Biomechanics of Body Tissue PDF

Biomechanics of Body Tissue Huntington University Nate Short, PhD, OTD, CHT, FAOTA  Part I: Bone 2 main structural components: 1) Collagen: organic material connective tissue (40% dry weight) 2) Hydroxyapatite: calcium based mineral (6...

Biomechanics of Body Tissue Huntington University Nate Short, PhD, OTD, CHT, FAOTA  Part I: Bone 2 main structural components: 1) Collagen: organic material connective tissue (40% dry weight) 2) Hydroxyapatite: calcium based mineral (60% dry weight) Bone makeup changes with age: Woven bone: immature bone in children; random cartilage More flexible & resilient Increased flexibility in children  Objectives Explore properties of various body tissues & relationship to function & occupation Examine types of muscle tissue & characteristics that affect force production Understand external factors that affect strength & function of tissue  What is wrong with these hands? Case courtesy of Ryan Thibodeau, Radiopaedia.org, rID: 167401 Case courtesy of Frank Gaillard, Case courtesy of Ian Radiopaedia.org, rID: 7546 Bickle, Radiopaedia.org, rID: 46441  Maturing Process Mineralization: Osteoclasts: tunnels into bone Osteoblasts: line tunnels with collagen fibers Collagen mineralized Osteocytes: older osteoblasts; control mineralization process  Osteons Result of osteoclast & osteoblast activity: Osteons: series of tubes lined with bone; primary structural unit of bone Also provide a passageway blood vessels & nerves  Mature Bone When osteons replace woven bone, bone is considered “mature” 2 primary categories: Cortical Bone: hard, dense; found in mid-shaft of long bones Cancellous Bone: “spongy” bone filled with spaces; found in bone ends Bone type distributed based on function  Bone Shape Long bones: Diaphysis (central shaft) Epiphysis: rounded end to provide articulation Metaphysis: between diaphysis & epiphysis; part of growth plate & ossifies with age. Periosteum: outer covering of bone  Bone Strength Individual bone strength depends on mineral composition, density, & structure of individual bone Elasticity: collagen makeup of a bone gives each bone a certain degree of viscoelasticity More Collagen = Increased elasticity Less collagen = more brittle  Bone Strength Increased use/weight-bearing = increased strength Increased osteoblast activity With age & decreased activity, bone density & strength decrease Estimates suggest resistance to fracture decreases 4% every 10 years Osteoporosis: loss of bone density caused by failure of osteoblasts to lay down new bone in pores created by osteoclast (regulated by hormones)  Fracture Healing Case courtesy of Matt Skalski, Radiopaedia.org, rID: 57418  Part II: Skeletal Muscle Made up of progressively smaller units:  Sarcomeres: contain myofilament chains Myosin: thick with “oars” Actin: long thin strands https://slideplayer.com/slide/13928821/  Connective Tissue Muscles also contain non-contractile connective tissue that binds muscle fibers together (fascia): Epimysium: surrounds entire muscle belly Perimysium: surrounds individual fascicles of muscle fibers Endomysium: surrounds individual muscle fibers Connective tissues converge at ends of muscle to create tendons which attach muscle to bone Also provides tensile strength  Muscle Contraction Muscle Contraction: electrical stimulus from motor unit Calcium: binds w/ protein troponin which causes actin to bind with myosin via “cross-bridges” Strength of contraction depends on number of cross-bridges which are increased with frequency of muscle stimulus.  Muscle Contraction Muscle relaxes as stimulus ceases Myofilament contraction progresses through muscle fibers, fascicles, & entire muscle belly, producing contraction Muscle contraction produces pull on bone via tendon attachment & creates motion at associated joint  Fiber composition & orientation affects contraction: Number of sarcomeres in muscle fiber Length of muscle fibers (contract 50-60% total length) Muscle fiber arrangement: Parallel: fibers parallel to entire muscle w/ long fibers Pennate: shorter fibers connected to tendon that extends throughout muscle Muscle Design  Muscle Moment Arm Muscle with longer moment arm (distance from force to joint) must shorten more than muscle with shorter moment arm to produce same motion: Example: biceps vs brachioradialis for elbow flexion Biceps has shorter moment arm & requires less shortening to produce elbow flexion  Muscle Strength Many factors affect strength Different ways to interpret strength: Amount of manual resistance sustained without motion Amount of weight a person can lift Dynamometer to measure force exerted  Muscle Strength Factors that affect muscle strength include: Muscle size Muscle moment arm Stretch of muscle Contraction velocity Level of Fiber Recruitment Types of Muscle Fibers  Muscle Size Most important factor determining tensile strength produced (length X width) Wider muscle, more muscle fibers present to contract Longer the muscle, more potential excursion of fibers PCSA (physiological cross-sectional area): cross-section that passes through ALL fibers  Effects of Exercise on Muscle Bulk* Resistance training leads to microtrauma (injury) to muscle proteins Complex cellular process causes “repair” & growth of muscle fibers More muscle proteins synthesized & creation of new sarcomeres Prolonged process…weeks or months to see physical changes Influenced by type/frequency of resistance, diet, lifestyle factors *Kwon, Y., and Kravitz, L. (2004). How do muscles grow? [Peer commentary on the article "Cellular and molecular regulation of muscle regeneration" by S.B. Charge and M.A. Rudnicki]. Retrieved from http://www.unm.edu/~lkravitz/Article%20folder/musclesgrowLK.html.  Muscle Length & Strength Strength depends on cross-links of actin/myosin chains Number of cross-links depends on proximity of actin/myosin chains Resting Length: full length of actin/myosin strands in contact As muscle shortens, contraction force decreases as the actin/myosin chains interfere with one another (“runs out of room”) As muscle lengthens, fewer cross-links are present In most cases, maximum strength is present in mid-range Myofascial Trigger Points (MTrPs) Ball, A.; Perreault et l. (2022) Ultrasound Confirmation of the Multiple Loci Hypothesis of the Myofascial Trigger Point and the Diagnostic Importance of Specificity in the Elicitation of the Local Twitch Response. Diagnostics, 12, 321.  Parallel Elastic Components As contractile fibers of muscle decrease in efficiency with muscle stretch, non-contractile, or passive, structures exert a pull against stretch (spring effect) Structures include connective tissue throughout muscle & related tendons at each end of muscle As muscle stretches, active force contraction decreases however passive tension of parallel elastic components increases  Clinical Application: Active Insufficiency Length affects ability to contract/produce force Active Insufficiency: muscle cannot shorten further Make a fist with your wrist flexed; Now try with wrist extended: Which is easier? Why? Flexion shortens wrist/digit flexors causing active insufficiency Extended wrist stretches flexors & increases passive tension, increasing muscle contraction force Active vs. Passive Insufficiency  Contraction Velocity Change in length of a muscle per unit of time Inversely related to contractile strength As contraction velocity increases, contractile force decreases Isometric Contraction: zero contraction velocity – no visible change in muscle length Produces more force than concentric contraction of same magnitude  Contraction Velocity Eccentric Contraction: contraction with lengthening of muscle Lowering weight w/ elbow = eccentric biceps contraction Capable of generating 1.5 – 2x maximum strength vs. isometric/concentric Also results in more muscle injuries Types of Muscle Contraction  Level of Fiber Recruitment Muscles made up of smaller units called motor units Motor nerve & fibers innervated by particular motor unit When muscle contracts, it recruits only amount of motor units needed to achieve strength of signal it receives from brain  Level of Fiber Recruitment Single stimulus produces muscle twitch – as stimulus is repeated, single twitches collectively produce a sustained (tetanic) contraction Muscle may produce a maximal (all motor units recruited) or submaximal (partial recruitment of motor units) contraction Muscle with greater mechanical advantage for motion requires less motor unit recruitment for needed muscle contraction  Muscle Fiber Type Varying degrees of contractile properties w/ mix of fiber types Metabolic classification system classifies muscle fibers as: Type I: Slow velocity; low force; fatigue resistant Type IIa: Moderate velocity, variable force, somewhat fatigue resistant Type IIb: Fast velocity, high force, quickly fatigue  Muscle Adaptations Activity Level: Increased activity causes muscle hypertrophy & increased cross- section of muscle bulk Decreased activity causes atrophy & decreased cross-section of bulk Prolonged Stretch: Induces protein synthesis & sarcomere production Increased overall strength of muscle fibers  Prolonged Shortening/Immobilization: Atrophy acceleration & loss of sarcomeres Adaptive Shortening: change in muscle’s resting length as a result of prolonged positioning Disrupts agonist/antagonist muscle balance & affects joint motion/function Example: Tightness of pec minor Muscle tissue is highly adaptive to external forces!!  Muscle Action & Classification Agonist muscle Prime mover (primary contributor) Antagonist muscle Contrasting/inhibiting muscle Fixators: Provide stability at origin Synergist: Muscles that assist prime mover  Force Couples Muscles that work together Act in different directions to produce same motion or stabilize a joint  Summary Muscles of our body provide support to our bone structure & allow joint motion & function of extremities Muscle strength is multi-factorial depending on muscle bulk, number of fibers, moment arm, fibers recruited, & joint position All of these factors must be considered when dealing with muscle dysfunction as a clinician  Part III: Articular Cartilage (Hyaline) Cartilage is living material composed of: Chondrocytes: only cells in cartilage; produce/maintain cartilage components Water: 70-85% of total weight of entire tissue Proteoglycans: protein core with attached sulfates Collagen: fibrous protein makes up 60-70% of dry weight Superficial: high permeability/water; horizontal collagen fibers Middle: random collagen fibers Deep (Radiate): perpendicular collagen; less water Calcified (tidemark): between cartilage & subchondral bone  Cartilage Nutrition Cartilage has no blood vessels & receives nutrition from diffusion of nutrients in synovial fluid as it is compressed Nutrients pass through superficial layers easily & to deeper layers with extended compression Cartilage aneural & not direct source of pain with arthritis Also avascular with limited ability to repair itself when damaged  Cartilage Compression Cartilage is designed to absorb compressive & sheer forces between bones as we move & bear weight through our joints: Proteoglycans have a negative charge & when compressed, repel each other, resisting compressive force Water content compresses throughout cartilage matrix allowing it to absorb compressive forces  Deeper layers of cartilage are progressively less permeable With rapid compressive loads, cartilage acts as single, elastic solid & superficial layers absorb most of compressive force (running) With extended compression, cartilage displaces as fluid content goes into deeper layers for increased support (extended stand)  Cartilage Damage With age, cartilage weakens & decreases in O2 content, wearing down more quickly Can also be damaged by excessive/repetitive loading or shear forces with acute injury May not be symptomatic until affects reach surrounding joint structures or underlying bone as cartilage is aneural  When cartilage breaks down, compressive forces on actual bone increase & cause further breakdown Pain associated with OA & cartilage breakdown is generally inflammation of surrounding joint capsule Causes: Hereditary predisposition Excessive/Repetitive loading – obesity, strenuous work Injury – traumatic osteoarthritis  Summary Articular (Hyaline) cartilage provides “cushion” between synovial joints Capable of functioning for lifetime but susceptible to age- based changes & damage due to excessive & repetitive loading Many factors lead to cartilage breakdown and subsequent osteoarthritis  Part IV: Tendons/Ligaments Made up of connective tissue & classified as dense, regular connective tissue. Fibers densely packed & resistant to stretch Provide joint stability to provide & maintain form in body Tendons – attach muscle to bone Ligaments – attach bone to bone  Composition: Fibroblast: manufactures proteins Extracellular Matrix: collagen and elastin fibers Collagen: primary fibrous component – strength similar to steel  Structure Tendons ligaments, like muscle, are made up of increasingly smaller fibers that make up entire unit:  Tendon/Ligament Strength Tendons & ligaments subjected to various degrees of tensile (pulling) stress Recall that tendons have bone & muscular attachments & ligaments have two bone attachments Therefore, tendon stress is related to muscle stress  During normal motion, elongation does not exceed 4% total length These stresses are elastic & tissue returns to its normal length Beyond this stress, tendon & ligament tissue may have plastic response & be unable to return to original shape & length Beyond 8% elongation, tendon or ligament will typically rupture – may rupture tissue itself or pull away portion of bone (avulsion) Avulsion Fracture Case courtesy of Francis Deng, Radiopaedia.org, rID: 71785  Temperature Increasing heat of tendon/ligament tissue: Below 37ºC: no change in viscoelasticity of tissue (normal) 37ºC - 40ºC: thermal transition; stress relaxation increases (therapeutic temperature) 40ºC & above: structural damage to collagen; possible rupture 59º-60ºC: irreversible shrinkage; used in thermal capsulorraphy to tighten lax joint capsule/ligament  Age-Based Changes Maximal tissue strength is reached at skeletal maturity (when growth plates close) Gradual decline throughout adulthood into old age Hormonal Changes: Cortisol – excessive levels reduce collagen production Relaxin – produced during pregnancy to increase extensibility of pelvic ligaments for women to give birth  Clinical Application: Immobilization Prolonged tendon/ligament immobilization reduces strength of tissue & decreases collagen synthesis TISSUE ADAPTS TO POSITION AND FORCE PLACED ON IT!! Clinical Application: safe position of hand for immobilization Maintains tension on collateral ligaments & intrinsic muscles  Clinical Application: Post-Immobilization After prolonged immobilization/casting, soft tissues shortened & are tight but are mechanically weaker & more susceptible to rupture Shortened tissues respond MUCH better to prolonged, low-load stretching than aggressive quick loading which can damage weakened tissue How can we provide low-load, prolonged stretch in and out of the clinic?  Tendon/Ligament Healing Tendons & ligaments have varying degrees of blood supply Have arterioles from adjacent muscle & anastomoses (connections) with small vessels in tendon sheaths which surround tendons & provide protection & tendon gliding  Tendon/Ligament healing has 4 overlapping stages: Hemorrhagic: gap filled with a blood clot Inflammatory: macrophages destroy debris, neovascularization Proliferative: fibroblasts produce new collagen & other proteins Remodeling: collagen organizes, scar strengthens Healing varies depending on blood supply and external forces acting on tissue  Clinical Application: Flexor Tendon Repair Soft tissue injuries & surgical repairs involve local scarring that may develop adhesions with surrounding tissues Research shows that for strong flexor tendon repairs, early protected active motion promotes tendon gliding & limits adhesions (Trumble et al., 2010) Griffin et al., 2012 N. Short, personal photo  Summary Tendons/ligaments provide stability to joints of body at rest & with motion Collagen is primary tensile component of tendon & ligament tissue Strength is affected by age, nutrition & blood supply to tissue, & external stresses applied to tissue Damage or imbalance to tendons & ligaments can affect kinematics & functional motion of joints of body  References Griffin, M., Hindocha, S., Jordan, D., Saleh, M., & Khan, W. (2012). Suppl 1: An overview of the management of flexor tendon injuries. The Open Orthopaedics Journal, 6, 28. Kwon, Y., and Kravitz, L. (2004). How do muscles grow? [Peer commentary on the article "Cellular and molecular regulation of muscle regeneration“ by S.B. Charge and M.A. Rudnicki]. Retrieved from http://www.unm.edu/~lkravitz/Article%20folder/musclesgrowLK.html. Oatis, C. A. (2009). Kinesiology: The mechanics and pathomechanics of human movement. 2nd ed. Philadelphia, PA: Lippincott,Williams, and Wilkins. Short, N., Vilensky, J., & Suarez-Quain, C. (2021). Functional Anatomy for Occupational Therapy. Books of Discovery. Images, unless otherwise cited, are courtesy of Books of Discovery (copyright 2021) and may not be used without expressed written consent