Connective Tissue Proper Flashcards
Cell types of CT proper
fibrocyte
fibroblast
CT Proper fibers
collagen, elastic and reticular fibers
CT proper matrix
Ground substance (PGs, GAGs) Tissue fluid
Fibrocyte
Quiescent cell, low activity for maintaining fibers and ground substance of ECM
Stimulated to become active (fibroblast) upon injury or tissue damage (for wound healing)
Fibroblasts
Intense synthetic activity for collagen and ground substance molecules
Cytoplasm
- large amounts of ER
- well developed Golgis
ECM Molecules
Collagen-main fiber; resists tensile force to provide strength to tissue
Elastin-provide resiliency allows stretching
Proteoglycans-filamentous protein core with attached GAGs; provide framework
Glycoproteins-PRO bound to small CHO molecues provides framework for ECM
Collagen is what percent of dry weight
30%
Four groups of collagen
collagen that forms fibrils
fibril-associated collagen
collagen that forms anchoring fibrils
collagen that forms networks
Type 1: fibroblast/osteoblast
Bone tendon ligaments= resist tension
Type 2: chondroblast
cartilage= resist compressive forces, shear forces at surface
Type 3: fibroblast
pliable tissues; blood vessels, uterus, GI tract, skin, muscle=structural maintenance in expandable organs; initial collagen of wound repair
Type 4: fibroblast
basement membranes; muscle cells, epithelial cells, adipoctyes=support of delicate structures; filtration
Tropocollagen
protein unit that polymerizes to form collagen fibrils
differences in the chemical structure of these polypeptide chains are responsible for the various types of collagen
Collagen fibrils
thin, elongated structures
several micrometers long (type 2)
Collagen fibers
fibrils aggregate to form fibers (types 1 and 3)
collagen bundles
collection of collagen fibers (type 1)
Type 2=no fibers/bundles
Type 4=no fibrils or fibers
Ehlers-Danlos Type VII
decrease in procollagen peptidase activity
increased articular mobility; frequent sublux
Scurvy
lack of Vit. C (no procollagen formed) Ulceration of gums; hemorrhages; weak bones
Osteogenesis imperfecta
Change of one nucleotide in genes for collagen Type I
Spontaneous fractures;
Cardiac insufficiency
Keloid scarring
Hyper-production of collagen
Local swelling that forms in scars of the skin
Elastic Fibers AAs
Amino acids: Desmosine and Isodesmosine provide covalent bonds that form cross-links between elastin fibers
5x more extensible than rubber
Elastic fibers
synthesized by: fibroblast; smooth muscle cells
Located: pliable tissue i.e. blood vessels, uterus, etc.
main fxn: elongation w/o deformation
With advanced age:
Elastic fibers are replaced by Type I collagen; tissues lose elasticity (more easily deformed)
Marfan Syndrome
Genetic mutation; disrupts proper elastic fiber synthesis
Tissues rich in elastic fibers are most affected
(i.e. large/medium-sized arteries contain large amounts of elastin)
Creates non-compliant (brittle) tissue, especially arteries, that are prone to rupture
Ground substance fxn
Fills spaces between cells and fibers of CT and provides a pathway for waste and nutrient exchange
Fluid provides for lubrication of ECM
Provides a barrier to penetration of foreign (infectious) agents
Tendons Fxn
Function
Connect muscle to bone
Transmit mechanical force generated by muscle to bone to create joint movement
Tendons Innervation
Innervation Golgi Tendon Organ (GTO) Pain fibers (free nerve endings)
Tendons nutrient supply
Nutrient supply
Limited vascular supply
Synovial membrane (tendon sheath)
Synovial sheath layers
dense irregular CT
Visceral layer
Parietal layer
b/w the layers is a cavity for fluid
provides lubrication for tendons to slide w/in their fibrous sheath
Ligament Functions
Connects bone to bone
Controls and guides normal movement of joints
Limits excess motion
Contain more elastic vs. tendons
Ligament Innervation
Proprioceptive fibers
Free nerve endings (pain)
Ligament nutrient supply
Limited vasculature
Loose CT proper with aging
decreased elasticity
decreased hydrophilic capabilities
decreased ROM
increased work to overcome inelasticity
Dense Irregular CT proper with aging
decreased elasticity
decreased hydrophilic capabilities
decreased ROM
increased work to overcome inelasticity
Dense Regular CT proper with aging
decreased in size decreased protein synthesis decreased tensile force decreased load to failure fiber degradation
Imobilization changes in CT proper
generates contracture
Tendons and ligaments immobilized
decrease tensile force generation
decreased load to failure
decreased GAGs/H20
Increased cross-linking of collagen: makes them less flexible
Synovial sheath becomes adherent to tendons–preventing full ROM
CT proper changes with acute activity
increased temperature and increased elasticity micro tears (that are repaired): create stronger and larger ligament/tendon prevention of cross links to maintain extensibility
CT proper changes with chronic activity
Hypertrophy of ligament/tendon – allows the CT to transmit (accept) increased amounts of force
↑ deposition of type I collagen, ↑ load to failure
↑ ROM if stretched
