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General Pathology > Bone and Joint Diseases > Flashcards

Bone and Joint Diseases Flashcards

1
Q

List the components of bone

A
  1. Organic - osteoid - 35% (type I collagen, GAG, proteins)
  2. Inorganic - mineral - 65% (hydroxyapatite)
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2
Q

List the histologic forms of bone

A
  1. Woven
    -Made rapidly during development or fracture repair
    -Less structural strength
    -When present in adults it is always abnormal
  2. Lamellar
    -Slowly produced parallel collagen fibers
    -More structural strength
  3. Other bone structural forms
    -Cortical (compact) bone - dense, thick layer on the outside of bone
    -Trabecular bone (cancellous, spongy) - thin, lattice-like network inside of bone. Makes bones light and may contain red marrow
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3
Q

List the bone cells

A

Osteoblasts
Osteocytes
Osteoclasts

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4
Q

Describe Osteoblasts

A

-Derived from stem cells under the periosteum and in the medullary space
-Live on the matrix surface
-Synthesize, transport and assemble bone matrix
-Regulate mineralization

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5
Q

Describe Osteocytes

A

-Osteoblasts that become encased in lacunar spaces in bone, interconnected by cytoplasmic processes through canaliculi
-Control calcium, phosphate levels
-Detect mechanical forces and translate into biologic activity

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6
Q

Describe Osteoclasts

A

-On the bone surface
-Specialized multinucleated macrophages (from circulating monocytes) causing bone resorption
-Bind to bone matrix through integrins forming a resorption pit
-Secrete acid and neutral proteases (mostly MMPs) that resorb bone

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7
Q

Describe bone remodeling

A

-Adult skeleton is constantly turning over in a tightly regulated process (i.e. remodeling) on the bone surface
-Changes signaled through 3 factors:
1. Activator of NF-kB (RANK) - made by osteoclast precursors
2. RANK ligand (RANKL) - made by osteoblasts and marrow stromal cells
3. Osteoprotegerin (OPG) - made by osteoblasts
-Peak bone mass occurs in early adulthood. In 4th decade, resorption exceeds formation resulting in decline in skeletal mass

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8
Q

Describe the signaling effects in bone remodeling

A

-RANK and RANKL binding stimulates differentiation into osteoclast –> bone resorption
-If osteoblast makes OPG this blocks RANK/RANKL binding –> prevents osteoclast differentiation

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9
Q

Describe the systemic factors that affect the balance of bone remodeling

A

-Increased bone turnover/breakdown favored by PTH, IL-1, glucocorticoids
-Decreased bone turnover/breakdown - growth factors, sex hormones favors OPG expression

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10
Q

List the congenital bone disorders

A

-Osteogenesis imperfecta
-Osteopetrosis

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11
Q

List the metabolic bone disorders

A

-Osteopenia and osteoporosis
-Rickets and Osteomalacia
-Hyperparathyroidism - covered in endocrine

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12
Q

List bone tumors

A

-Bone-forming tumors
-Cartilage-forming tumors
-Metastatic tumors

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13
Q

List the joint diseases

A

-Arthritis
-Osteoarthritis
-Rheumatoid arthritis
-Gout

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14
Q

Describe Osteogenesis Imperfecta

A

-Also known as “brittle bone disease”
-Group of disorders of Type I collagen maturation (insufficient or abnormal) –> inadequate bone formation with think cortices and trabeculae –> weak bones that break easily
-Most (>90%) case are autosomal dominant collagen mutation - causing fractures and deformity
-Mistaken for child abuse
-Most show blue sclera due to choroid showing through thin sclera
-Most types have “opalescent teeth” which is clinically and radiographically identical to dentinogenesis imperfecta (no pulp chamber, bulbous crown) but different mutation)

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15
Q

Describe Osteopetrosis

A

-Hereditary bone disorders where osteoclasts can’t remodel bone. They are hard but brittle

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16
Q

What is the pathogenesis of Osteopetrosis

A

Bone deposition without resorption –> thickening of cortical bone and sclerosis of cancellous bone, obliterating the marrow space

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17
Q

Describe outcomes of Osteopetrosis

A

-Myelophthisic anemia and extramedullary hematopoeisis with hepatosplenomegaly
-Deafness and blindness due to constriction of nerve ostea
-Dense, opaque, solid tubular bones on radiographs become easily infected causing osteomyelitis
-Autosomal dominant type (most common) - pt survives, less severe effects
-Autosomal recessive types - death due to marrow failure

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18
Q

What is Osteopenia

A

Decreased bone mass (1-2.5 SD below mean peak bone mass)

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19
Q

What is Osteoporosis

A

Severe osteopenia with significantly increased risk of fracture (>2.5 SD below mean peak bone mass)

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20
Q

Describe the pathogenesis of Osteopenia and Osteoporosis

A

Imbalance between osteoblastic and osteoclastic activity leading to progressive loss of trabeculae and trabecular thickness (net loss of bone). (Note: collagen and mineralization are normal)

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21
Q

Describe the pathophysiology and associations of Osteopenia and Osteoporosis

A

-Peak bone mass at young adulthood; bone turnover continues with net deficit over time. Reduced peak bone mass in adolescent girls - tend to have low Ca2+ intake
-Osteoblasts less effective with age
-Aging and disuse (muscular loading stimulates bones)
-Dietary: low Ca2+, Vit D, increased PTH
-Estrogen is protective: prevents resorption caused by pro-inflammatory cytokines (IL-1, IL-6, TNF) and increases OPG
-Steroids, anticoagulants, alcohol, tobacco, proton pump inhibitors

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22
Q

What is the risk associated with Osteopenia and Osteoporosis?

A

bone compression and fractures (hip, vertebral, wrist) –> immobility which can lead to life-threatening complications (ex: embolism, pneumonia)

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23
Q

How do you diagnose Osteopenia and Osteoporosis

A

-Not seen on plain films until 30% bone loss
-DEXA scan (more sensitive method to show bone density)

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24
Q

What is the prevention and tx for Osteopenia and Osteoporosis?

A

-Increased calcium in diet and exercise
-Estrogen replacement after menopause
-Bisphosphonates - Fosamax and Actonel - kills and inactivates osteoclasts

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25
Q

Rickets and Osteomalacia are what type of defect?

A

Vit. D deficiency causing impairment of mineralization and a resultant accumulation of unmineralized bone matrix

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26
Q

Describe Rickets

A
  1. Vitamin D deficiency in children
    -Dietary deficiency (formular-fed infants)
    -Inadequate sunlight
  2. Soft, deformable bones
    -Bowed legs
    -Pigeon breast (protruding sternum)
  3. Enamel hypoplasia
27
Q

Describe Osteomalacia

A
  1. Vit D deficiency in adults
    -Pancreatic, intestinal or biliary diseases causes fat malabsorption
    -Reduced sunlight and dietary intake
  2. Poor remodeling of existing bones
    -New matrix is poorly mineralized resulting in weak bones of normal contour
28
Q

Describe Vit D-resistant Rickets

A

-X-linked dominant inheritance
-Kidney cannot resorb phosphate (causes hypophosphatemia)
-Same clinical appearance as rickets (short stature) but does not respond to Vit D
-Dental: elongated pulp horns causes pulp exposures at DEJ

29
Q

What is Hypophosphatasia

A

-Inherited condition (dominant and recessive forms)
-Deficiency of tissue alkaline phosphatase
-Bony findings resembling rickets (short stature, bowed legs, fractures)

30
Q

What are the dental findings with Hypophosphatasia?

A

-Wide pulp canals
-Early deciduous tooth loss because of poorly formed cementum (ex: Md incisors)

31
Q

What diagnostic tests are performed with Hypophosphatasia?

A

-Urinary phosphoethanolamine
-Low serum alk phosphatase

32
Q

Describe Paget Disease of Bone

A
  • Increased/uncontrolled generalized bone remodeling resulting in distortion and weakening of bone; unknown etiology
    -Older pts (rare <40yrs), Anglo-saxon ancestory; decreasing incidence
    -Asymptomatic or Bone pain +/-, usually >1 bone (polyostotic) enlarges
    -Elevated serum alkaline phosphatase; Ca+2 and PO4 normal
33
Q

What do you see in the H&N with Paget Disease? In Radiographs?

A

H&N:
-Skulls, jaws - Mx/Md - hat/denture won’t fit, spaces between teeth (due to jaw expansion)
Radiographs:
-thick cortices, “cotton wool” appearance at late stage, generalized hypercementosis

34
Q

What is the tx for Paget Disease?

A

Bisphosphonates

35
Q

Describe the Histologic Phases of Paget Disease of Bone

A
  1. Osteolytic phase: initial resorption with numerous enlarged osteoclasts
  2. Osteoblastic phase: increased osteoblastic activity (“cotton wool” appearance)
  3. Osteosclerotic (Burned out) phase: dense “mosaic” bone with prominent reversal lines
36
Q

Describe Fibrous Dysplasia

A
  1. A developmental condition: continual production of immature bone matrix
  2. Bone expands but is soft and immature
  3. Disease severity increases the earlier the mutation occurs during development
    -Albright syndrome: severe polyostotic fibrous dysplasia + precocious puberty in females + cafe-au-lait spots on skin
    -Polyostotic - many bones affected
    -Monostotic disease - only one bone affected
37
Q

What is the pathogenesis of Fibrous Dysplasia?

A

Spontaneous G protein mutation –> continual adenylyl cyclase production of cAMP –> bone matrix formation

38
Q

What are the clinical findings of Fibrous Dysplasia?

A

-Slow growing, firm, painless, fusiform bone expansion starts in childhood and stops after growth is complete
-Bone is weak and deformable
-Most common in ribs, long bones, jaws, skull

39
Q

What is the histology of Fibrous Dysplasia

A

Cellular fibrous stroma with haphazard, woven bone trabeculae (“Chinese character letters”) without osteoblastic rimming

40
Q

What is the tx for Fibrous Dysplasia

A

Surgical reduction after growth stops. Don’t radiate, b/c can cause sarcoma

41
Q

Describe Osteomyelitis

A

-Inflammation of bone and marrow, virtually always secondary to infection
-Primary focus of disease or complication of systemic infection
-All types of organisms but most often pyogenic bacteria
-Spread to bone: hematogenous, direct extension or implantation (ex: fracture)

42
Q

Describe Acute Osteomyelitis

A

-Bacterial growth and neutrophilic rxn in first 48 hours –>
-Bone necrosis and spread along the periosteum. If periosteum ruptures –>
-ST abscess which can exit the skin as a draining sinus tract
-After 1 week, fibrous tissue ingrowth and reactive vital bone forms at periphery (involucrum) around the dead infected bone (sequestrum)

43
Q

Describe Chronic Osteomyelitis

A

-Up to 25% of acute cases don’t resolve and persist as a chronic infection. Can have spontaneous acute flareups or occur after years of dormancy
-Marrow fibrosis, sequestrum and chronic inflammation (lymphocytes, plasma cells)

44
Q

Describe Osteoma

A

-Benign bone tumor often growing on bone surface (periosteal)
-Painless, slow growing
-Multiple osteomas of facial/jaw bones could represent Gardner Syndrome (precancerous colon polyps leading to colon cancer)

45
Q

Describe Osteoblastoma

A
  • 2-4cm up to 10cm
    -Pain common, not well relieved by salicylates
    -Expansile, well/ill-defined RL with patchy to diffuse mineralization
    -Reactive sclerosis not always present
46
Q

Describe Osteoid Osteoma (OO)

A
  • <2cm
    -Pain, usually nocturnal, relieved by salicylates because tumor makes prostaglandins (usually extragnathic lesions)
    -Non-expansile, usually well circumscribed RL with variably thick reactive sclerosis
    -Small RO nidus may be present (target-like)

(RL = radiolucent)
(RO = radiopaque)

47
Q

Describe Osteosarcoma

A

-Malignant appearing cells producing bone
-2nd decade peak occurrence; also occurs in older adults with Paget disease, bone infarcts or previous radiation
-Genetic mutation - often RB gene
-Painful enlarging mass
-Knee joint - most common site; 8% in the jaw
-Radiograph: expansile RL/RO mass that pushes out the periosteum
-Sunburst appearance due to reactive bone formation
-Hematogenous spread to lungs
-Tx: neoadjuvant chemotx (chemo before surgery), surgery, chemtx

48
Q

Describe Chondroma

A

Benign cartilage producing tumor that often occur in the hands but never found in the jaws. Any cartilage tumor seen in the jaws is malignant

49
Q

Describe Chondrosarcoma

A

-Malignant tumor producing cartilage not bone
-Painful, enlarging mass
-Seen in adults (>40 yrs)
-Pelvis, shoulder, ribs
-Radiograph: mixed RL/RO mass
-Variable grades - higher grades spread through blood to lungs
-Tx: surgery

50
Q

Describe Ewing Sarcoma

A

-Small round cell tumor (resembles lymphocytes) of neuroectoderm
-Medullary bone in children and young adults
-Most in leg bones and pelvis; some in jaws
-Rapid growth with pain and expansion, can mimic acute infection
-Radiograph: ill-defined radiolucency and periosteal reaction produces “onion-skin” layers of reactive bone
-Tx: surgery and chemotx

51
Q

Describe Metastatic tumors

A

-Mets to bone are much more common than primary bone cancer
-75% of skeletal metastases originate from cancers of the prostate, breast, kidney, and lung
-Typically axial skeleton (often vertebral) and can be multiple lesions
-Poor prognosis

52
Q

Describe the clinical presentation of Metastatic tumors

A

-Pain, possible paresthesia
-Can cause hypercalcemia
-Can replace marrow –> myelophthisic anemia

53
Q

Describe the radiographic presentation of Metastatic tumors

A

-Irregular, ill-define radiolucency most often
-Prostate or breast mets can cause mixed or radioopaque lesions

54
Q

List the types of joints

A
  1. Solid (nonsynovial) joints or synarthroses
  2. Cavitated (synovial) joints
55
Q

Describe Solid (nonsynovial) joints or syarthroses

A

-Provide structure and only minimal movement
-No joint space
-Fibrous tissue (i.e. cranial structures, periodontal ligaments) or cartilage bridge (sternum/ribs, pelvis) at ends of bones

56
Q

Describe Cavitated (synovial) joints

A
  1. Have a joint space for range of motion
  2. Enclosed by a synovial membrane lined by synoviocytes that make synovial fluid (plasma filtrate) containing hyaluronic acid (liubrication) and nutrition for articular cartilage
  3. Hyaline cartilage: elastic shock absorber and wear-resistant- had no blood supply, lymphatic drainage or innervation
    -Water (70%) and proteoglycans resist compression and limit friction
    -Type II collagen - resists tensile stress and transmits vertical loads
    -Chondrocytes - make and digest matrix
57
Q

Describe Osteoarthritis

A

-“Degenerative joint disease” (DJD)
-Degeneration of cartilage without repair, leading to failure of the joint
-A disorder of cartilage not an inflammatory process
-Most common joint disease; increases exponentially >50yrs

58
Q

What is the pathogenesis of Osteoarthritis?

A

Genetic and mechanical factors predispose to chondrocyte injury –> they release cytokines (TGF-beta, TNF) and factors (MMPs) that change the ECM (degradation exceeds synthesis) –> chondrocyte loss and degraded matrix

59
Q

What is the clinical presentation of Osteoarthritis?

A

-Hips, knees, lower spine, phalanges (Heberden nodes-osteophytes in women); can affect the TMJ
-Pain that increases with use; morning stiffness for about 30 min; crepitus; limited range of motion
-Joint deformity but not joint fusion can occur; see bony outgrowths from the joint = osteophyte (bone spur)

60
Q

What is the tx of Osteoarthritis?

A

Pain management and inflammation reduction with NSAIDs, intra-articular steroids, reduce use, joint replacement (arthroplasty)

-Unfortunately, can’t prevent or halt progression

61
Q

Describe Gout

A

Acute inflammatory arthritis due to formation of urate crystals (tophus) in joints (big toe, ankle and wrists); can also affect kidney and ear lobes

62
Q

What is the pathogenesis of Gout?

A

Excess uric acid (from purine metabolism) –> hyperuricemia and urate crystal precipitation

63
Q

What is the pathophysiology of Gout?

A

Precipitated urate is extremely irritating and evokes an acute inflammatory response causing extreme pain, redness and swelling

64
Q

What is the tx for Gout?

A

Colchicine; avoid red meat and alcohol

General Pathology (32 decks)

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