2.01 Flashcards

1
Q

Describe the structure and composition of compact bone

A

Hard outer layer, resistant to breaking and bending, made of Haversian canal. No bone marrow and highly ordered. Mostly mineralized tissue.

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2
Q

Describe the structure and composition of cancellous bone

A

Layers of less structured bone, vulnerable to fracture, forms the inner layer of bones, found in vertebrae and ribs. Has bone marrow but no Haversian canals.

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3
Q

What is woven bone?

A

Consists of collagen laid down in a disorganised fashion following bone fracture or disease. Laid down quickly (advantage) - strength is repaired when osteoclasts and osteoblasts invade and rebuild (forms lamellar bone)

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4
Q
  1. Osteoblasts
  2. Osteoclasts
  3. Osteocytes
  4. Osteoid and osteoid seam
A
  1. Actively secrete matrix, after building bone, become lining cells/osteocytes
  2. Break down bone by producing acid (protons), initiate resorption and remodelling + secrete growth factors to recruit new osteoblasts
  3. Bone maintenance, sensing mechanical forces, signals bone remodelling
  4. Osteoid is a cell where the matrix isn’t fully mineralized. Osteoid seam is the maturing collagen between cell and mineralization front.
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5
Q

Composition of bone matrix

A
  1. Collagen (type 1) - gives bone tensile strength
  2. Non-collagenous proteins - alkaline phosphatase (marker for bone formation), proteoglycans, growth factors (attract osteoblasts)
  3. Minerals - hydroxyapatite (calcium and phosphate crystals) - give compressive strength
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6
Q

Bone turnover - Why? How?

A
We need it for 3 reasons
1. Bone shape changes as we grow
2. In response to changing load
3. Repair of microdamage
It is done via osteoclasts resorbing bone, osteoblasts then build bone and either become lining cells (quiescent and unable to secrete matrix) or apoptose.
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7
Q

Coupling in terms of bone turnover

A

Osteoblasts activity and osteoclast activity are coupled → Bone formation and remodeling are balanced. Growth factors are embedded in bone:
▪ Osteoclastic activity causes release of GF
▪ GF causes osteoblast differentiation

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8
Q

Importance of RANKL

A

Osteoblasts have RANKL on surface
▪ RANKL binds with RANK receptor on pre-osteocytes (monocytes) to cause osteoclast differentiation
▪ Osteoprotegerin: “Decoy” RANK receptor that binds and blocks RANKL

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9
Q

Types of bones

A

Long bone, flat bone, irregular bone

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10
Q

Different types of cartilage

A

Hyaline cartilage – type 2 collagen fibers, GAGs, proteoglycans, (precursor for for bone formation, in utero it’s called endochondral ossification, found in articular surfaces, trachea, bronchi, larynx, nose)
Elastic – elastic fibers and lamellae, GAGs, proteoglycans, chondrocytes (surrounded by perichondrium, ear and epiglottis, has elastic lamellae in matrix)
Fibrocartilage – type 1 collagen fibers, GAGs, proteoglycans, chondrocytes and fibroblasts (no perichondrium, combination of dense regular CT and hyaline, shock absorber)

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11
Q

Histology of hyaline cartilage

A

Surrounded by perichondrium (dense CT) except at articular surfaces – source of new chondrocytes for cell turnover
Matrix is unstructured, produced by chondrocytes, variations in staining reflect variations in concentrations of matrix components, reflect pressure loads
Chondrocytes seen singularly or in clusters of recently divided cells, produce matrix in response to pressure loads

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12
Q

Explain the processes of endochondral bone growth, remodelling and repair of bone

A

Endochondral ossification is the process by which growing cartilage is systematically replaced by bone to form the growing skeleton. Remodelling and repair mediated by osteoblasts and osteoclasts.

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13
Q

Describe the different types of joints

A

Fibrous - Fibrous joint – bones united by dense regular CT, e.g. sutures in skull.
Cartilaginous - Cartilaginous joints are a type of joint where the bones are entirely joined by cartilage, either hyaline cartilage or fibrocartilage.
Synovial - A synovial joint is the type of joint found between bones that move against each other, such as the joints of the limbs (e.g. shoulder, hip, elbow and knee). Characteristically it has a joint cavity filled with fluid.

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14
Q

Types of bony fractures

A

Single Traumatic event/Stress Fracture (Repetitive stress in normal bone)/Pathological Fracture (Normal stress in abnormal bone)
Open fracture: bone pokes through the skin and can be seen, or a deep wound exposes the bone through the skin. Closed fracture, the bone is broken, but the skin is intact.
A simple fracture is a result of excessive force or impact on the bone, resulting in a break.
Comminuted fracture refers to a bone that is broken in at least two places
Greenstick fracture occurs when a bone bends and cracks, instead of breaking completely into separate pieces
Extra-articular fracture does not extend into the joint
Intra-articular - An intra-articular fracture refers to a fracture that extends from the bone into the nearby joint

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15
Q

Le Fort facial fractures

A
  • Le Fort I – Horizontal fracture of alveolar rim
  • Le Fort II – Pyramid fracture; apex above nose bridge and extends inferolaterally through infraorbital rim
  • Le Fort III – Involves zygomers, infraorbital rims, maxilla, and paranasal sinuses
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16
Q

Identify the common types of mandibular fracture

A

The more common sites are the condyle, body, angle, and parasymphyseal area of the mandible.

17
Q

Explain factors that can impede healing of fractures

A

Large gap between fragments
Movement of fragments
Low blood supply to fracture
Other patient characteristics include age, socioeconomic status, pre-injury health

18
Q

Describe the essential features of the processes involved in healing of a bony fracture

A

Stages of Bone Healing:
1. Haematoma formation – solid swelling of clotted blood within tissue
2. Inflammation/cellular proliferation
3. Callus formation
o Only forms if fracture sites move → Stabilizes joint and bridges gap
o Indirect healing = Callus forms between fragments
o Direct healing = Fragments are immobile and no callus forms
4. Consolidation
5. Remodelling

19
Q

Describe some of the complications of fractures, such as neurovascular complications, non-union and mal-union, compartment syndromes and infection

A

Early complications - vascular, nerve injury, compartment syndromes
Late – delayed union, malunion, avascular necrosis, growth disturbance, joint impairment, pain syndromes
Neurovascular injury = Damage to neurovascular vessels near fracture site
Compartment syndrome = Tight casts causes pressure to build up due to swelling at fracture.
o Pressure can occlude capillaries, leading to ischema
o Necrosis of muscle and nerves ensues
• Non-union = Failure for bones to unite
o Hypertrophic Non-union = Periosteal of new bone is formed but needs better stability; biology is ok.
o Atrophic Non-union = No signs of healing; biology needs to be improved
• Mal-union = Bones heals in unsatisfactory position

20
Q

Describe the main components of peripheral nerves (motor, sensory & autonomic fibres)

A

Sensory: Connects the brain and spinal cord to your skin and allow you to feel pain and other sensations. Autonomic: Controls involuntary function (e.g., blood pressure, digestion, heart rate). Motor: Connects the brain and spinal cord to muscles to stimulate movement.

21
Q

Basic principles associated with nerve conduction, regeneration & degeneration

A

For communication between cells, the electrical signals generally are converted into chemical signals conveyed by small messenger molecules called neurotransmitters
Degeneration - Loss of functional activity and trophic degeneration of nerve axons and their terminal arborizations
Regeneration - Occurs, depends on level of injurt sustained

22
Q

Types of Mechanoreceptors

A

Nociceptors - detect pain/noxious stimuli
Parcinian Corpuscles - Senses high frequency vibrations (>500Hz)
Meissner’s Corpuscles - senses low frequency vibrations
Merkel-cell-neurite Complex - sense pressure
Rufini Organ - responds to stretching

23
Q

Types of nociceptors

A

Thermal, mechanical, polymodal Respond to multiple stimuli), silent (Only activated when a very specific cytokine is present; produce a completely novel sensation)

24
Q

Nociceptor fiber types

A
A-delta fibers
o Thermal and pain sensors
▪ Pain
▪ Temperature
o Myelination
o Larger diameter
o Relatively fast conduction
▪ Causes “first pain” = Sharp mechanical pain
• C fibers
o Polymodal sensors
▪ Temperature
▪ Pain
▪ Itch
o No myelination
o Small diameter
o Slow conduction
▪ Causes “second pain” = Visceral aching pain
25
Q

Nociceptor activation - experience of pain

A

Tissue damage causes release of nociceptor-activating
mediators:
o Bradykinin, Prostaglandins, K+
• These mediators activate nociceptors only
• Nociceptors send pain signal to spinal cord
Retrograde activation - Sensory axons send signal away from spinal cord. Substance P is released and activates mast cells which release histamine which increase swelling and sensitivity of nociceptors. Histamine and Substance P acts on vessels → More bradykinin, PGs, and histamine from blood further activates and sensitizes nociceptors.

26
Q

Allodynia and hyperalgesia

A
Allodynia = Previously touch stimulus become painful
Hyperalgesia = Noxious stimuli are now perceived as more noxious
27
Q

What is referred pain?

A

Referred pain is pain perceived at a location other than the site of the painful stimulus/origin. It is due to the convergence of axons in the ganglion.

28
Q

Different types of pain

A

Acute versus chronic pain - Acute pain happens quickly and goes away when there is no cause, but chronic pain lasts longer than six months and can continue when the injury or illness has been treated
Nociceptive versus neuropathic - noxious stimuli detected by nociceptors / neuropathic pain refers to nerve issue/dysfunction and inflammatory pain - spontaneous hypersensitivity to pain caused by inflammation
Cutaneous (pain perceived from the skin) deep somatic (pain receptors deeper in the body including tendons, joints, bones, and muscles) and visceral pain (pain related to the internal organs in the midline of the body)
Cancer versus non-cancer pain

29
Q

Facial nerve palsy

A

Bell’s palsy is facial muscle weakness or paralysis resulting from damage to the facial nerve (CN7). Pain and discomfort usually occur on one side of the face or head. Direct anesthesia to the facial nerve can force a rapid onset that occurs while the anesthetic agent is being injected, reflex vasospasms of the external carotid artery can lead the ischemia of facial nerve, and dental infections may secondarily effect the facial nerve