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Musculoskeletal and Skin > Bone Pathology > Flashcards

Bone Pathology Flashcards

1
Q

Basic Structure and Function of Bone

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2
Q

Cellular Components of Bone: Osteoblasts

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3
Q

Cellular Components of Bone: Osteoclasts

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4
Q

Woven or Lamellar?

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5
Q

Explain Endochondral Ossification

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6
Q

Explain Endochondral Ossification: Primary Spongiosia

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7
Q

Explain Itramembranous ossification

A
  • flat bones
  • formed direct from osteoblasts
    • no cartilage anlagen
  • enlargement- new bone on pre-exsisting surface
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8
Q

Roles of GH, T3, PTHrP, Int, SOX9, RUNX2, and FGF3

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9
Q

Remodeling

A
  • constant turnover of bone; tightly regulated process
  • ~10% of skeleton is replaced annually
  • takes place at BMU
    • coupled osteoblast and osteoclast activity on bone surface
    • orderly sequence of osteoclast attachment, resorption, osteoblast attachment and proliferation, and matrix synthesis
  • Regulated by cell-cell interaction and cytokines
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10
Q

Cytokines in remodeling

A

RANK- osteoclast precursor

RANKL- osteoblasts

OPG- “decoy” receptor; bind RANKL and prevent interaction with RANK

RANK-RANKL activate NF-kB

M-CSF produced by osteoblasts; stimulates tyrosine kinase cascade leading to osteoclast differentiation

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11
Q

Explain this and balance of remodeling

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Bone formation and remodeling modulated by connection between RANK and WNT pathways

factors affecting balance: hormones, vit D, cytokines, growth factors

paracrine crosstalk between osteoclasts and osteoblasts: as bone is broken down substances are released that stimulate osteoblasts

peak bone mass achieved in early adulthood: by 4th decade resorption exceeds formation and steady decline in skeletal mass

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12
Q

Achondroplasia

A

most common skeletal dysplasia

autosomal dominant

retarded cartilage growth

shortened proximal extremities

enlarged head with bulging forehead

gain of function mutations in FGFR3

normally FGFR3 inhibits endochondral growth

constitutive activation = surpassed growth

approx. 90% are new mutation: almost all in paternal allele

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13
Q

Osteogenesis Imperfecta (OI)

A

Deficiencies in synthesis of type I collagen - osteoid

most common inherited disorder of connective tissue

bone and other tissue rich in collagen: joints, eyes, ears, skin, teeth

autosomal dominant mutations in a1 and a2 chains of type I collagen: effective assembly of collagen polypeptides

too little bone > extreme skeletal fragility

blue sclerae > decreased collagen (think sclerae)

hearing loss > impaired conduction

dental abnormalities > deficient dentin

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14
Q

Types of osteogenesis imperfect

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15
Q

Osteopetrosis

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  • AKA marble bone disease or Albers-Schonberd disease
  • reduced bone resorption and diffuse, symmetric skeletal sclerosis
  • Imparied formation or function of osteoclasts
  • mutations interfere with acidification of osteoclast resorption pit
    • i.e. CA2 required to generate protons from CO2 and H2O
    • Lack of CA2 prevents acidification of resorption pit: prevents osteoclast activity
  • lack medullary canal
  • ends long bones are misshapen: Erlenmeyer flask deformity
  • small neural foramina compress nerves
  • primary spongiosia persists
  • no room for marrow elements
  • woven bone remains because mature trabecular cannot form
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16
Q

Severe Infantile form of osteopetrosis

A

Autosomal recessive

evident in utero or soon after birth

fracture, anemia, hydrocephaly

death early

repeated infections du etc leukopenia

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17
Q

Mild Adult form of Osteopetrosis

A

Repeated fractures

mild cranial nerve deficits

anemia

*kaplan- carbonic anhydrase deficiency

18
Q

Acquired Disorder: Osteoporosis

A

osteopenia (decreased bone mass)

osteopenia severe enough to significantly increase risk of fracture

bone mass >2.5 STDs below mean peak bone mass

localized and generalized

senile and postmenoposal most common

normal bone but decreased in quantity (thin)

some bones more severely impacted

Senile- cortex thinned

post menopausal- trabecular plates perforated and thinned

clinical manifestations depend on involved bones

cant be reliably detected by x-rays

19
Q

Best screenings for osteoporosis

A

Quantitative CT and DEXA scans

20
Q

Osteoporosis: prevention and treatment

A

exercise, calcium, vitamin D, bisphophonates

21
Q

Paget Disease (osteitis deformans)

A

increased disorder bone (uncoupling of BMU)

usually begins in late adulthood

both environmental and genetic causes

22
Q

phases of Paget Disease

A

Initial osteolytic phase: osteoclast activity. with resorption pits: osteoclasts are giant with abundant nuclei

Mixed phase: osteoclasts persist, now with osteoblastic rimming; marrow replaced by loose connective tissue; osteoprogenitor cells and blood vessels

Sclerotic phase: mosaic pattern of lamellar bone; prominent cement lines; periosseous tissue replaced by normal marrow, thickened trabecular and soft, porous cortices.

23
Q

Stage of Paget?

A

Stage 3: sclerotic phase

24
Q

Clinical findings and treatment of Paget disease

A

variable

majority of patients asymptomatic; incidental radiographic finding

most symptoms are mild; readily created with calcitonin and bisphophonates

25
Q

Hyperparathyroidsim

A

osteoclast activation - increased bone resorption and calcium mobilization; due to increased RANKL expression. on osteoblasts

increased calcium resorption by renal tubules

increased urinary excretion of phosphates

increased synthesis of active vitamin D by kidneys; calcium absorption from the gut; induces RANKL on osteoblasts thus mobilizing bone calcium

26
Q

Hyperparathyroidism associated disorders

A

Osteoporosis: generalized; phalanges, vertebrae, proximal femur

dissecting osteitis - osteoclasts tunnel through trabecular; marrow spaces replaced by fibrovascular tissue

brown tumor- bone loss leads to micro fractures and secondary hemorrhage; influx of macrophages and fibrous tissue; can undergo cystic degeneration

osteitis fibrosa cystica- hallmark of severe hyperparathyroidism; increased bone cell activity; peritrabecular fibrosis; cystic brown tumors

27
Q

?

A

brown tumor and osteitis fibrous cystica caused by hyperparathyroidism

28
Q

Secondary response to hyperparathyroidism

A

chronic hypocalcemia

compensatory overactivity of parathyroids, increased PTH

renal failure most common cause; inadequate vitamin D sythesiss; affects Gi calcium absorption

decreasing bone mass leads to more susceptible to fractures, bone deformation, and joint problems

treatment: decreased PTH levels reverses bone changes

29
Q

Renal Osteodystrophy and mechanisms of skeletal deformities

A

skeletal changes in chronic renal disease

mechanisms of skeletal deformities with renal disease

  • tubular dysfunction- renal tubular acidosis; low pH dissolves hydroxyapatite and demineralizes and osteomalacia
  • generalized renal failure- affects glomerular and tubular function; reduced phosphate excretion; chronic hyperphosphatemia; hypocalcemia; secondary hyperparathyroidism
  • decreased production of secreted factors- involves BMP-7, FGF23, Klotho; results in osteopenia and osteomalacia
30
Q

3 main types of Renal Osteodystrohpy

A

High turnover- increased bone resorption and formation

low turnover (aplastic)- little osteoblastic and osteoclastic activity; osteomalacia less commonly

mixed pattern

31
Q

Osteocnecrosis

A

infarction of bone and marrow

medullary cavity or medulla and cortex

usually due to fractures or steroids

all cause vascular insufficiency by: mechanical injury; thromboembolism; external pressure, venous occlusion.

32
Q

?

A

Osteonecrosis:

•Medullary infarcts – geographic•Cortex not affected•Collateral blood flow•In subchondral infarcts – wedge shaped necrosis•Overlying articular cartilage viable•Supplied by synovial fluid

33
Q

?

A

Osteonecrosis:

•Empty lacunae surrounded by necrotic adipocytes•Healing response – osteoclasts resorb necrotic trabeculae•Remaining trabeculae act as scaffolding for new bone•With subchondral infarcts the pace of replacement is too slow•à Collapse of the necrotic bone and distortion, fracture, and sloughing of articular cartilage

34
Q

Osteonecrosis symptoms

A

•Symptoms depend on location & extent of infarction•Subchondral – pain with activity initially•Constant later•Collapse à severe secondary arthritis•Medullary – small & clinically silent•Exceptions Gaucher disease & sickle cell anemia

35
Q

Osteomyelitis

A
  • Inflammation of bone & marrow•Secondary to infection
  • Pyogenic bacteria & mycobacteria most common
  • Infection through: hematogenous spread, extension from contiguous site, direct implantation
  • Staphylococcus aureus 80%-90% of culture positive cases
36
Q

Infections pathogens of osteomyelitis

A
  • GU infections & IV drug users – E. coli, Pseudomonas, Klebsiella•Neonates – H. influenzae and Group B strep
  • Sickle cell patients – Salmonella
  • Mixed infections – direct spread/inoculation•50% - no organism isolated
37
Q

?

A

Osteomyelitis:

  • Acute – bacterial proliferation
  • Neutrophils•Necrosis of bone marrow
  • Subperiosteal abscess may form•Lifting of periosteum à impaired blood supply ànecrosis
  • Dead bone = sequestrum - surrounded by involucrum
  • Ruptured periosteum can drain to skin
38
Q

?

A

Osteomyelitis

  • After a week, chronic inflammatory cells release cytokines causing
  • Osteoclastic bone resorption
  • Ingrowth of fibrous tissue
  • Deposition of reactive bone
  • Involucrum – shell of living tissue around infected bone
39
Q

disease and treatment?

A

Osteomyelitis

  • May manifest as acute systemic illness or minimal subtle symptoms
  • Characteristic radiographic finding

s•Lytic bone destruction with surrounding sclerosis

  • Tx: antibiotics & surgical drainage
  • Up to 25% persist as chronic infection
  • Causes•Delay in diagnosis•Extensive bone necrosis•Inadequate therapy•Weakened immune system•Spontaneous acute flare-ups
  • Complications: pathologic fracture, secondary amyloidosis, endocarditis, sepsis, malignancy
40
Q

Mycobacterial osteomyelitis

A

•1-3% of patients with TB have osseous involvement•Infection may persist for years•Localized pain, low grade fevers, chills, weight loss•Usually solitary•Caseating granulomata•Destructive & treatment resistant than pyogenic

•Pott disease – tubercular spondylitis•Multiple vertebrae•Extends into soft tissue•Permanent compression fractures•Scoliosis or kyphosis•Neurologic defects due to spinal cord & nerve compression•Other complications•Arthritis, sinus tract, abscess, amyloidosis

41
Q

Skeletal Syphilis and types

A
  • Treponema pallidum (spirochete)•Congenital syphilis – lesions appear around 5th month of gestation•Areas of active endochondral ossification & periosteum
  • “Saber shin” – massive reactive periosteal bone deposition
  • Acquired syphilis – tertiary stage•Nose, palate, skull, extremities
42
Q

???

A

Skeletal syphilis

Musculoskeletal and Skin (17 decks)

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