Synovium non synovial joints and bone physiology and diseases
1 / 32

Synovium, non-synovial joints, and bone physiology and diseases - PowerPoint PPT Presentation

  • Uploaded on

Synovium, non-synovial joints, and bone physiology and diseases. Lecture 8 Tuesday, January 30, 2007 Ref. Wheater’s Functional Histology Chapter 10, Ross and Pawlina Chapter 8, Chapter 6 Medical Physiology p. 1088-1090 Basic Pathology p. 756-761. Synovium.

I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
Download Presentation

PowerPoint Slideshow about ' Synovium, non-synovial joints, and bone physiology and diseases' - ophira

An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.

- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript
Synovium non synovial joints and bone physiology and diseases

Synovium, non-synovial joints, and bone physiology and diseases

Lecture 8

Tuesday, January 30, 2007

Ref. Wheater’s Functional Histology Chapter 10, Ross and Pawlina Chapter 8, Chapter 6

Medical Physiology p. 1088-1090

Basic Pathology p. 756-761

Synovium diseases

  • Specialized connective tissue not epithelium

    • Surface is a discontinuous layer up to 4 cells deep.

    • Lining cells are not connected by junctional complexes.

    • Lining cells are not resting on basement membrane.

    • Contains vessels and nerves.

    • May be loose (areolar), fibrous, adipose, folded, or villi.

  • Two synovial cell types

    • Type A synoviocytes - majority, plump, have numerous lysosomes

    • Type B synoviocytes - fibroblast-like, secretory

Synovium wfh 10 29 plump cells are type a fibroblast like cells are type b
Synovium WFH 10.29 diseasesPlump cells are type A; fibroblast like cells are type B

Synovial fluid
Synovial Fluid diseases

  • A specialized form of ECM

    • Hyaluronic acid, glycoproteins,

      • Secreted by type B synoviocytes

    • Fluid component is a transudate from capillaries

  • Diffusion of oxygen, nutrients and metabolites between blood and synovial fluid.

  • Viscous, transparent

  • Few leukocytes (<100/µl)

Non synovial joints
Non-synovial joints diseases

  • Dense fibrous

    • Syndesmoses e.g. sutures of skull

    • Become synostoses after replacement by bone.

  • Hyaline cartilage

    • Synchondrosis or primary cartilaginous joint

    • In adult human- vertebrocostal ribs with the sternum

  • Fibrocartilage

    • Symphyses or secondary cartilaginous joints

    • Apposing bones are covered by hyaline cartilage and directly connected by fibrocartilage.

    • e.g. pubic symphysis and intervertebral disks

Intervertebral joints diseasesWFH 10.29Two types: fibrocartilage between bodies of vertebrae andsynovial between vertebral arches

Intervertebral disc
Intervertebral disc diseases

  • Annulus fibrosus

    • Concentric rings of fibrocartilage surround a central cavity

  • Nucleus pulposus

    • Viscous fluid supporting tissue that is a remnant of the notochord. (Notochord is derived from mesoblast of embryo and defines the primitive axis of the body)

    • ECM consists of ground substance only

    • Cells suspended in fluid are physaliphorous cells.

    • Acts as a shock absorber.

Disc herniation
Disc herniation diseases

  • Annulus fibrosis weakens with age.

  • Compression may cause herniation of the nucleus pulposus.

  • Weakest ligaments are posterior lateral.

  • Extruded material puts pressure on spinal cord or spinal nerve root.

  • Herniations are usually in the lumbar or cervical areas.

Bone physiology
Bone physiology diseases

  • Remodeling is continual process

    • 80% total bone is compact

    • 20% is trabecular-higher fractional rate of turnover

  • Osteocytic osteolysis

    • Transfer of Ca++ from interior to surface via interconnected osteocytes

  • Nutritional requirements

    • Vitamin C, vitamin D, Calcium

Normal bone formation resorption
Normal bone formation/resorption diseases

  • Osteoblast

    • Makes osteoid

    • Influences osteoclast differentiation via

      • RANKL (also on stromal cells and T cells) interaction with RANK on precursor monocytes

      • Secretion of M-CSF

    • Makes osteoprotegerin that binds to RANK ligand preventing RANK ligand from stimulating osteoclasts

    • Has receptors for hormones and cytokines, IL-1, TNFa and secretes mediators that influence osteoclast activity

  • Factors released from the digested bone matrix (cytokines, growth factors) trigger osteoblast to deposit an equivalent amount of new bone.

Bone pathology overview
Bone Pathology Overview diseases

  • Abnormalities of quality/quantity of bone

    • Osteoporosis, osteopetrosis, osteomalacia

    • Osteogenesis imperfecta

    • Paget’s disease

  • Infection

    • Osteomyelitis (bacterial, fungal)

  • Neoplasia

    • Primary malignant, benign, or metastatic

Osteoporosis diseases

  • Relative excess of osteoclastic function.

  • Net loss of bone.

  • Trabecular bone is more active metabolically and lost more rapidly.

  • Increased incidence of fractures

    • Forearm, vertebrae, and hip

Types of osteoporosis
Types of osteoporosis diseases

  • Involutional-primary, senile

  • Disuse

    • Immobilization (local or weightlessness)

  • Secondary

    • Drug related e.g. corticosteroids

      • Corticosteroids increase the production of RANK ligand but decrease the production of osteoprotegerin-- bone loss

    • Endocrine

    • Gastrointestinal

    • Neoplasia

Involutional osteoporosis
Involutional osteoporosis diseases

  • Most common

  • Affects both men and women

  • Peak bone mass is reached in early adulthood and depends on

    • Genetic factors (vitamin D receptor)

    • State of nutrition

    • Level of physical activity

    • Hormonal status

Estrogen s effects on bone
Estrogen’s effects on bone diseases

  • Estrogen inhibits secretion of IL-1, IL-6, and TNFa

  • Estrogen stimulates production of TGFb

    • TGFb increases apoptosis of osteoclasts

  • Net effect of estrogen treatment is to reduce or arrest bone loss

  • Other inhibitors of osteoclasts are bisphosphonates

Osteopetrosis diseases

  • Rare, hereditary, autosomal recessive or dominant

  • Stone-like bone, solid on radiographs

  • Actually brittle, fractures easily

  • Pressure on nerves

    • Optic nerve atrophy

  • Caused by osteoclast dysfunction

  • Lack of bone marrow

    • Increased infections, lack of precursors for osteoclasts

Rickets and osteomalacia
Rickets and osteomalacia diseases

  • Defect in matrix mineralization

  • Often due to vitamin D deficiency

  • Rickets in children

    • Weakness and bowing of weight-bearing bones

    • Defects in teeth

    • Hypocalcemia

  • Osteomalacia in adults

    • Vulnerable to fractures, especially vertebrae and femoral neck

Actions of vitamin d
Actions of vitamin D diseases

  • Increase calcium absorption from GI tract

  • Increase reabsorption of calcium in kidneys

  • Stimulate synthetic activity of osteoblasts

    • secrete osteocalcin which binds Ca++

    • secrete M-CSF which causes proliferation of osteoclast precursors

  • Required for mineralization of matrix

  • With other hormones controls calcium metabolism

Osteogenesis imperfecta
Osteogenesis Imperfecta diseases

  • A group of diseases due to deficiencies in synthesis of type I collagen

    • Autosomal dominant or recessive

    • In some forms mutant allele acts as a dominant negative

    • Fragile, brittle bones

    • Joint laxity

    • Eyes- blue sclera

    • Teeth

  • 4 major types-most common is autosomal dominant

  • Variable signs from mild to lethal in utero

    • suspicion of child abuse

Bone disease associated with hyperparathyroidism
Bone disease associated with hyperparathyroidism diseases

  • Excess parathyroid hormone activates osteoclasts

  • Primary

    • Rare, tumor of parathyroid gland

  • Secondary

    • Renal disease factors in addition to high PTH:

      • Decreased production of vitamin D.

      • Decreased calcium absorption from gut.

      • Metabolic acidosis.

    • Paraneoplastic syndrome

    • Nutritional

      • Lack of calcium in diet

Paget disease osteitis deformans
Paget Disease (Osteitis Deformans) diseases

  • Etiology unknown, possibly paramyxovirus

    • Higher incidence in whites in England, France, Australia, New Zealand, USA

    • Rare in Scandinavia, China, Japan, and Africa

  • Affects middle-aged or older adults

  • Often asymptomatic

  • 3 phases (repeating and overlapping)

    • Osteolytic, haphazard, inappropriate osteoclastic activity

    • Mixed- osteolysis and rapid bone formation

    • Osteosclerotic

  • Net effect more bone (woven bone), but weaker

    • Pain and predisposition to fractures and tumors

Paget Disease Mosaic pattern PBD 28-13 diseasesBP 21-5New bone is woven bone--lacks normal lamellar architecture.

Osteomyelitis infection of bone and marrow
Osteomyelitis (infection of bone and marrow) diseases

  • Acute osteomyelitis

    • Pyogenic bacteria

      • 80-90% are Staphylococcus aureus

      • Pneumococci and gram negative organisms

      • Mixed bacteria -- common after trauma

  • Route

    • Hematogenous - more common in infants and young children

    • Penetrating injury- compound or open fracture

    • Extension from adjacent infection

  • Sequestrum (necrotic bone)

    • complicates healing

    • Acts as a foreign body and haven for microorganisms

Chronic osteomyelitis with sequestrum bp 21 3 pbd 28 19 often draining tracts open onto the skin
Chronic osteomyelitis with sequestrum diseasesBP 21-3PBD 28-19Often draining tracts open onto the skin.