
Chapter 6
Forces and its Effects
 When forces act, two potential effects; 1- acceleration 2- deformation.
 Tissues sustain force two primary factors dictate injury. 1- size (magnitude) of force, 2- materials
properties of the involved tissues.
 Everything has a yield point (a point the material will deform or break) Tearing or FX of a tissue
or bone.
 Direction in which force is applied has important implications for injury:
 Axial Force(Compression) are forces that act along the long axis (Standing),
 Tensile Force are forces that pull things apart (Ankle Sprain)
 Shear Force is forces that include Compression/Tension forces, which cause one part to slide or
displace w/respect to another.
 Torque is the product of a force and its moment arm (Rotary Force) Door Hinge
 Combination forces along a long bone (Compression/Tension) generates a torque known as
Bending, which causes a FX
 Torsion is a product of torque which is twisting effect W/shear force.

Chapter 6
Soft-Tissues
 Skin- Compose of two major regions:
 Outer (Epidermis) multiple layers containing the pigment, hair, nails, sebaceous glands, and
sweat glands.
 The Dermis contains blood vessels, nerve endings, hair follicles, sebaceous glands, and sweat
glands.
 Tendons connect bone to muscle and ligaments connect bone to bone.
 Muscle could only be Strain.
 Ligaments could only be Sprain.
 Muscle is viscoelastic which means that muscle has extensibility; the ability to be stretched
(increase in length) and elasticity is the ability to return to normal length after lengthening or
shortening.
 Chapter 6
Skin Injury Classifications
 Abrasions: cause by a shear force (common) scraped.
 Blister: repeated application of shear in one or more directions (shoe rubs back and forth
against a foot).
 Skin bruises: compression forces delivered by a blow damaging the capillaries that causes
accumulation of blood.
 Incisions :( surgery),
 Lacerations: (irregular cut/tear) tension/shear force,
 Avulsion: (severe lacerations; results in complete separation from the skin).
 Puncture: something that penetrates the skin.
 Contusions (Bruise) Heavy blow, Ecchymosis (tissue discoloration), Hematoma: Hard mass
compose of blood and dead tissue.
 Chapter 6
Strains and Sprains Classification
 1st degree: mild discomfort, local tenderness, mild/no swelling, no loss of ROM
 2nd degree: more severe pain, some instability, and muscle weakness, ecchymosis, loss of half of
ROM
 3rd degree: Severe pains, very unstable, severe ecchymosis, complete loss of ROM.
Chapter 6
Cramps and Spasms, Itis’s
 Cramp is an involuntary contraction: Clonic (alternating contraction/relaxation) Tonic
(continued contractions)
 Spasms are an involuntary contraction of short duration cause by reflex action cause by a blow
to the muscle.
 Myosits, Fasciitis, Tendinitis, Tenosynovitis, Bursitis: Classified in four stages; 1) Pain after
activity only
 2) Pain during activity, does not restrict performance
 3) Pain during activity, restricts performance
 4) Chronic, unremitting pain, even at rest
 Hypertrophy (increase in size)
 Atrophy (decrease in size)
Chapter 6
Bone Injury
 Primary constituents of bone are Ca+ Carbonate, Ca+ phosphate, collagen, and H2O. 60-70% of
bone weight provides stiffness and strength resist compression/tension, Collagen provides bone
with some of its flexibility. Aging cause the loss of Collagen and increase the bone brittleness.
 Bone growth will continue as along the epiphyseal plates exist. Most close around 18 but could
be present until 25. (Bone diameter continues for life)
 Bone is constantly rebuilding, some cells build while the others resorb bone; cells that form new
bone are call osteoblasts and the ones that resorb are called osteoclasts. (the balance between
the two are equal until the age of 40’s women and 60’s for men)
 Bone is at its strongest in Compression and weakest in Shear.
Chapter 6
Bone FX Types
 Tibial Fx (Torsional and bending)
 Spiral Fx (Shear/Tension)
 Impacted Fx (Compression force) fx on opposite side
 Greenstick Fx (child due to high levels of Collagen, more flexible) bending/torsion forces
 Avulsion Fx (tensile) tendon or ligament pulling away from the bone.
 Stress Fx (micro trauma)
 Chapter 6
Epiphyseal Injury Classifications
 Type I: Compete separation of the epiphysis from the metaphysis with no fx
 Type II: Separation of the epiphysis and a small portion of the metaphysis
 Type III: Fx of the epiphysis
 Type IV: Fx of the part of the epiphysis and metaphysis
 Type V: Compression of the epiphysis w/o fx, resulting in compromised epiphyseal function.
Chapter 6
Bone Healing
 Three Phase healing:
 Acute inflammatory: Last 4 days results formation of a hematoma, vasodilation, edema,
chemical changes.
 Repair/Regeneration Phase: Osteoblasts build new bone and osteoclasts resorb damage bone
tissue. A callus is formed between the fx bone (Callus is weak immature bone tissue that
strengthens with remodeling) Direct bone healing: When bone fx are immobilized in direct
contact with both ends, this enables an interwoven bone tissue to be deposit w/o a callus build
up.
 Maturation and Remodeling Phase: the osteoblasts activity on the concave is (Compress side)
and osteoclasts on the convex side (tension) continue until shape and strength returns to
normal. This takes up to 8 weeks.
Chapter 6
Nerves Injury Classification
 Spinal nerve is formed from Ant. /Post roots that unite to form the intervertebral foramen.
Posterior branches (Afferent) sensory nerves transmit to skin, tendons, ligaments and muscle.
 Anterior branches (Efferent) motor nerves transmit control signal to the muscle (highly
myelinated)
 Tensile/ Compression forces: most common injuries. Tensile: high speed accidents and football
collisions (stingers).
 Grade I: Neurapraxia (mild lesion) conduction block, temporary loss of sensation/motor.
Recovery within few days to weeks
 Grade II: Axonotmesis disrupts the axon myelin sheath, significant motor loss and mild sensory
deficits that last at least two weeks. Axonal growth occurs at a rate of 1-2mm per day.
 Grade III: Neurotmesis severe injury with poor prognosis, with motor and sensory deficit
persisting up 1 year. Surgery is sometime need to avoid poor or imperfect regeneration.
 Nerve regeneration rate is 1mm per day or about 2.5cm per month.
Soft Tissue Healing
Inflammatory Phase (0-6days)
 The acute inflammatory response is of relatively brief duration and involves activities that
generate exudates- plasma like fluid that exudes out of tissue or its capillaries and is composed
of protein and granular leukocytes (white blood cells).
 In the Chronic inflammatory response is of prolonged duration and involves the presence of
nongranular leukocytes and the production of scar tissue.
 Soft Tissue Healing
Inflammatory Phase (0-6days)
 The acute phase involves three mechanisms that act to stop blood loss from the wound:
 1). Local vasoconstriction occurs, lasting a few seconds to as long as 10 min. Larger vessels
constrict due to neurotransmitters and capillaries and smaller arterioles and venules constrict
due to the influence of serotonin and catecholamines released from platelets. The resulting
reduction in the volume of blood flow in the region promotes increased blood viscosity or
resistance to the flow, which further reduces blood loss at the injury site.
 2). The platelet reaction provokes clotting as individual cells irreversibly combine with each
other and with fibrin to form a mechanical plug that occludes the end of a ruptured blood
vessel. The platelets also produce an array of chemical mediators in the inflammatory phase:
serotonin, adrenaline, noradrenaline, and histamine. Also ATP is use for energy in the healing
process.
 Soft Tissue Healing
Inflammatory Phase (0-6days)
 3). Fibrinogen molecules are converted into fibrin for clot formation through two different
pathways. Following vasoconstriction, vasodilation is brought on by a local axon reflex and the
complement and kinin cascades, approximately 20 proteins that normally circulate in the blood
in inactive form become active to promote variety of activities essential for healing.
Phagocytosis- is the activation of neutrophils and macrophages to rid the injured site debris and
infectious agents. As the blood flows to the injured area slows, these cells are redistributed to
the periphery, where they begin to adhere to the endothelial lining. Mast cells and basophils are
also stimulated to release histamine, further promoting vasodilatation. Bradykinin also
promotes vasodilation and increase blood vessel wall permeability, contributing to the
formation of tissue exudates.
 Approximately 1 hour post injury, swelling, or edema, occurs as the vascular walls become more
permeable and increased pressure within the vessels forces a plasma exudate out into the
interstitial tissues. These only happen for a few minutes in cases of mild trauma, with a return to
normal permeability in 20-30 minutes.
 Soft Tissue Healing
Inflammatory Phase (0-6days)
 More severe traumas can results in a prolonged state of increased permeability, and sometimes
result in delayed onset of increased permeability, with swelling not apparent until some time
has elapsed since the original injury.
 Mast cells are connective tissue cells that carry heparin, which prolongs clotting and histamine.
Platelets and basophil leukocytes also transport histamine, which serves as a vasodilator and
increases blood vessel permeability.
 Bradykinin, a major plasma protease present during inflammation, increases vessel permeability
and stimulates nerve endings to cause pain
Soft Tissue Healing
The Proliferative phase (3-21 days)
 The Proliferative phase involves repair and regeneration; it takes place for approximately 3 days
following the injury through the next 3 to 6 weeks. These processes include the development of
new blood, fibrous tissue formation, generation of new epithelial tissue, and wound contraction.
This happens when the hematoma’s size is sufficiently diminished to allow room for the growth
of new tissue.
 Soft tissue does not have the ability to regenerate new tissue, so it is replace with scar tissue.
Healing through scar formation begins with the accumulation of exuded fluid containing a large
concentration of protein and damaged cellular tissues. This accumulation forms a highly
vascularized mass of immature connective tissues that include fibroblasts, which are cells
capable of generating collagen.
 The developing connective tissue at the wound site is primarily Type I and III collagen, cells. Type
III collagen is useful in this stage because of its ability to rapidly form crosslink's that contribute
to stabilization of the wound site.
Soft Tissue Healing
Maturation Phase (up to 1 year)
 The maturation or remodeling phase involves newly formed tissue into scar tissue. This includes
decreased fibroblast activity, increased organization of the extracellular matrix, decreased tissue
water content, and reduced vascularity and normal histochemical activity. In soft tissue this
process begins at 3 week post injury.
 Type I and III continue to increase, replacing immature collagen resulting in contraction of the
wound. Although the epithelium has typically completely regenerated by 3-4 weeks, the tensile
strength of the wound at this time is only approximately 25% of normal strength. After several
months strength mat still be as much as 30 % below preinjury strength. The collagen turnover
rate in a newly healed scar is also very high, so that failure to provide appropriate support for
wound site can result in a lager scar.
 Scar tissue is fibrous, inelastic, and nonvascular; it is less strong and less functional than the
original tissue. The development of the scar also typically causes the wound to shrink, resulting
in decreased flexibility of the affected tissue. The tensile strength of scar tissue may continue to
increase for as long as 2 years post injury.
 Soft Tissue Healing
Maturation Phase (up to 1 year)
 Muscle fibers are permanent cells that do not reproduce in response to injury. Reserve cells in
the basement membrane of each muscle fiber that are able to regenerate muscle fiber following
an injury. Following severe injury, muscle may regain only about 50 % of its preinjury strength.
 Tendons and ligaments have few reparative cells, healing of these structures is a slow process
that can take more than a year. Regeneration is enhanced by proximity to other soft tissues that
can assist with supply of the chemical mediators and building blocks required. This is why the
isolated anterior cruciate ligament (ACL) has a poor change of healing. If tendons and ligaments
are under high tensile stress before scar formation is complete, the newly form tissues can be
elongated and cause joint instability.
 Because tendons, ligaments, and muscles hypertrophy and atrophy in response to mechanical
stress, complete immobilization of the injury leads to atrophy, loss of strength, and decreased
rate of healing in these tissues. Although immobilization may be necessary to protect the injury
tissues during the early stages of recovery, strengthening exercises should be implemented as
soon appropriate during rehabilitation of the injury.