III. Phases of Healing
The Natural Process of Healing
During the natural cellular process of healing there are three key phases, with specific functional cellular processes, and durations....
The phases and associated relative timeline of tissue repair. (Watson, 2006)
Phase I: **Acute Inflammation**
Vascular response, cellular infiltrate, polymorphonuclear leukocytes, macrophages, neovscularization, synthesis of granulation tissue.
Duration: 1-7 days post injury
The key phases of the tissue repair process. The phases identified are shown as separate entities, when they are actually interlinked! Specific cellular cascades of events act in sequence stimulating the following phase.
(Watson, 2006)
Phase II: **Proliferative**
Cellular proliferation, macrophages, fibroblasts, collagen synthesis (TIII), endothelial cell proliferation, mature formation of granulation tissue, increased mechanical strength.
Duration: day 4 up to 6 weeks post injury **occurs all the time in the background**
The proliferation process. (Watson, 2006)
Phase III: **Maturation**
Collagen remodelling (TIII-TI), increased wound strength, decreased vascularity, macrophages, fibroblasts, formation of scar tissue.
Duration: 2-3 weeks post injury, to months or years.
The remodelling process. (Watson, 2006)
The tensile strength of tissues, comparing injured and uninjured tissue during the phases of healing. (Watson, 2006)
**To gain a conceptual understanding of individual prognosis, we need to differentiate the soft tissue injury sequelae from pathologic degeneration.**
Following soft tissue injuries, the body will undergo three natural phases of healing: acute inflammatory, proliferative (repair/regeneration) and maturation (remodeling). During the acute inflammatory phase, the injured site is infiltrated with blood products to remove injured cells and necrotic debris. The proliferative phase entails the replication of native tissue cells to replace the injured or damaged tissues. This phase is disorganized and physiologically unstable, leading to scar tissue formation. The remodelling phase involves rearrangement of disorganized tissue cells into more organized structures and recover the physiologic properties. If the maturation phase is suboptimal scar tissue will contract and become imbedded in the native tissue. The potential of the body to heal with regenerated native tissue, without scarring, is now possible with the use of orthobiologics, followed by an appropriate physical therapy rehabilitation program.
Wound Healing: Factors leading to Impaired Healing Response
Key factors, primary or secondary, will inevitably lead to impaired healing response. It's important to manage injuries early, decreasing prolonged swelling, and subsequent re-injury/recurring microtrauma. This includes implementing acute management strategies.
When injuries occur, they need to be managed properly, and it involves more than protection, rest, ice, compression, and elevation (P.R.I.C.E), no heat, alcohol, running or massage (No H.A.R.M) in the initial 48 hours following an acute injury, and no NSAIDs. To facilitate healing and prevent further tissue damage, physical therapy will help get you back into action - effectively, efficiently and better than you were before your injury happened. This process involves taking a thorough medical history, including your present signs, symptoms, mechanism of injury, past medical history, completing a physical examination including a functional orthopaedic assessment and creating a treatment plan.
Electrophysiological Agents (EPAs) and manual therapy are required to improve joint mobility/soft tissue extensibility, facilitate healing, and reduce pain/inflammation. Specifically designed exercises will improve joint range of motion, motor control, muscular strength and endurance. It is essential each exercise is performed correctly, through a full pain free range of motion, and progressed appropriately. Individuals will work through each stage of my *7 Phase Management Plan* to optimize recovery.
Primary Factors:
Hypoxia, bacterial colonization, ischemia, reperfusion injury, altered cellular response, collagen synthesis defects due to: systemic illnesses/chronic conditions - diabetes, smoking, malnutrition.
Local Factors:
Tissue edema, hypoxia, infection, maceration, dehydration.
Bone
Bone: Composition.
Bone: "lines of stress"; topographic trabeculae.
According to Wolff's Law (1892), the external shape and internal architecture of a bone is determined by the external stresses acting on it. The initial structure of the trabecular bone firstly undergoes secondary changes, becoming thicker and denser resisting external loading. The porosity percent of trabecular bone is within the range of 0.2-0.8g/cubic centimeter (Meyers, M et al. 2014), effecting its strength. The micro structure is typically oriented and the "grain of porosity" is aligned in a direction at which mechanical stiffness and strength are the greatest. The range of young's modulus [a mechanical property that measures the stiffness of a solid material, defining the relationship between stress (force per unit area) and strain (proportional deformation)], for trabecular bone is 800-14000 MPa and the strength failure is 1-100 MPa. (Carter, D. 1976).
The compressive strength of trabecular bone arises from compressive stress. On the stress-strain curves for both trabecular bone and cortical bone, there are three stages:
I. Linear Region: where the individual trabecula bend and compress, as the "bulk tissue" is compressed.
II. After Yielding: when trabecular bonds start to fracture
III. Stiffening: when trabeculae stiffen
Stress-Strain Comparisons: Steel, glass and bone.
Throughout adulthood, bone density steadily decreases with age, including a loss of trabecular bone mass. If bone mineral density is measured as 1 standard deviation below the mean it is defined as "osteopenia"; if it is measured as more than 2.5 standard deviations below the mean, it is defined as "osteoporosis" (World Health Organization). Low bone mineral density increases the risk for stress fractures.
Cartilage
Cartilage is a resilient and smooth elastic tissue, covering and protecting the ends of long bones at the joints, is a structural component of the thoracic rib cage, and IVDs. It is composed of specialized cells, chondrocytes, which produce collagenous extracellular matrix, abundant of ground substance (rich in proteoglycan and elastin fibers).
It is classified as: elastic, hyaline, and fibrocartilage; all differing in amounts of collagen and proteoglycans.
Cartilage has a limited repair capability as chondrocytes are bound in lacunae, they cannot migrate to damaged areas. Hyalin cartilage does not have a blood supply, and the deposition of new matrix is slow. Damaged hyalin cartilage is usually replaced by fibrocartilaginous scar tissue. Recently, bioengineering techniques are being developed to generate new cartilage, using cellular "scaffolding" material and cultured cells to grow artificial cartilage.
Ligaments
Ligaments are fibrous connective tissue connecting bones to other bones. The major constituents of ligaments are: collagen, elastin, glycoproteins, protein polysaccharides, glycolipids, water, and cells (mostly fibrocytes). The greatest quantities of constituents found in ligaments are collagen and ground substance. For practical purposes, the physical behavior of ligaments is usually predicted based on the content and organization of these substances alone.
Collagen constitutes 70–80% of the dry weight of ligament, the majority being type I collagen, which is also found in tendon, skin, and bone. Collagen has a relatively long turnover rate, with its average half-life being 300 and 500 days, which is slightly longer than that of bone. Therefore, several months may be required for a ligament to alter its structure to meet changes in physical loading conditions or to repair itself after injury. Water makes up about 60–80% of the wet weight of ligaments.
Hierarchial organization of a tendon.
Tendons:
Tendons are tough bands of dense, fibrous connective tissue, connecting muscles to bones, capable of withstanding tension. Normal healthy tendons are composed mostly of compact, parallel arrays of collagen fibers. The collagen portion (86%), is composed of 97-87% TI collagen; each collagen molecule is about 300nm long, 1-2 nm wide, and the diameter of the fibrils formed range from 50-300 micrometers. The fibrils assemble to form fascicles, which then form into a tendon fibre. The fascicles are bound by the endotendineum, a delicate, loose connective tissue containing collagen fibrils. They function to transmit forces; passively modulating forces during functional movements, providing additional stability with no active work. Tendons throughout the body have differing functional roles; due to their elastic properties they can function as "springs". They store and recovery energy at high efficiency; as tendons stretch, muscles are able to function with less or even no change in length, allowing greater force generation.
The mechanical properties of tendons are dependent on the collagen fiber diameter and orientation. Collagen fibrils allow tendons to resist tensile stress; their proteoglycans allow resistance to compressive stress. Energy storing tendons utilize significant amounts of sliding between fascicles enabling the high strain characteristics they require, whilst positional tendons rely heavily on sliding between collagen fibres and fibrils. Recent literature suggests fascicles are twisted, or helical, in nature providing their spring-like behaviour.
Tendons are viscoelastic structures, exhibiting both elastic and viscous behaviour. When stretched they exhibit typical "soft tissue". They respond favourably to changes in mechanical loading with growth and remodeling processes, akin to bones. As tendons heal, in response to repetitive microtrauma, they become more fibrous, resulting from increased production of type I collagen and the fibrils align in the direction of mechanical stress. The final maturation phase may take up to 10 weeks, where there is an increase in crosslinking of collagen fibrils, increasing stiffness.
Through the cellular process of mechanotransduction, tenocytes respond to the mechanical forces of exercise, facilitating healing at a cellular level. Mechanical forces create alterations to gene expression, protein synthesis, and cell phenotype, changes the tendon structure.
Force Responses in tendons: normal activity, strenuous activity, and initial failure.
Stress-Strain Response: physiologic response, overuse injury and ligament rupture.
Density Comparison: Bone, cartilage and ligament.