acute/chronic inflam mm, ligament tendon healing Flashcards
Acute Inflammation
rapid host response lasting mins hours or days that serves to deliver leukocytes and plasma proteins such as antibodies to sites of infection or tissue injruy
Granuloma Formation:
Outcome of acute inflammation
then Progession to chronic inflammation
Some bacteria cant broken don and remain cenclosed within their macrophage host
Commonly occurs: substantial tissue damage, inability if the tissue to regenerate, extensive fibrinous exudate
Abscess formation: acute inflammation
a creamy yellow pus may accumulate in the wound or site of injury
Dead, dying neutrophils, broken down cells tissues & dead pathogens
Inflammation fails to clear this area of debris, collagen fibres may be laid down to wall off the sac of pus
Outcomes of inflammation:
Complete resolution
Healing: clearance or cessation of injurous stimuli
removal of exudate, fibrin, debris
Revascularisation
Remodelling
Cardinal Signs
redness, swelling, heat, pain
Complement
stimulates histamine release which attracts neutrophils and promotes phagocytosis
Leuoktrienes
are produced by mast cells and basophils and help phagocytes attach to pathogens
Prostaglandins
assist with inducing chemotaxis. They can intensify and prolong the pain caused by inflammation
Kinins
induce chemotaxis of leukocytes and prompt neutrophils to release lysosomal enzymes.
Kinins are responsible for much of the pain associated with inflammation
Chemical Mediators of Inflammation:
Histamine
promote vasodilation of local arterioles increasing blood flow to injured area
Removal and Repair stage of acute inflammation
step 3
Monocytes follow neutrophils to the injured area
Monocytes are poor phagocytes, after entering the tissues they swell and develop a large number of lyosomes becomig macrophages
Macrophages are the central cells in the disposal of cell debris as acute inflammation subsides
Recruitment: Phagocyte mobilisation
step 2
Leucocytosis: increase in neutrophils (WBC”S)
Margination: phagocytes’ cling to inner walls of endothelium.
Endothelium sprouts cell adhesion molecule’s that signal that is site of inflammation
Diapedesis: Chemical signalling prompts neutrophils (wbc’s) to squeexe b/w the endothelial cells of capillary walls
Chemotaxis: inflammatory chemicals released active the neutrophils,
within an hour neutrophils are collected at the stie and are devouring the foreign material
Events that occur during inflammation
(Recognition)
Step 1
Recognition:
1. Inflammatory chemical release
chemical alarm
INfmamaotry chemicals are released such as Histamine, kinins, Prostaglandins, Sedentary macrophages
Vascular events: Vasodialation, Increased vascular permeability(capillaries)
Chronic Inflammation
Prolonged duration (weeks or months) in whcih inflammation, tissue injury and attempts at repair co-exist, in varying combinations
Tissue Repair Ability, regenerative capacity
Extremely Well: Epithelial tissues, bone, areolar connective tissue, dense irregular connective tissue, blood forming tissue
Moderate: dense regular connective tissue, smooth muscle
Limited: skeletal mm, cartilage
None: cardiac muscle, nervous tissue in brain and spinal cord
Acute Inflammation
rapid host response lasting mins hours or days that serves to deliver leukocytes and plasma proteins such as antibodies to sites of infection or tissue injruy
Systemic Manifestations signs and symptoms
Malaise: tissue malnutrition due to higher overturn of proteins in chronic inflammatory process
Fever: due to presence of inflammatory mediators
Leukocytosis: greater number of white blood cells in blood due to persistent inflammation
Lymphadenitis: inflammation of lymph nodes
Depression: due to continuous pain associated with chronic inflammation
Frequent infections: due to compromised immune system
Chronic Inflammation:
duration, weeks months years,
Caridnal signs same however reduced
Predominant cells:
Outcome:
Marcophages, b and T lymphocytes, plasma cells and fibroblasts
chronicn inflammtion will be ongoing, unless the intial cause is removed
mechanincal stress, antiboides, foregin obect bacteria or chemical agent
Granuloma
Nodular lesion formed by collection of macrophages, lymphocytes, mononuclear cells and fibroblasts that constitutes a special form of chronic inflammation.
Chronic Inflammation morpholgical features
Infiltration with immune cells:
macrophages (innate immune system)
lymphocytes and plasma cells (adaptive immune system)
Progressive tissue destruction caused by the offending agent as well as the inflammatory cells
Fibrosis (scar tissue) formation by fibroblasts, in an attempt to heal the tissues
New blood vessel proliferation (angiogenesis) to assist blood supply to healing tissues
Aeitology of chronic inflammtion
persistent infections
Persistent mechanical injury
Prolonged exposure to toxic agents
Presence of a foreign body eg talc, splinter
Autoimmune diseases (self antigens)
Chronic Inflammation
prolonged inflammatory response, tissue destruction and repair proceed simultaneously
Granuloma
Nodular lesion formed by collection of macrophages, lymphocytes, mononuclear cells and fibroblasts that constitutes a special form of chronic inflammation.
Chronic Inflammatory cells
Plasma cells, macrophages, lymphocytes, fibroblasts
Tendon & Ligament Repair
Inflammation Stage (hours-days)
Haemostasis- bleeding is ceased
Acute inflammtion, stets stage for repair,
Inflammotry cells release cyotkines and growth factors
Ligament Strain Grades info
Grade 1, 0-50% fibre disruption, normal range
Grade 2- 50-80% fibre disruption, increase laxity however end point
Grade 3, compete tear of ligament, excessive joint laxity no firm end point.
Remodelling Phase (weeks to months)
Muscle Strain
Formation of mature contractile apparatus which fuse with existing myofibers
Attachment of new myofibre to intervening scar tissue
Repair Phase (days to weeks)
of muscle strain
Clearance of necrotic tissue by macrophages
Fibroblasts produce collagen which later develops into scar tissue
Myogenic reserve cells differentiate into myoblasts and begin repair of myofibre
MM strain, repair to myofibers Inflammation Phase (hours to days)
Haematoma fills the gap b/w the torn myofibers
Ruptured myo-fibres contract & sealed by a new sarcolemma
Infiltration by acute inflammatory cells
I
Muscle Strains grading
Grade 1: small no. fibres affected localised pain but no loss of strength
Grade 2: greater no. fibres affected with associated pain and weakness
Grade 3: complete tear of mm, considerable pain and complete loss of function
(biarthrodial Mm) hammies, quads, gastrocs
Acute vs Chronic Musclotendious injuries
Acute Mm, strain/tear
contusion
Acute Tendon, tear (partial/complete
Chronic: mm strain,
Chronic tendon injuires: tendionopathy, tendinits tendinosis, tensosynovitis
Osteopathic Implications of Mm, tendon and Ligament Injuries
Acute soft tissue
treatemtn within the first week
Acute Soft Tissue Injury Management- R.I.C.E
treatment within the first week -effleurage to reduce swelling, soft tissue, mechanical loading, examination and treatment of biomechanically related region, if bad after 5-7, consider MRI
Tendon & Ligament Repair
Remodelling Phase (weeks and months)
Collagen maturation beings: collagen type 3- collagen type 1
Alignment continues as ligament/tendin undergoes mechanincal loading
Cross-linking, increase strength of connective
becomes stronger but never at pre-injury strength
Repair Phase (days[weeks)
tendon and ligament repair
DENSE REGULAR
Proliferation of fibroblasts- synthesise new extracellular matrix and collagen fibres
Collagen formation consists of collagen type 3 which is smaller diameter than collagen type 1.
within few weeks collagen being to align along the long axis of the ligament in response to loading
Tendon & Ligament Repair
Remodelling Phase (weeks and months)
Collagen maturation beings: collagen type 3- collagen type 1
Alignment continues as ligament/tendin undergoes mechanincal loading
Cross-linking, increase strength of connective
becomes stronger but never at pre-injury strength
Osteopathic Implications
Return to daily activities or Sport- Specific Training
Clincal features if present 3-5 days post injury, recovery period greater than 4 weeks
Brusiing/haematoma, tenderness to palape, lack of complete ROM
Pain during isometric mm contraction
Osteopathic Implications
Risk Factors that predispose soft tissue injury
History, inappropriate training program
Overloading, freq, intensity
poor warm, cool down
ADLS, technique, equipment
Osteopathic Implications of Mm, tendon & Ligament Injures
Rehab
Rehab- tissue loading results in remodelling, maturation and alignment of connective and scar tissue
Mm strain, rehab, include strengthening, lengthening, speed and agility training
Ligament strain, joint rang emotion, proprioception, balance training and mm strength to increase joint stability
Osteopathic Implications of Mm, tendon and Ligament Injuries
Acute soft tissue
treatemtn within the first week
Acute Soft Tissue Injury Management- R.I.C.E
treatment within the first week -effleurage to reduce swelling, soft tissue, mechanical loading, examination and treatment of biomechanically related region, if bad after 5-7, consider MRI
