interact with certain matrix components to change their shape and initiate clot formation.
The platelet-rich fibrin clot releases growth factors that are necessary for healing and provides a platform on which many cellular events occur. Several growth factors have been identified, each playing a specific role in the inflammatory process. Vascular Endothelial Growth Factor aids in new blood vessel formation, which increases vascularity in injured areas. Fibroblast Growth Factor promotes the growth of the cells involved in collagen and cartilage formation.
When stimulated by growth factors, neutrophils, monocytes, and other immune cells migrate to the injured tissue to initiate matrix turnover by ingesting and removing debris and damaged cells during the inflammatory phase. The tissue formed initially appears as disorganized scar tissue with more blood vessels, fat cells, fibroblastic and inflammatory cells than normal ligament tissue. Over the next several weeks, fibroblast cells deposit various types of collagen, proteoglycans, other proteins and glycoproteins to the matrix.
The collagen becomes aligned with the long axis of the ligament during this time, however, the newly formed type of collagen fibrils are abnormal and smaller in diameter than normal ligament tissue.
After a few weeks, the proliferative phase merges into the remodeling phase in which collagen maturation occurs for months to years after the initial injury. With time, the tissue matrix starts to resemble normal ligament tissue, however, critical differences in matrix structure and function persist.
See Figure 2. In fact, evidence suggests that the injured ligament structure is replaced with tissue that is grossly, histologically, biochemically, and biomechanically similar to scar tissue. The remodeling phase of ligament repair can continue for months to years, during which time collagen and ligament matrix are continually overturned by processes of tissue synthesis and degradation.
This provides ongoing opportunities for the ligament to adapt with functional improvement, or degrade and fail with applied loads. The persisting abnormalities present in the remodeled ligament matrix can have profound implications on joint biomechanics depending on the functional demands placed on the tissue.
Because remodeled ligament tissue is morphologically and biomechanically inferior to normal ligament tissue, ligament laxity results, causing functional disability of the affected joint and predisposing other soft tissues in and around the joint to further damage. Some of the identifiable differences in remodeled matrix verses normal ligament matrix include altered proteoglycan and collagen types, 23, 24 failure of collagen crosslinks to mature, 7, 25 persistence of small collagen fibril diameters, 22, 26 altered cell connections, 28 increased vascularity, 22, 25 abnormal innervation, increased cellularity and the incomplete resolution of matrix flaws.
After injury, fibroblasts primarily synthesize type III collagen and to a much lesser extent Type I collagen. The abnormal collagen cross-linking and smaller collagen fibril sizes of the repaired ligament create weaknesses in tissue strength and stiffness which remain for months to years after initial injury.
In order to understand ligament healing, many studies use the medial collateral ligaments MCLs of rabbits as experimental models. Remodeled MCLs also exhibit inferior creep properties, elongating more than twice as much as normal MCLs, even at low tensions. When the knee or any joint is unstable, sliding between joint surfaces increases, and the efficiency of muscles surrounding the joint decreases. This creates alterations in the load distribution of the joint, which disrupts the underlying cartilage and bone, causing wear and increasing shear, eventually leading to osteochondral degeneration or osteoarthritis.
Animal studies have shown that different ligaments heal at different rates 15, and combined ligament injuries heal with inferior rate and quality than isolated injures. This may be related to the specific properties of the particular ligament that was injured, the type of ligament injury partial or full disruption , or interventions employed after ligament injury.
As discussed earlier, ligament healing is slow and often incomplete. Joint laxity caused by ligament injury improves slowly over a period of six weeks to a year. However, at six weeks to one year after injury, a large percentage of patients still have objective mechanical laxity and subjective joint instability.
While each of these therapies can help with the subjective symptom of pain following ligament injury, they do not all contribute to the cellular repair and healing of ligament tissue.
In fact, some of these therapies have been shown to be detrimental to the ligament healing process by suppressing and inhibiting certain cellular processes that are required for ligament tissue repair. Other therapies have been shown to contribute to healing through their stimulation of certain cellular processes involved in the regeneration of ligament tissue. Injured limbs are traditionally rested by splinting or casting.
While immobilization of the affected joint has long been prescribed following ligament injury, it has since been discovered that healing ligaments are dramatically affected by the presence or absence of joint motion. The theory is that rest or immobilization will prevent further tissue damage in the joint by limiting movement, thereby decreasing pain and swelling. It is also thought that rest may improve recovery time, decrease functional problems, and reduce long-term pain.
However, immobilizing a joint with a ligament injury can cause detrimental side effects, such as synovial adhesions, 62 increasing collagen degradation with decreasing collagen synthesis, 7 and a greater percentage of disorganized collagen fibrils. Immobilization causes ligament physiology to progressively switch from an anabolic to a more catabolic state. One study that measured collagen fiber bundle diameters in the normal and repaired ligaments of dogs, clearly documented that increased or decreased levels of exercise will greatly influence the strength of ligaments.
The study showed that the amount of exercise performed by the animal was directly correlated with the number of collagen fibrils, their arrangement, and their average thickness within the ligament. Prolonged limb immobilization decreases the glycosaminoglycan and water content and the degree of orientation of the matrix collagen fibrils within the ligaments.
Ultimately this causes the ligaments to have less mass and strength. See Figure 3. Decreased ligament loading has a profound effect on decreasing the strength of the ligament-bone junction fibro-osseous junction because immobilization causes subperiosteal osteoclasts to resorb much of the bony inserts of the ligaments. This causes a substantial decline in the tensile strength at the bone-ligament interface.
Early controlled resumption of activity after injury, including repetitive loading on injured soft tissue structures such as ligaments and tendons has profoundly beneficial effects including enhanced cellular synthetic and proliferative effects, increased strength, size, matrix organization and collagen content of ligaments and tendons.
Under loading conditions, cells within the ligament detect tissue strains and respond by modifying the tissue. Results of numerous animal studies have shown that the strength of repaired ligaments is greater in animals which were allowed to continue to exercise, rather than to rest.
Patients who treated their ligament injuries with motion, versus immobilization, were able to return to work quicker, return to sport quicker, and demonstrated less objective instability as tested by stress X-ray.
NSAIDs have been a mainstay treatment of ligament injuries for many years, especially for acute sports injuries, but new research has shown that NSAIDs are only mildly effective in relieving the symptoms of most muscle, ligament, and tendon injuries and are potentially deleterious to soft tissue healing.
NSAIDs specifically block the cyclooxygenase enzymes which catalyze the conversion of arachidonic acid to prostaglandins which play a significant role in ligament healing. One study looked at the use of Piroxicam in the treatment of acute ankle sprains in the Australian military. While the recruits were able to resume training more rapidly, in the long-term, an increase in ankle instability was evidenced by a positive anterior drawer sign in the Piroxicam group.
Corticosteroid injections have long been used to treat musculoskeletal disorders including ligament injuries. Although steroid injections have been shown to be effective in decreasing inflammation and pain of ligament injuries for up to six to eight weeks, the histological, biochemical, and biomechanical properties of ligament healing are inhibited.
Corticosteroid injections into injured ligaments have an adverse effect on healing. Corticosteroid injections into ligaments and tendons have been known to inhibit fibroblast function and thus collagen synthesis even causing collagen necrosis at the injection site.
Prolotherapy has emerged as an injection therapy treatment option for musculoskeletal and arthritic pain. It involves the injection of a small amount of various proliferant solutions such as hypertonic dextrose, sodium morrhuate, platelet rich plasma at the painful entheses of ligaments and tendons, as well as trigger points and adjacent joint spaces to induce healing of the injured structures. Prolotherapy is given to the articular ligaments of the entire spine, pelvis and peripheral joints to tighten unstable joints.
Case series have documented the efficacy of Prolotherapy for ligament injuries of the sacroiliac joint, low back, , neck, , shoulder, elbow, knee, , temporomandibular joint, , and other articulations. Ligament healing is often slow and incomplete. Joint laxity caused by ligament injury improves slowly over a period of six week to a year. However, at six weeks to one year after injury, a large percentage of patients still possess objective mechanical laxity and subjective joint instability.
Numerous strategies have been employed over the year attempting to improve ligament healing after injury or surgery. One of the most important advances in the treatment of ligament injuries has come from the understanding that controlled early resumption of activity can stimulate repair and restoration of function, and that treatment of ligament injuries with prolonged rest may delay recovery and adversely affect the tissue to repair.
Likewise, although steroid injections and nonsteroidal anti-inflammatory medications have been shown to be effective in decreasing inflammation and pain of ligament injuries for up to six to eight weeks, the histological, biochemical, and biomechanical properties of ligament healing are inhibited. Regenerative medicine techniques, such as Prolotherapy, have shown success in case series involving ligament injuries of the spine and peripheral joints, but studies in more controlled settings and with large numbers are needed in the future.
Ligament structure, physiology and function.
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