|
|
| (68 intermediate revisions by 5 users not shown) |
| Line 1: |
Line 1: |
| − | <big><center>[[Bones|'''BACK TO BONES''']]</center></big>
| + | ==Changes to normal structure== |
| | | | |
| | + | ===Damage to Periosteum=== |
| | + | *Invokes a hyperplastic reaction of the inner layer |
| | + | *Is painful |
| | + | *Exostoses can remodel or remain |
| | | | |
| − | ===Introduction===
| + | Lifting of periosteum causes new bone formation below |
| − |
| |
| − | *Bone is a hard, highly specialised connective tissue
| |
| − | *Consists of interconnected cells embedded in a calcified, collagenous matrix
| |
| − | *Living, dynamic, responsive tissue, growing and remodelling throughout life
| |
| − | *Pathogenesis of many bone diseases is complex
| |
| − | **May involve genetic defects, diet or infection or a combination of these
| |
| − | *'''Function''':
| |
| − | **Support/protection
| |
| − | **Movement
| |
| − | **Stem cell storage
| |
| − | **Mineral storage
| |
| | | | |
| | + | Circumferential incision (e.g. during [[Bones Fractures - Pathology|fracture]]) |
| | + | *Longitudinal bone growth results |
| | + | *May be only on one side where periosteum is damaged |
| | + | **Used by surgeons to treat [[Angular Limb Deformity|angular limb deformities]] |
| | | | |
| − | ===Normal structure=== | + | ===Physis (Growth plate)=== |
| | | | |
| − | *'''Cells''' | + | *Site of many '''congenital''' or '''nutritional''' bone diseases in the growing animal |
| − | **'''Osteoblasts'''
| + | *'''Open''' in neonates and growing animals |
| − | ***Mesenchymal cells
| + | **Chondrocyte proliferation balances cell maturation and death |
| − | ***Arise from bone marrow stroma
| + | *'''Closes and ossifies''' at maturity |
| − | ***Produce bone matrix = '''osteoid''' | + | **Regulated by androgens |
| − | ***Cell membranes are rich in alkaline phosphatase (ALP) | + | *If growth teporarily stops -> layer of bone seals the growth plate -> moves into metaphysis when growth resumes -> forms '''Harris lines''' |
| − | **'''Osteocytes'''
| |
| − | ***Osteoblasts that have become surrounded by mineralised bone matrix | |
| − | ***Occupy cavities called '''lacunae''' | |
| − | **'''Osteoclasts'''
| |
| − | ***Multinucleated cells
| |
| − | ***Derived from haematopoietic stem cells
| |
| − | ***Responsible for bone resorption (have a brush border for this)
| |
| − | *'''Matrix'''
| |
| − | **Type I collagen forms the backbone of the matrix
| |
| − | **Mineral – accounts for 65% of bone and includes Ca, P, Mg, Mn, Zn, Cu, Na
| |
| | | | |
| | + | ==Test yourself with the Bone and Cartilage Pathology Flashcards== |
| | | | |
| − | ===Bone organisation===
| + | [[Bones_and_Cartilage_Flashcards_-_Pathology|Bones and Cartilage Flashcards]] |
| | | | |
| − | *Patterns of collagen deposition:
| |
| − | **'''Woven bone''':
| |
| − | ***"Random weave" which is only a normal feature in the foetus
| |
| − | ***In adults it is a sign of a pathological condition (e.g. fracture, inflammation, neoplasia)
| |
| − | **'''Lamellar bone''':
| |
| − | ***Orderly layers which are much stronger than woven bone
| |
| − | ***Two main types:
| |
| − | ****'''Compact bone''' (cortical)
| |
| − | *****Forms 80% of total bone mass
| |
| − | *****Forms the shell of long bone shafts - contain '''Haversian systems'''
| |
| − | ****'''Cancellous bone''' (spongy or trabecular)
| |
| − | *****In vertebrae, flat bones and epiphyses of long bones
| |
| − | *****Contains no Haversian systems
| |
| | | | |
| − | | + | [[Category:Bones - Pathology|A]] |
| − |
| |
| − | ===Periosteum and blood supply===
| |
| − | | |
| − | *Specialised sheath of connective tissue covering bone except at the articular surfaces
| |
| − | *Inner layer
| |
| − | **Merges with the outer layer of bone
| |
| − | **Contains osteoblasts and osteoprogenitor stem cells
| |
| − | *Damage to the periosteum invokes a hyperplastic reaction of the inner layer
| |
| − | *The blood supply to the mature bone enters via the periosteum
| |
| − | | |
| − | | |
| − | ===Bone development===
| |
| − | | |
| − | *Two main types of bone development:
| |
| − | **'''Endochondral ossification''' (cartilage model)
| |
| − | ***Long bones mainly
| |
| − | ***Vascularised
| |
| − | ***Developed centres of ossification
| |
| − | ****Primary (diaphyseal)
| |
| − | ****Secondary (epiphyseal)
| |
| − | **'''Intramembranous ossification'''
| |
| − | ***Flat bones mainly (e.g. skull)
| |
| − | ***Mesenchymal cells differentiate into osteoblasts
| |
| − | ***No cartilage precursor template
| |
| − | | |
| − | Physis
| |
| − | • The cartilage model remains only at the junction of the diaphyseal and epiphyseal centres to become the physis or growth plate. This is an important site since many congenital or nutritional bone diseases in the growing animal are manifest at this site.
| |
| − | | |
| − | • In neonates and growing animals, the growth plate is “open”, i.e. chondrocyte proliferation balances cell maturation and death (Fig 2). The growth plate “closes” and ossifies at maturity.
| |
| − | | |
| − | | |
| − | | |
| − | | |
| − | Fig 2. Growth plate cartilage is divided into zones
| |
| − |
| |
| − | Bone resorption
| |
| − | • Mediated by two hormones
| |
| − | o Parathyroid hormone (PTH) which is produced by chief cells in the parathyroid glands in response to decreased serum calcium
| |
| − | | |
| − | o Calcitonin which is produced by C-cells in the thyroid glands in response to increased serum calcium
| |
| − | | |
| − | PTH
| |
| − | ↓
| |
| − | Osteoclasts increase in number
| |
| − | ↓
| |
| − | Osteoclasts attach to bone and resorb mineralised matrix
| |
| − | | |
| − | Osteoclasts do not have receptors for PTH so how do they do this?
| |
| − | Answer:
| |
| − | | |
| − | LOW CALCIUM → INDUCES PTH SECRETION →
| |
| − | BONE RESORPTION → CALCIUM
| |
| − | | |
| − | CALCITONIN HAS THE OPPOSITE EFFECT - IT INHIBITS OSTEOCLASTS
| |
| − | | |
| − | Bone dynamics
| |
| − | | |
| − | Bone growth and maintenance of normal structure are directly related to mechanical forces which generate bioelectrical potentials (piezoelectricity). These potentials strengthen bone and inactivity reduces them, thereby leading to bone loss. In neonates, bone growth predominates and modelling is important. In adults, formation of bone is balanced by resorption; this is known as remodelling. It continues in a subtle but active way throughout life under the influence of hormones and mechanical pressure. Bone resorption may exceed formation in pathological states (hormonal, trauma, nutritional) or in old age and disuse.
| |