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Craniofacial Bone Biology > Lecture 8 > Flashcards

Lecture 8 Flashcards

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1
Q

OSTEOCLAST FORMATION REGULATION AND ACTIVITY (3 STEPS)

A
  1. ) PROLIFERATION/DIFFERENTIATION - MONONUCLEAR PRECURSOR CELLS W/ HEMATOPOIETIC LINEAGE FUSE => MULTINUCLEATED OSTEOCLASTS
  2. ) ACTIVATION OF OSTEOCLAST PRECURSOR WHEN RANKL BINDS TO RANK ON OSTEOCLAST SURFACE (OPG CAN INTERFERE W/ THIS REACTION AND STOP OSTEOCLAST ACTIVATION BY BINDING TO RANKL)
  3. ) RUFFLED MEMBRANE SECRETES H+ ENZYMES => ACIDIC ENVIRONMENT (PROMOTES DEGRADATION OF ORGANIC/INORGANIC PORTION OF BONE INTO COMPARTMENT
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2
Q

RUFFLED MEMBRANE

A
  • CA CATALYZES FORMATION OF H2O AND CO2 W/IN RUFFLED MEMBRANE AND COMBINES THEM TO FORM BICARBONATE (PROVIDES H+ IONS FOR ACIDIC ENVIRONMENT)
  • DEGRADATION PRODUCTS FROM BREAKDOWN OF BONE INTO CA2+ AND PO4(3-) AND COLLAGEN FRAGMENTS ARE REABSORBED BY RUFFLED MEMBRANE AND EXCRETED VIA VESICULAR EXCRETION
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3
Q

ENZYMES INVOLVED IN OSTEOCLASTIC BONE BREAKDOWN

A

1.) LYSOSOMAL ENZYMES
2.) MATRIX METALLOPROTEINASES
RELATIONSHIP BETWEEN ENZYMATIC AND CHEMICAL ACTIVITY IS IMPORTANT

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4
Q

TUMOR CELL EFFECTS ON OSTEOCLASTIC ACTIVITY

A

TUMOR CELLS PRODUCE FACTORS (PTHrP - PARATHYROID HORMONE-RELATED PROTEIN) THAT PROMOTE FORMATION/ACTIVATION OF OSTEOCLASTS => BONE RESORPTION AND RELEASE OF FACTORS BY BONE MATRIX (TGF-β) WHICH STIMULATES TUMOR CELL PROLIFERATION

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5
Q

PTHrP

A

BLOCKS OPG AND ACTIVATES RANKL

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6
Q

BONE GROWTH

A

BONE GROWS IN LENGTH @ THESE VARIOUS SITES -
1) CARTILAGE GROWS ON THE ENDS OF THE ARTICULAR CARTILAGE
2) CARTILAGE REPLACED BY BONE ON THE INSIDE OF THE ARTICULAR CARTILAGE
3) CARTILAGE GROWS AT THE EPIPHYSEAL PLATE OUTER EDGE
4) CARTILAGE REPLACED BY BONE AT THE EPIPHYSEAL PLATE INNER EDGE
THIS OCCURS UNTIL EPIPHYSEAL PLATES (COMPOSED OF HYALIN CARTILAGE) CLOSE

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7
Q

BONE REMODELING IN SPONGY/CORTICAL BONE

A

DIAPHYSIS IS REMODELED -
SPONGY BONE IS REMODELED EVERY 3-4 YEARS
CORTICAL BONE IS REMODELED EVERY 10 YEARS
PROCESS IS CONTINUAL - NEVER AT METABOLIC REST
PRODUCES LYSOSOMAL ENZYMES AND ACIDS

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8
Q

BONE REMODELING

A
  1. ) BONE RESORBED AT BONE HEAD/NECK JUNCTURE
  2. ) BONE ADDED BY APPOSITIONAL GROWTH AT THE SURFACE OF THE EXTERIOR DIAPHYSIS
  3. ) BONE RESORBED ON THE INTERIOR SURFACE OF THE DIAPHYSIS
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9
Q

REMODELING UNITS

A

MADE UP OF A COMPOSITE OF OSTEOBLASTS AND OSTEOCLASTS

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10
Q

EPIPHYSEAL PLATE CARTILAGE ORGANIZATION

A

Real People Have Career Options

  1. ) RESTING ZONE - SMALL INACTIVE CARTILAGE CELLS
  2. ) PROLIFERATION ZONE - QUICKLY DIVIDING (REPEATED MITOSIS) CHONDROBLASTS (PUSH EPIPHYSIS AWAY FROM DIAPHYSIS => LENGTHENING)
  3. ) HYPERTROPHIC ZONE - OLDER CHONDROCYTES ENLARGE AND SIGNAL TO THE SURROUNDING MATRIX TO CALCIFY
  4. ) CALCIFICATION ZONE - MATRIX BECOMES CALCIFIED AND CHONDROCYTES DIE LEAVING BONE-LIKE TISSUE (NOT BONE YET)
  5. ) OSSIFICATION ZONE - OSTEOCLASTS DIGEST CALCIFIED CARTILAGE AND OSTEOBLASTS REPLACE IT W/ ACTUAL BONE TISSUE IN THE SHAPE OF CALCIFIED CARTILAGE => BONE TRABECULAE
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11
Q

FUSION OF EPIPHYSIS

A

AT FULL BONE LENGTH CELLS IN EPIPHYSEAL CARTILAGE STOP PROLIFERATING AND BONES OF DIAPHYSIS AND EPIPHYSIS THEN BECOMES CONTINUOUS

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12
Q

ACHONDROPLASIA

A

DEFECT IN CARTILAGE FORMATION (MOST COMMON CAUSE = DWARFISM)

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13
Q

SALTER-HARRIS FRACTURES

A

INVOLVE EPIPHYSEAL PLATES (INTERFERES W/ GROWTH AND HEIGHT)

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14
Q

OSGOOD-SCHLATTER DISEASE

A

STRESS ON EPIPHYSEAL PLATES IN THE TIBIA LEAD TO EXCESS BONE GROWTH AND A PAINFUL LUMP IN THE BONE

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15
Q

SOMATOTROPIN

A

PRIMARY GROWTH FACTOR THAT AFFECTS BONE GROWTH
STARTS IN THE HYPOTHALAMUS
-TROPIN = TO NOURISH/STIMULATE

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16
Q

HYPOTHALAMIC PITUITARY AXIS

A

RELEASES GROWTH HORMONE RELEASING HORMONE (GHRH) WHICH CAUSES A RELEASE OF SOMATOTROPIN FROM THE ANTERIOR PITUITARY WHICH THEN TRAVELS TO THE LIVER AND STIMULATES THE RELEASE OF NEW GROWTH FACTOR, INSULIN-LIKE GROWTH FACTOR WHICH ACTS AS A NEGATIVE FEEDBACK LOOP AND BINDS TO THE HYPOTHALAMUS TO TELL IT TO STOP RELEASING GHRH VIA SOMATOSTATIN (GROWTH HORMONE INHIBITING HORMONE) AND PROMOTES FEMUR AND MUSCLE GROWTH

17
Q

GIGANTISM

A

EXCESSIVE GH SECRETION THAT STARTS IN YOUNG ADULTS/ADOLESCENTS
RARE, RESULTING FROM A TUMOR OF SOMATOTROPES
PITUITARY DISORDER

18
Q

ACROMEGALY

A

EXCESSESIVE SECRETION OF GH IN ADULTS AS A RESULT OF A BENIGN PITUITARY TUMOR
CLINICAL SIGNS -
1.) OVERGROWTH OF EXTREMITIES
2.) SOFT TISSUE SWELLING
3.) ABNORMALITIES IN JAW STRUCTURE - MAX/MAN PROGNATHISM (ONLY AFFECTED DUE TO 2˚ CARTILAGE)
4.) CARDIAC DISEASE
CAUSES HYPERGLYCEMIA - NO EFFECTS ON HEIGHT B/C EPIPHYSEAL PLATES ARE ALREADY CLOSED

19
Q

ESTROGEN’S ROLE IN CLOSURE OF EPIPHYSEAL PLATES DURING EARLY SEXUAL MATURATION

A

ESTRADIOL-17β (E2) HAS AN INDIRECT EFFECT ON THE E2/α-ESTROGEN RECEPTOR WHICH STIMULATES GROWTH HORMONE SECRETION AND YIELDS INCREASED LONGITUDINAL BONE GROWTH

20
Q

ESTROGEN’S ROLE IN CLOSURE OF EPIPHYSEAL PLATES DURING LATE SEXUAL MATURATION

A

E2 HAS A DIRECT EFFECT ON THE E2/α-ESTROGEN RECEPTOR WHICH INHIBITS CHONDROCYTE PROLIFERATION AND YEILDS A CESSATION OF LONGITUDINAL BONE GROWTH

21
Q

EPIPHYSEAL PLATE CLOSURE IN MALES

A

ANDROSTENEDOINE ————-> ESTRONE (LESS POTENT)
TESTOSTERONE ————> ESTRADIOL
SAME PROCESS AS FEMALES BUT GROWTH OCCURS FOR LONGER PERIODS OF TIME IN MALES

22
Q

BONE RESORPTION ESSENTIAL POINTS

A

RESORPTION BAYS - GROOVES FORMED BY OSTEOCLASTS AS THEY BREAK DOWN BONE MATRIX

23
Q

RESORPTION INVOLVES OSTEOCLAST SECRETION OF

A
  1. ) LYSOSOMAL ENZYMES THAT DIGEST ORGANIC MATTER
  2. ) HCL THAT CONVERTS CA2+ SALTS INTO SOLUBLE FORM
  3. ) BROKEN DOWN PRODUCTS ARE ENDOCYTOSED AND RELEASED INTO INTERSTITIAL FLUID/BLOOD
24
Q

BONE RESORPTION MECHANISM

A
  1. ) CA SYNTHESIZES HCO3- FROM CO2 AND H2O
  2. ) HCO3- IS CHANNELED TO THE SITE OF CACO3 SYNTHESIS
  3. ) POLYPHOSPHATE IS FORMED AND STORED W/IN CELL VESICLES AND NEUTRALIZED BY METAL IONS
  4. ) POLYPHOSPHATE IS RELEASED INTO EXTRACELLULAR SPACE AND HYDROLYZED BY ALKALINE PHOSPHATE
  5. ) ORTHOPHOSPHATE AND CA2+ (COMPONENTS OF SYNTHESIS OF HAP) ARE LIBERATED TO FORM CA5(PO4)3(OH)
  6. ) DEPOSITION OF HAP PROCEEDS ONTO CACO3 CRYSTALS
25
Q

A DIET RICH IN…

A

PROTEIN, VITAMIN C/D/A, CALCIUM, PHOSPHORUS, MAGNESIUM, AND MANGANESE IS REQUIRED FOR BONE DEPOSITION

26
Q

(1) OSTEOID SEAM AND (2) CALCIFICATION FRONT

A
  1. ) UNMINERALIZED BAND OF BONE MATRIX

2. ) BETWEEN THE OSTEOID SEAM AND THE OLD MINERALIZED BONE

27
Q

BONE GROWTH CESSATION

A

AT AGE…
21 FOR MALES
18 FOR FEMALES

28
Q

HORMONAL CONTROL OF BONE AND CALCIUM HOMEOSTASIS

A
  1. ) PARATHYROID HORMONE - (PTH) INCREASES THE NUMBER AND ACTIVITY OF OSTEOCLASTS, PROMOTES RECOVERY OF CALCIUM FROM URINE AND PROMOTES FORMATION OF CALCITRIOL (PART OF PARAFOLLICULAR TISSUE - CELLS IN THE THYROID OUTSIDE OF THE FOLLICULAR GLAND)
  2. ) CALCITONIN - INHIBITS ACTIVITY OF OSTEOCLASTS, SPEEDS UP CALCIUM ABSORPTION FROM BLOOD AND ACCELERATES CALCIUM DEPOSITION BY BONES
  3. ) VITAMIN D - CALCIUM AND PHOSPHATE ABSORPTION AND REABSORPTION, SIMILAR STRUCTURE TO ANDROGEN AND ESTROGEN
29
Q

VITAMIN D

A

ACTIVATED BY THE RUPTURE OF THE BETA RING BY UV LIGHT FROM THE SUN
ONCE ACTIVATE THE MOLECULE IS MOVED TO THE LIVER, TRANSFORMED AND MOVED TO THE KIDNEY WHERE IT IS OFFICIALLY ACTIVATED AND ALLOWED TO ACT ON VARIOUS TISSUES
INTESTINES - INCREASES DIET CALCIUM AND PHOSPHATE ABSORPTION
KIDNEYS - DECREASES CALCIUM LOSS IN THE URINE
BONE - INCREASES CALCIUM MOBILIZATION FROM THE BONE

30
Q

VITAMIN D ENDOCRINE ACTIONS

A 
INTESTINAL CALCIUM TRANSPORT
BONE METABOLISM
RENAL CALCIUM ABSORPTION
BLOOD PRESSURE
INSULIN SECRETION
31
Q

VITAMIN D AUTOCRINE/PARACRINE ACTIONS

A

INHIBITION OF CELL PROLIFERATION
PROMOTION OF CELL DIFFERENTIATION
IMMUNE REGULATION

32
Q

PTH BALANCE

A

INCREASED PTH INHIBITS RELEASE FROM OSTEOBLASTS/STROMAL CELLS OF OPG THAT INHIBITS OSTEOCLASTS
INCREASE PTH => INCREASED RANKL AND DECREASED OPG => INCREASED OSTEOCLASTS => INCREASED CALCIUM IN THE BLOOD

33
Q

HORMONAL REGULATION OF CALCIUM

A

RISING CALCIUM LEVELS TRIGGER THYROID TO RELEASE CALCITONIN (INHIBITS BONE RESORPTION AND STIMULATES CALCIUM SALTS TO BE DEPOSITED IN THE BONE)
FALLING CALCIUM LEVELS SIGNAL PTG TO RELEASE PTH (SIGNALS OSTEOCLASTS TO DEGRADE BONE MATRIX AND RELEASE CALCIUM INTO THE BLOOD)

34
Q

BONE COMPOSITION

A

60% INORGANIC MATERIAL - FORMED FROM HAP
25% ORGANIC MATERIAL - COMPOSED OF TYPE I COLLAGEN AND GF
15% WATER

35
Q

BONE REMODELING CYCLES

A

COUPLED AND BALANCED - OSTEOCLAST ACTIVITY = OSTEOBLAST ACTIVITY
COUPLED AND UNBALANCED - OSTEOCLAST ACTIVITY > OSTEOBLAST ACTIVITY
UNCOUPLED - OSTEOCLAST ACTIVITY&raquo_space; OSTEOBLAST ACTIVITY

36
Q

MECHANICAL STRESS ON BONE

A

INCREASES OSTEOBLAST ACTIVITY

37
Q

OSTEOPOROSIS

A

BONES BECOME FRAGILE AND MORE LIKELY TO FRACTURE, BONE LOSES DENSITY (I.E. CALCIUM AND MINERALS IN THE BONE)

Craniofacial Bone Biology (11 decks)

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