{"id":5358,"date":"2026-01-05T00:00:36","date_gmt":"2026-01-04T23:00:36","guid":{"rendered":"https:\/\/akvetmed.cz\/?p=5358"},"modified":"2026-01-03T03:39:53","modified_gmt":"2026-01-03T02:39:53","slug":"hojeni-poraneni-pohyboveho-aparatu-a-rehabilitace","status":"publish","type":"post","link":"https:\/\/akvetmed.cz\/en\/uncategorized\/hojeni-poraneni-pohyboveho-aparatu-a-rehabilitace\/","title":{"rendered":"Healing of musculoskeletal injuries and rehabilitation"},"content":{"rendered":"
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\u00a0 \u00a0 \u00a0 \u00a0 \u00a0 \u00a0 Injuries of various aetiologies and to different parts of the musculoskeletal system are frequent in veterinary surgeries. Injury can be defined as a violation of the anatomical, physiological and functional integrity of the tissues in the body.<\/span>2<\/sup> The treatment of these injuries can be divided into immediate treatment after their occurrence and treatment leading to restoration of the existing function of the injured part of the musculoskeletal system, if possible restoring full functionality. Today's veterinary medicine offers a wide spectrum of acute treatments for musculoskeletal injuries using a variety of procedures. In most cases, the aim is to restore anatomical and physiological integrity. The restoration of functional integrity is the subject of rehabilitation. In most cases, immobilisation of the limb is an integral part of the treatment of these injuries, which may cause further damage to the associated tissues.<\/span><\/p>

Rehabilitation of patients with acute or chronic orthopaedic injuries involves the application of controlled procedures to tissues to improve their strength, condition and function. It is important to know how to safely remobilize tissues after injury and after a period of immobilization. Rehabilitation can sufficiently affect the tissues to positively impact their recovery. Conversely, if the tissue is overloaded, it can damage the tissue and prolong the healing time or cause further disability. A balance must be struck between the need to protect tissues from further damage and promote healing and the need to prevent tissue damage by not using them. In order to find this balance and to be able to time rehabilitation treatments correctly in these patients, we should have an understanding of the healing process of each tissue.<\/p>

General tissue healing<\/b><\/p>

\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 With each injury, a complex series of processes begin to take place in the tissues that involve cellular and biochemical responses to the injury, ultimately leading to healing of the injury. These microscopic processes are initiated, mediated and maintained by biochemical mediators called cytokines and growth factors.3<\/sup> The number of these processes depends on the severity and number of injured tissues. The goal is regeneration or repair of damaged or traumatized tissues. Regeneration and repair are part of healing. Wound healing usually occurs in three main phases: inflammation, repair (proliferation or fibroblastic phase) and remodelling (matriculation). There are no sharp boundaries between these phases; one gradually transitions into the other, and we may find evidence of two phases of healing at any one time, although they generally build on each other as we will discuss below. This is influenced by the type of tissue damaged and the severity of the damage.1,2<\/sup><\/p>

  1. Inflammatory phase<\/b><\/li><\/ol>

    This phase of healing can be further divided into an acute vascular response followed by cell infiltration. The immediate vascular response is actually hemostasis in the wound. The disruption of blood vessels at the wound allows extravascular movement of blood elements and contact of extravascular collagen with platelets, which is the start for the coagulation cascade. The coagulation cascade results in the formation of the fibrin network necessary for the formation of the hemostatic plug, which then serves as a site for cellular infiltration.<\/p>

    The cellular aspect of the inflammatory phase follows the vascular response. The release of cytokines in conjunction with the hemostatic plug and increased vascular permeability begins chemotaxis of cells into the wound. Neutrophils are the first cells to migrate to the wound site, appearing about 6 hours after injury, and their migration to the wound site peaks on day 2-3. The role of neutrophils is the initial debridement and phagocytosis of microorganisms, thereby minimizing the emergence of potential infection. The extent of neutrophil action in the wound depends on the severity of the injury and the degree of contamination. The contribution of neutrophils in an uncontaminated wound is not important for normal wound healing.<\/p>

    The second type of cells that appear at the site of injury are macrophages. These appear at the site of injury about 24 to 48 hours after neutrophil migration. The presence of macrophages at the site of injury is crucial for the transition from the inflammatory to the reparative phase. They have five main functions: phagocytosis, wound debridement, regulation of matrix synthesis, cell drainage and activation, and angiogenesis. Phagocytosis and wound debridement occur with the release of oxygen radicals, nitric oxide and collagenases. In cooperation with neutrophils, macrophages create the optimal environment for the initiation of the reparative (fibroblastic) phase of wound healing. This activity is at its peak during the first 3 to 4 days after injury. In addition, macrophages release cytokines, growth factors, prostaglandins and enzymes that subsequently activate and control angiogenesis and fibroplasia. Macrophages probably play a central role in the control of cellular and biochemical processes in wound healing. The presence of macrophages attracts and activates lymphocytes. Lymphocytes secrete lymphokines such as interferons and interleukins, which stimulate fibroblast migration and collagen synthesis. Their activity peaks about 6 days after injury.<\/p>

    1. Reparative phase<\/b><\/li><\/ol>

      The reparative (proliferative or fibroblastic) phase of wound healing is characterized by the cellular response of endothelial cells and fibroblasts. Fibroblast proliferation and migration predominate and are followed by matrix synthesis of collagen, elastin and proteoglycans. Fibroblasts begin to appear at the site of injury within 3 days after its occurrence. After the lag phase, which lasts 2 to 3 days, they begin to form collagen and proteoglycans. Matrix synthesis then increases over the next few weeks, simultaneously increasing the tensile strength at the injury site.<\/p>

      In addition, at this stage, endothelial cells begin to proliferate and form new capillaries that gradually migrate into the wound. The newly formed capillaries are formed immediately after the onset of fibroblast migration and collagen network formation and continue until normal oxygen tension is established at the wound site. This dense network of macrophages, fibroblasts, and neovascularization during the proliferative phase is called granulation tissue.<\/p>

      1. Remodelling (matriculation) phase<\/b><\/li><\/ol>

        The remodelling phase is the final phase of wound healing, during which collagen fibres reorient parallel to the lines of force and fibres oriented across these fibres then form a stable network. This is the most important aspect of connective tissue wound healing because appropriate collagen deposition and positioning are important for the development of adequate tensile force in the healed tissue. Although collagen deposition peaks 2 to 3 weeks after injury, tensile strength increases progressively over a 1-year period. This period is characterized by the removal of biomechanically inferior collagen fibers (type III) and their replacement with fibers suitable for the specific tissue (generally type I collagen). In addition, the reduced concentration of proteoglycans leads to a decrease in water content, resulting in compression of the collagen fibres. The tighter the fibres are together, the greater the area for crossing them and thus the greater the tensile strength. Therefore, the balance between collagenolysis and matrix accumulation is important.1,2<\/sup><\/p>

        \u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 In musculoskeletal injuries, the following tissues can be injured: bone, tendons, ligaments and articular cartilage. We will discuss their healing process and their influence on rehabilitation in the next section of this article<\/p>

        Bone healing<\/strong><\/p>

        Bone is a tissue that heals by direct cellular regeneration and restores 100% of its biomechanical properties. Bone healing can be divided into primary bone healing and secondary bone healing.<\/p>

        Primary healing of the bone occurs when there is a minimal gap (up to 0.5 mm) between the fracture parts and the fracture is stable. Primary healing of the fracture occurs by contact or gap healing. Contact healing occurs in fractures with a gap between the fragments of less than 0.1 mm. A resorption cavity is formed in the fracture line, where osteoclast action removes bone and calcified matrix, followed by osteoblast activity. If the gap between the fracture fragments is greater than 0.1 mm but not greater than 0.5 mm, so-called gap healing occurs. This gap cannot be directly repaired by the resorption cavity. The gap is filled with lamellar bone and only then is it replaced by a resorption cavity as in contact healing. In primary bone healing, minimal radiological callus forms and the fracture line gradually disappears. Although in primary healing, new bone forms immediately without the formation of fibrous or cartilaginous tissue, this does not reduce the healing time of the fracture. Weeks to months are needed for complete union. Early stability decreases with primary healing of the bone compared to secondary healing, therefore longer periods of time are required for removal of stabilizing implants.<\/p>

        Secondary healing occurs in unstable fractures with a gap between fragments greater than 0.5 mm. This healing is characterised by the formation of a sludge. The size of the sludge is determined by the size of the fracture instability. Healing of such a fracture follows the general pattern of wound healing. During 24 to 72 hours, the inflammatory phase takes place. In the reparative phase, a fibrous and cartilaginous soft callus forms during the first 3 weeks. The function of the callus is to fuse the ends of the fracture and reduce the movement of the fragments. The remodelling phase then begins with the transition from soft fibrocartilaginous callus to hard - ossified callus, which occurs by endochondral ossification. Once the ossified callus is formed, remodelling to the original lamellar bone occurs. After the formation of the callus, we can stimulate the actual remodeling of the bone by controlled micro-movements.<\/p>

        Primary and secondary healing take place at approximately the same time intervals. The callus in secondary healing appears radiologically 10 to 12 days after the injury. Disappearance of the fracture line occurs after 30 days. Primary bone healing takes longer. Complete remodeling of the callus occurs 90 days after fracture healing. Primary bone healing without callus creates less stability than secondary healing and therefore it is necessary to leave stabilizing implants in place for a longer period of time than in secondary healing. Bone healing and strength is faster in secondary healing. Healing is influenced by the stress between fragments, minimal age, the nature and location of the fracture, the presence or absence of concomitant disease, and the surgical method of fixation. Clinical union defined as resistance to loading such that fixation can be removed. Clinical fusion occurs differently according to the age of the injured animal. The table shows the age of the dog and the time at which clinical union occurs.<\/p>

        Table: age of the dog and time of clinical fracture union<\/b><\/p>

        Age of the dog<\/p><\/td>

        Clinical association of fracture<\/p><\/td><\/tr>

        Puppy up to 3 months<\/p><\/td>

        2 - 4 weeks<\/p><\/td><\/tr>

        Puppy 3 - 6 months<\/p><\/td>

        4 - 12 weeks<\/p><\/td><\/tr>

        Puppy 6 - 12 months<\/p><\/td>

        5 - 8 weeks to 3 - 5 months<\/p><\/td><\/tr>

        Adult dog over 1 year<\/p><\/td>

        7 - 12 weeks to 5 - 12 months<\/p><\/td><\/tr><\/tbody><\/table>

        \u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 (Millis, 2014)\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0<\/p>

        Impact on rehabilitation\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0<\/b><\/p>

        During the inflammatory phase, we strive to control pain, minimize soft tissue inflammation, maintain joint health, and provide safe, controlled mobility depending on the stability of the fracture. During the reparative phase (3 days to 4-6 weeks) we may perform small, slowly increasing cyclic stretches to increase micro-movements and improve muscle formation and continue to maintain joint health through active and passive range of motion.1<\/sup><\/p>

        Muscle healing<\/strong><\/p>

        Muscle injuries occur through laceration, contusion, rupture, ischemia and strain. A strain is described as an injury to a muscle or tendon with a tendency to occur near the myotendinous junction. A common cause of non-penetrating injury is severe contraction of the muscle with passive extension. Damage to the muscle results in tearing of the muscle fibers and disruption of the vascular and connective supporting tissue.<\/p>

        The healing of the muscle follows the same stages as general wound healing. After the formation of a hematoma, edema and ischemia occur, resulting in necrosis of the surrounding ruptured muscle fibers. The initial inflammatory phase continues with the removal of the necrotic debris by neutrophils and macrophages within 24 to 72 hours. An essential component of muscle injury healing is the restoration of blood supply to the injured fibers. The reparative phase follows and involves the processes of regeneration of functional muscle fibers or formation of fibrous scar tissue, depending on the size of the injury. Reparation into scar tissue is not desirable because it creates a greater chance of re-injury and a reduction in the contractile force of the muscle by about 50%. The reparative phase involves the production of extracellular matrix by fibroblasts. Myoblastic germ cells from around the wound and mononuclear leukocytes migrate to the viable end of the muscle fibers and fill the gap, providing a source for the formation of myotubes. An alternative form of muscle healing occurs when there is an inadequate source of myoblasts, insufficient vascularization, inadequate innervation, or excessive stress on the injured site. In these situations, excessive collagen deposition occurs and fibroblast activity leads to the formation of fibrous tissue.<\/p>

        Prolonged immobilization allows penetration of regenerating muscle fibres and reduces fibrous tissue formation. However, muscle fibers tend to orient incorrectly to the line of stress and strain. This reduces the tensile strength of the muscle fibers and when more fibrous tissue is formed during the remodeling phase, there is a significant loss of muscle strength. Initial immobilization for 3 to 5 days followed by controlled mobilization accelerates the appearance of type I collagen fibers and consequently increases tensile strength. Considering normal healing, the recommendation is 4 to 6 weeks of protected activity before increasing activity. Timing of appropriate stress and movement at the site of injury are important to the type of healing. For optimal muscle fiber healing and return to maximum function, movement at the site of injury should not begin unless healing is in the reparative or early remodeling phase. During these phases, the muscle fibers straighten parallel to the line of applied appropriate stress. With excessive movement, the gap widens and the muscle heals with more fibrous tissue.<\/p>

        Impact on rehabilitation<\/b><\/p>

        The decrease in muscle contractile force is related to the degree of injury and fibrous tissue ingrowth. Rehabilitation depends on the extent of the injury (e.g., degree of stretch, rupture). For mild stretch, 3-5 days of immobilization followed by active muscle contraction shows better penetration of muscle fibers through scar tissue and greater muscle strength and volume. When the muscle is torn, immobilization for a minimum of 2-3 weeks is recommended to promote repair, promote new collagen formation and better tolerate remobilization stress. When rehabilitating a complete muscle tear, moderate activity is recommended for 4-8 weeks after injury. After 8-12 weeks, unrestricted activity is possible.1<\/sup><\/p>

        Tendon healing<\/strong><\/p>

        The tendon healing process follows the same phases as general wound healing with initial fibroplasia and collagen deposition followed by matriculation and reorientation of collagen fibres. The primary difference in tendon healing is whether the tendon is covered by tissue with blood vessels called paratenon or synovium. In the former case, fibroblasts and capillaries readily penetrate the injured tendon. In the latter case, more time is needed to achieve adequate tensile strength and healing, because the healing process depends on the actual blood supply or inflammatory infiltration of the healing tissue. Therefore, immobilization is extremely important in the initial phase to prevent the formation of a gap at the healing site.<\/p>

        In the early stage of tendon healing, cells from the surrounding tendon tissue penetrate the tendon to allow phagocytosis, fibroplasia and subsequent collagen deposition. This is an external healing process. The inflammatory stage is evident during the first 3 days and is rapidly followed by deposition of randomly oriented collagen fibers by the fifth day. The reparative phase follows with increasing amounts of deposited collagen during the first 4 weeks. Collagen production is greatest on days 5-12 after injury and decreases significantly by day 60. Research has shown that tendon healing by collagen deposition requires a minimum of 28 days for the fibers to orient parallel to the line of stress, In addition, collagen bundles are recognizable from normal tendon up to 112 days after injury. The intrinsic healing process can be stimulated by controlled mobilization, reducing the risk of adhesion formation and generating greater tensile strength, allowing the collagen fibers to be properly positioned along the stress line. Ideally, controlled passive movement begins on day 21 of repair; however, the duration and extent of movement for optimal healing is unknown. The goal of therapy is to minimize adhesion formation and return maximum function. The appropriate therapy is surgical apposition of the injured tendon ends. With healing, the tendon reaches 56% of normal tensile strength at week 6 and 79% at 1 year. The synovial (avascular) tendon needs a longer healing time than the vascular tendon.<\/p>

        Impact on rehabilitation<\/b><\/p>

        Post reparative immobilization for large tendons may be necessary for 6 weeks. This prolonged immobilization can be harmful. Complete immobilization longer than 21 days results in reduced vascularization. For complete or partial transection and surgical repair, it is optimal to begin passive mobilization 5 days after surgery. With controlled passive mobilization continued for 21 days to promote internal healing, increase tensile strength, and reduce adhesion formation. Conservative movement with light loading can begin at 6 weeks because the tendon already has 25-50% of normal tensile strength and is able to withstand normal muscle force. We perform light loading for at least 12 weeks. Moderate movement helps to maintain the normal range of motion of the joints. Sufficient tensile strength for normal activity is achieved after months.<\/p>

        Healing of ligaments<\/strong><\/p>

        Vases heal differently depending on their location. For example, the healing potential of the medial collateral ligament of the knee is good, but the cranial cruciate ligament of the knee does not show a healing response after injury. Ligaments heal by the same mechanisms described for general healing processes. Immediately after injury, an organized hematoma forms, and the surrounding tissue becomes edematous. Inflammatory cells, monocytes and macrophages enter the site of injury. This stage lasts 48 to 72 hours. The reparative phase begins 2 to 3 days after the injury and lasts about 6 weeks. Matrix formation and cellular colonization predominate. The defect is filled with granulation tissue with blood vessels. The resulting scar contains many cells for the first weeks, mainly fibroblasts, which synthesize collagen. The remodelling phase can last more than 12 months. At this time, the tensile strength is only 50 to 70% of the original strength. Part of the loss of tensile strength is due to bone loss at the insertion site of the ligament. Healing of the ligament is faster than healing of the bone. Factors important to the actual healing of the tissue are ligament end apposition, nutritional status, endocrinologic imbalances, severity of injury, blood supply, and mechanical stress on the healing tissue. Depending on the degree of injury, healing takes several days to more than a year. At 1 year, the healed ligament reaches a tensile strength of 50-70%. The healing properties and rate depend on which ligament is damaged. A torn medial collateral ligament of the knee has a tensile strength of 52% after 14 weeks of healing<\/p>

        Impact on rehabilitation<\/b><\/p>

        The time to start rehabilitation varies greatly depending on the ligament that is damaged. The parameters for healing of the ligament may be as follows. The reduction in tensile force is slowed or reduced by immobilizing the joint and reducing stress. Short-term (30 minutes) and more frequent (6 days per week) exercise is best for gaining ligament strength, as found in a study in horses.1<\/sup><\/p>

        Cartilage healing of the joint<\/strong><\/p>

        The limiting factor for cartilage healing is its avascular nature. Damage to the articular surface results in two different responses depending on whether the damage occurs on the cartilage surface or also affects the subchondral bone. Injury to the cartilage surface alone results in local chondrocyte death and subsequent loss of matrix. In this defect, there is no fibroblastic response and the local chondrocytes must proliferate and fill the defect with new matrix. Chondrocytes respond initially with increased mitotic activity. However, the chondrocytes cannot completely fill the defect and the lesion persists. The injury reaching the subchondral bone allows access of stem cells from the bone marrow and blood capillaries to the cartilage defect. Thus, the same stages of healing as in general wound healing take place here. After the initial debridement and inflammatory phase, the defect begins to fill with collagen and fibrous cartilage is formed within 5 to 7 days. After 2 months, the defect is filled with a matrix rich in proteoglycans. Healing of the wound continues with remodelling and matting. At 6 months, the concentration of glycosamines decreases significantly and a higher content of dermatan sulphate, whose molecule is smaller and less durable compared to glycosaminoglycans, is found in the repaired cartilage. The healed cartilage is more fibrous and is biomechanically inferior to the original hyaline cartilage. One concept in healing articular defects is that of early continuous passive motion, because prolonged immobilization adversely affects the biomechanical and biochemical capacity of the newly formed articular cartilage.<\/p>

        Impact on rehabilitation<\/b><\/p>

        Continuous passive movement after cartilage injury improves healing, especially with hyaline cartilage, as demonstrated by studies in rabbits.1<\/sup><\/p>

        Conclusion<\/b><\/p>

        \u00a0Wound healing in most tissues involves an initial process of haemostasis followed by inflammation. This allows debridement of the injured area and subsequent chemotaxis of appropriate cells to form reparative tissue. Generally the process of repair involves the production of collagen, bone or myofibrils. Matting occurs over time when appropriate collagen and tissue support occurs to increase resistance and tensile strength. Initiating physical rehabilitation in the postoperative period is important, and techniques must be used to increase the matriculation phase to maximize the earliest return to tensile strength and function. Timing of the various therapeutic modalities is important, and knowledge of the basic healing processes is imperative.<\/p>

        Literature:<\/p>

        1. Millis D., Levine D. Canine Rehabilitation and Physical Therapy. Elsevier Saunders, 2014, 79 - 91<\/li>
        2. Amalsadvala T., Swaim S.F.. Management of Hard - to - Heal Wounds. Vet Clin Small Anim 36 (2006), 693 - 711<\/li>
        3. Hosgood G.. Stages of Wound Healing and Their Clinical Relevance. Vet Clin Small Anim 36 (2006), 667-685<\/li><\/ol>\t\t\t\t\t\t<\/div>\n\t\t\t\t<\/div>\n\t\t\t\t\t<\/div>\n\t\t\t\t<\/div>\n\t\t\t\t<\/div>","protected":false},"excerpt":{"rendered":"

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