Term
| What is the normal concentration for calcium in the ECF? The normal phosphate concentration? |
|
Definition
1. 9.4mg/dL
2. 3-4 mg/dL in adults and 4-5 mg/dL in children |
|
|
Term
| What percentage of the body's calcium if in the ECF? ICF? Bones? |
|
Definition
|
|
Term
| What are the forms of calcium found in the plasma and what percentage of the calcium plasma content are they? Which are diffusible through plasma membranes? |
|
Definition
1. combined with plasma proteins (41%), combined with anionic substances (9%), ionized (50%)
2. ones combined with anionic substances and ionized calcium |
|
|
Term
| How percentage of the body's phosphate is in the ECF? ICF? Bones? |
|
Definition
|
|
Term
| In what forms is phosphate found in the blood and what percentage of the phosphate plasma content are they? |
|
Definition
1. HPO4- and H2PO4-
2. They vary a lot, due to both being buffers (conjugate base forms of phosphoric acid) |
|
|
Term
| What negative effect does low phosphorus have? High phosphorus? |
|
Definition
1. No significant effect short term, but long term in combination with hypocalcemia can lead to bone loss
2. No significant effect |
|
|
Term
| What is outer bone called? Inner spongy bone? |
|
Definition
1. compact bone
2. trabecular bone |
|
|
Term
| What is the usual rate of intake for calcium? How much is absorbed? How much is used in the blood or bones? |
|
Definition
1. about 1000 mg/day
2. Only about 35% (350 mg) will be absorbed
3. Only about 10% (100 mg) will be used, because 25% (250 mg) is secreted in the GI juices after being absorbed and is then sloughed by mucosal cells |
|
|
Term
| How much phosphate from the daily intake is absorbed? |
|
Definition
| Almost all of the phosphate, except for the phosphate attached to the unabsorbed calcium |
|
|
Term
| How much of the plasma calcium can be filtered? How much of that portion is filtered? Where? How much of it is reabsorbed? Where? How much is excreted per day? |
|
Definition
1. 59%
2. 99%
3. mostly the proximal tubules, loops of Henle, and early distal tubules
4. 10%
5. late distal tubules and early collecting ducts
6. about 100 mg, depending on calcium ion content and need |
|
|
Term
| How much of the plasma phosphate is reabsorbed? |
|
Definition
| The amount reabsorbed is directly proportional to the additional increase in plasma phosphate, unless concentrations drop below 1 mmol/L, at which point the kidneys absorb all the phosphate from the filtrate |
|
|
Term
| What are the consequences of hypocalcemia? At what levels do these problems start? What is a lethal low level? Hypercalcemia? At what levels can these symptoms be noticed? |
|
Definition
1. ↑ Na+ membrane permeability → increased action potentials → peripheral tetany and possibly seizures, other symptoms include clotting issues, dilation of the heart, cellular enzyme activity changes, and increased membrane permeability in some cells
2. 6 mg/dL
3. 4 mg/dL
4. ↑ [Ca2+] → ↓ nervous system excitability, constipation, lack of appetite, and decreased QT interval
5. 12 mg/dL |
|
|
Term
| What is the signature spasm indicating calcium deficiency? |
|
Definition
| Carpopedal spasm, which occurs in the hand making it look like a crane hand gesture |
|
|
Term
| What it the general composition of bones? |
|
Definition
| 30% organic matrix and 70% calcium salts |
|
|
Term
| What is the organic matrix of bones composed of? |
|
Definition
| 90-95% collagen fibers with the remainder being homogenous gelatinous medium called ground substance |
|
|
Term
| What substance in the "ground substance" assists in calcium salt deposition? |
|
Definition
| proteoglycans (especially condroitin and hyaluronic acid) |
|
|
Term
| What are bone salts composed of? What is the name of the crystal in bone salts? |
|
Definition
1. calcium and phosphate mainly, but also some magnesium, sodium, potassium, and carbonate
2. hydroxyapatite |
|
|
Term
| What contributes to compression strength in the bone? Tensile strength? Shear strength? |
|
Definition
1. calcium salts
2. hydroxyapatite crystal bonds to collagen
3. the overlap of collagen fibers and the overlap of crystals |
|
|
Term
| What lays down the bone matrix? What lays down the calcium salts? |
|
Definition
1. osteoblasts
2. the salts precipitate by themselves |
|
|
Term
| What happens when an osteoblast becomes trapped in the bone matrix/bone salts? If that happens, what is the area in the bone that it sits in called? |
|
Definition
1. It becomes inactive and is called an osteocyte
2. a lacuna |
|
|
Term
| Why do calcium salts not precipitate throughout the body instead of just where the bones are? Why can calcium salts precipitate in some old blood clots and degenerative tissues? |
|
Definition
1. inhibitors exist to prevent the precipitation; those inhibitors are absent in the bones
2. the inhibitors are absent there |
|
|
Term
| Where does the calcium come from to maintain calcium levels in the ECF? How long does it take to reestablish calcium levels? |
|
Definition
1. calcium exchange initially occurs from the amorphous bone salts that have not formed hydroyxapatite yet; after that it can be pulled from hydroxyapatite crystals or from various cells that have them stored in their mitochondria
2. 30-60 minutes |
|
|
Term
| What cells break down bone? How? |
|
Definition
1. osteoclasts
2. they send out villi and release proteolytic enzymes and acids from them to break down collage fibers and bone salts respectively; the products are then released into the ECF |
|
|
Term
| How does PTH affect bone deposition/reabsorption? |
|
Definition
| PTH attaches to osteoblasts, causing the release of cytokines including osteoprotegrin ligand (OPGL); this causes the differentiation of preosteoclasts into mature osteoclasts; osteoclasts also produce RANK-ligand and colony-stimulating factor, which preosteoclasts have the receptors and cause the differentiation of preosteoclasts into osteoclasts |
|
|
Term
| What kind of stem cells for osteoclasts differentiate from? |
|
Definition
|
|
Term
| How does estrogen affect bone deposition/reabsorption? |
|
Definition
| estrogen stimulates osteoblasts to secrete osteoprotegrin (OPG), aka osteoclastogenesis inhibitory factor (OCIF); this inhibits bone reabsorption and binds to OPGL, preventing osteoclast maturation |
|
|
Term
| How does vitamin D affect bone deposition/reabsorption? |
|
Definition
| vitamin D attaches to osteoblasts, causing the release of cytokines including osteoprotegrin ligand (OPGL); this causes the differentiation of preosteoclasts into mature osteoclasts |
|
|
Term
| How does the osteoclast/osteoblast reabsorption/deposition cycle work under normal conditions? When does bone deposition in an area usually stop? |
|
Definition
1. osteoclasts form masses and reabsorb small areas of the bone for 3 weeks, until a very small tunnel is made; then osteoclasts disappear and osteoblasts fill the tunnel, depositing the bone back in the tunnel
2. when the blood vessel that supplies the area is encroached upon |
|
|
Term
| What it the area in the bone that holds a blood vessel supplying the bone? |
|
Definition
|
|
Term
| How does the deposition/reabsorption cycle change with physical stress? Lack of stress? |
|
Definition
1. When stress is inflicted on a bone, the osteoblasts will be stimulated to deposit more bone to adjust the strength of the bones for the stress inflicted upon them; bone shape may even change slightly due to this additional deposition
2. more bone will be reabsorbed over time and the bone will become brittle |
|
|
Term
| What cellular activity occurs in the bone immediately after a fracture? What happens if a fractured bone is set at an angle? |
|
Definition
1. osteoprogenitor cells that sit in the "bone membrane" (the surface tissue living the bone) differentiate into osteoblasts and are recruited to the site of the fracture; new bone matrix is then formed followed shortly by new calcium salt deposition in a formation of a callus
2. The parts of the fractured bone that are touching will receive more stress and the non-touching portions will receive less; over months or years (depending on many factors, especially age and activity of the osteoblasts/osteoclasts) the bone will fill in the portion that receives more stress and absorb the unstressed part, somewhat fixing the angle of the bone |
|
|
Term
| What is the active form of vitamin D? |
|
Definition
| 1,25-di-hydroxycholecalciferol (1,25(OH)2D3 or calcitriol) |
|
|
Term
| What type of hormone is vitamin D? Steroid, peptide, amine derivative, gas, or eicosanoid? |
|
Definition
|
|
Term
| How is vitamin D made in sunlight? Where is excessive vitamin D stored? |
|
Definition
1. irradiation of 7-dehydrocholesterol by UV light produces vitamin D3 (cholecalciferol), which can be converted into the precursor of the active form of vitamin D (25-hydroxycholecalciferol) in the liver and into the active form in the kidneys with the help of PTH
2. in the liver |
|
|
Term
| How is the vitamin D production regulated? |
|
Definition
| calcitriol provides negative feedback control to the liver's conversion of D3 to the precursor |
|
|
Term
| How long do the effects of vitamin D last? |
|
Definition
| The vitamin D stays attached to its receptor for 2 days, but the effects of its attachment for weeks |
|
|
Term
| What activity does vitamin D have in the intestine? How? |
|
Definition
| 1. it assists in the absorption of calcium from the intestine; decreased calcium causes increased conversion of D3 to the precursor, which allows that to be converted into calcitriol; increased calcitriol increases calbindin trancription and translation, which causes increased calbindin, which causes increased calcium absorption |
|
|
Term
| What is the concentration of vitamin D in the blood when there are normal calcium levels? Low calcium concentrations? High calcium concentrations? |
|
Definition
1. almost zero
2. very high
3. almost completely zero; precursor molecules would be converted into inactive forms |
|
|
Term
| Where is the receptor site for vitamin D? |
|
Definition
| 1. In the nucleus; it forms a complex with the retinoid-X receptor and then binds to DNA to activate transcription |
|
|
Term
| What effect does vitamin D have in epithelial cells? Renal cells? |
|
Definition
1. it promotes the transcription of calcium-stimulated ATPase in the brush border and alkaline phosphatase
2. it promotes absorption of phosphate and provides a weak effect of preventing the renal excretion of calcium and phosphate |
|
|
Term
| What is the effect of vitamin D in bones? |
|
Definition
| It promotes bone calcification of bones in small doses and the absorption of bones in large doses |
|
|
Term
| Where is the parathyroid glands located? How many are there? |
|
Definition
1. On the posterior portion of the thyroid gland
2. 4 |
|
|
Term
| What would happen if one parathyroid gland was removed? Two? Three? Four? |
|
Definition
1. The other glands would be able to maintain PTH levels
2. The other glands would be able to maintain PTH levels
3. PTH levels will be low and function will be depressed for a while until the remaining gland can hypertrophy to compensate for the loss of other glands
4. There will be a complete loss of PTH production |
|
|
Term
| What types of cells are in the parathryoid gland and what are their functions? |
|
Definition
1. chief cells, which are believed to produce most of the PTH and are the primarily cells
2. Oxyphil cells, which are believed to be inactive and/depleted chief cells |
|
|
Term
| What kind of hormone is PTH? Peptide, steroid, eicosanoid, amine derivative, or gas? How is it made? |
|
Definition
1. Peptide
2. It is formed as a preprohormone, cleaved into a prohormone, and then into a hormone and stored in granules/vesicles for when it is released; the fragments are released with it and they exhibit some PTH attributes as well |
|
|
Term
| What is the function of PTH? |
|
Definition
| It increases the reabsorption of calcium from the bones (beginning with the amorphous bone salts) and reduces calcium excretion; it also strongly promotes the excretion of phosphate from the kidneys |
|
|
Term
| How long does PTH activity last? |
|
Definition
|
|
Term
| How is PTH secretion regulated? |
|
Definition
| by calcium ion concentration; as [Ca2+] drops, PTH rises; as [Ca2+] rises, PTH drops |
|
|
Term
| How does sustained hypocalcemia affect the parathyroid glands? How about in rickets? Osteomalacia? Explain why for each. |
|
Definition
1. it causes the glands to hypertrophy, because if the calcium levels won't go up with large amounts of PTH that it already produces, the gland will need to grow to try to produce excess PTH
2 and 3. They both cause hypertrophy of the glands; rickets and osteomalacia both include vitamin D deficiency; vitamin D greatly increases the effectiveness of PTH, so, in the absence of vitamin D, PTH levels will have to dramatically increase to raise calcium levels in the blood |
|
|
Term
| How are parathyroid glands affect by pregnancy? Lactation? Why? |
|
Definition
| For both, the glands are enlarged and PTH levels are high because the mother's body needs to provide a large amount of calcium for the baby; the baby will be undergoing rapid bone growth in the womb, so calcium levels need to be high, and there need to be high calcium levels to provide adequate calcium in breast milk during lactation |
|
|
Term
| How will high calcium and vitamin D intakes in diet affect the parathyroid gland? |
|
Definition
| they will cause hypotrophy of the gland |
|
|
Term
| What is the receptor that monitors calcium levels? Is it cell-surface, intracellular, or nuclear? |
|
Definition
1. calcium-sensing receptor (CaSR)
2. cell-surface |
|
|
Term
| What second messenger system does CaSR use? |
|
Definition
| 1. g-protein, which activated PLC which eventually causes the release of calcium stores and inhibition of PTH secretion |
|
|
Term
| How is PTH transported to target tissues? |
|
Definition
| it is soluble in the blood |
|
|
Term
| Which bone cells does PTH signal for reabsorption? |
|
Definition
| 1. mostly osteocytes, but it signals osteoblasts as well, which subsequently signal preosteoclasts to differentiate into osteoclasts |
|
|
Term
| What is the osteocytic membrane system? |
|
Definition
| a network of processes that connect osteocytes throughout the bone and on the surface of the bone |
|
|
Term
| How does calcium get from the bones to the blood in bone reabsorption? |
|
Definition
| between the osteocytic membrane and the bone is a small amount of bone fluid; when PTH attaches to cell surface receptors, it causes an increased permeability in the cell membrane to calcium; osteocytes (stimulated by PTH) pump calcium from the bone fluid to the ECF on the other side, lowering the calcium concentration in the bone fluid and encouraging the deposited calcium to be absorbed into the fluid; the ECF calcium is then picked up by the blood to reestablish blood concentrations of calcium |
|
|
Term
|
Definition
| then process by which calcium phosphate salts will be absorbed from the bone, but does not disrupt the fibrous and gel matrix of the bone's structure; as such, this process can't involve proteases or acids |
|
|
Term
| Where in the nephron does PTH exert its influence? |
|
Definition
| PTH reduces reabsorption of phosphate in the proximal tubules and the thick ascending leg of the loop and increases reabsorption of calcium mainly in the late distal tubules, collecting tubules, early collecting ducts, and possibly the ascending loop of Henle; PTH also increases the rate of reabsorption of magnesium and hydrogen and decreases the rate of reabsorption for sodium, potassium, and amino acids |
|
|
Term
| What is hypoparathryoidism? What does it cause? How is it treated? |
|
Definition
1. low PTH secretion
2. decreased osteolytic activity, causing low calcium, which can cause tetany of the hands and laryngeal muscles, the later of which can cause obstruction of respiration
3. PTH, vitamin D, and calcium supplements can be used, but PTH supplements are expensive and the body may develop antibodies against it, so oftentimes very high calcium and vitamin D levels are used instead |
|
|
Term
| What is primary hyperparathyroidism? What does it cause? |
|
Definition
1. excessive productive of PTH, usually by a tumor in the PT gland(s)
2. excess PTH secretion causes increased osteolytic activity and proliferation of osteoclasts, causing increased bone reabsorption, causing large increases in plasma calcium and loss of bone mass and integrity; loss of bone mass causes the stimulation of osteoblastic activity which causes an increase in calcium and phosphate deposition, but it will not be enough to counteract PTH; the large increase of calcium cause depression of the PNS and CNS, celiary problems, muscle weakness, constipation, abdominal pain, peptic ulcers, lack of appetite, and depressed relaxation of cardiac muscle during diastole; if calcium and phosphate levels are high enough, calcium salts will be deposited in other areas of the body |
|
|
Term
| What is it called when calcium salts are deposited outside of the bones? Where are they despoited? How high does blood calcium have to be in order to cause such deposition? |
|
Definition
1. metastatic calcification or parathyroid poisoning
2. alveoli of the lungs, tubules of the kidneys, the thyroid gland, acid-producing area of the stomach mucosa, and walls of the arteries
3. 17 mg/dL |
|
|
Term
| What is osteitis fibrosa cystca? What does it cause? |
|
Definition
1. proliferation of osteoclasts
2. the bones become very weak and have large holes or tunnels in them from apparent osteoclast "tumors" (large masses of osteoclasts) |
|
|
Term
| What are kidneys stones? What causes them? What do kidney stones cause? How are they treated? |
|
Definition
1. precipitations of calcium oxalate
2. increased levels of calcium can cause this conditions and alkaline urine levels promote it; such calcium levels are sometimes due to slight hyperparathyroidism
3. kidney stones can cause severe pain and possibly damage to the kidneys
4. They are sometimes treated with acidotic diets and acidic drugs, but honestly most doctors just give a patient an Rx for a handful of vicodin and some flomax and tell him to pass the stone in the painful comfort of his own home |
|
|
Term
| What is secondary hyperparathyroidism? What causes it? |
|
Definition
1. excess PTH secretion not caused by a tumor
2. vitamind D deficiency or chronic renal disease (which makes the kidneys unable to produce sufficient active vitamin D) causes hypocalcemia, causing production of excess PTH |
|
|
Term
| What is rickets? What causes it? |
|
Definition
1. vitamin D deficiency in children
2. usually it is causes by insufficient exposure to sunlight, resulting in reduced vitamin D production; this often occurs in winter, when the child stays indoors because he has no sense of how fun cold weather can be and has a horrible diet because his parents don't care and the child's body uses up the vitamin D stores in the liver |
|
|
Term
| What are the consequences of rickets? How is it treated? |
|
Definition
1. lack of vitamin D means PTH activity will increase, causing a slight drop in calcium but a large drop in phosphate levels via excretion; increased PTH means increased osteoclastic activity, causing increased bone reabsorption, which will eventually cause increased osteoblastic activity; however, there will be a loss of calcium, meaning there will be bone remodeling without deposition of calcium salts, making the new bone weak and flexible; eventually low calcium can cause tetany
2. vitamin D, calcium, and phosphate supplementation |
|
|
Term
| What is osteomalacia? What causes it? What does it cause? |
|
Definition
1. vitamin D deficiency in adults
2. adults seldom have vitamin D deficiency, but sometimes the deficiency can occur due to steatorrhea (the inability to absorb fat); since vitamin D is fat soluble, it will remain in the gut
3. if calcium can also not be absorbed (due to a lack of vitamin D), the calcium will form insoluble soaps with the fat in the gut; tetany rarely results from osteomalacia, but bone compromise may result (by the same causation as rickets) |
|
|
Term
| What is renal rickets? What does it cause |
|
Definition
1. a kidney disease causing a reduction in the production of the active form of vitamin D
2. it causes the same problems as rickets |
|
|
Term
| What is congenital hypophosphatemia? What does it cause? How is it treated? |
|
Definition
1. kidneys congenitally have reduced reabsorption of phosphates
2. it causes the same problems as rickets because calcium salts will not form without phosphates
3. treated with phosphate supplementation |
|
|
Term
| What is the most common bone disease in adults? What causes it? What does it cause? |
|
Definition
1. osteoporosis
2. as one ages, osteoblastic activity reduces without a subsequent reduction of osteoclastic activity, causing bone reabsorption to exceed bone deposition; insufficient calcium, lack of vitamin C (necessary for secretion of intercellular substances), and malnutrition may cause it too; other causes include a lack of stress on the bones, menopause causing a lack of estrogen (estrogen decreases the number and activity of osteoclasts), other effects of old age (reduction in metabolism, reduced hGH, etc), and Cushing's syndrome, the latter of which causing excessive glucocorticoids which cause protein catabolism and inhibit protein deposition, which means osteoblasts would be inhibited
3. it causes a loss of organic bone matrix, causing a loss of bone density |
|
|
Term
| What kind of hormone is calcitonin? Eicosanoid, gas, steroid, peptide, or amine derivative? How is it synthesized? |
|
Definition
1. peptide
2. it is synthesized as a preprohormone, cleaved to a prohormone, then to a hormone and stored in vesicles in the parafollicular cells or the C cells lying in the interstitial fluid between the thyroid follicles |
|
|
Term
| What does calcitonin cause? What is its secretion in response to? |
|
Definition
1. decreased plasma calcium concentrations by deposition of calcium salts on bone surfaces
2. high calcium concentrations |
|
|
Term
| What is the mechanism of action of calcitonin? |
|
Definition
| 1. it causes an immediate decrease in absorptive activities of the osteoclasts and the osteocytic membrane, resulting in a favor of calcium deposition, meaning decreased plasma calcium concentrations; decrease in osteoclastic activity decreases the number of osteoclasts eventually and, since osteoclastic activity promotes osteoblastic activity, calcitonin eventually decreases both |
|
|
Term
| How long does calcitonin activity last? |
|
Definition
| Not long; in fact, calcitonin activity is, in effect, essentially transient |
|
|
Term
| Does calcitonin have more effect in adults or children? Why? |
|
Definition
1. children
2. because their osteoclasts and osteoblasts are more active and more bone remodeling occurs |
|
|
Term
| Besides the bones and their calcium stores, how else can the body replenish plasma calcium concentrations? |
|
Definition
| reabsorption of calcium from the filtrate, absorb more calcium from the gut, or release calcium from mitochondrial stores |
|
|
Term
| What is the role of teeth in digestion? |
|
Definition
| They increase the surface area of food, allowing digestive enzymes to work more efficiently |
|
|
Term
| How much force can the front teeth exert? The back teeth? |
|
Definition
1. 50-100 lbs
2. 150-200 lbs |
|
|
Term
| From superficial to deep, what are the layers of the teeth? |
|
Definition
| enamel, dentin, pulp, cementum (deep to the outside of the mouth, but superficial to the center of the tooth) |
|
|
Term
| From superior to inferior, what are the parts of the tooth? Define them. |
|
Definition
| crown (the portion visible above the gums/the part with enamel), neck (the portion where the root and crown meet), root (the portion that connects the crown with the jaw) |
|
|
Term
| What is the enamel of the tooth formed by? When? What is it composed of? |
|
Definition
1. ameloblasts
2. prior to the eruption of the tooth
3. large dense hydroxyapatite crystals with absorbed carbonate, magnesium, potassium, and other ions in a meshwork of protein similar to keratin |
|
|
Term
| What is the most corrosive-resistant substance of the body? |
|
Definition
|
|
Term
| What is the main body of the tooth composed of? What is it composed of? |
|
Definition
1. dentin
2. a strong meshwork of collagen fibers and hydroxyapatite crystals that are denser than regular bone |
|
|
Term
| How is dentin nourished? How is resistant to compression forces? Tensional forces? |
|
Definition
1. it is nourished by odontoblasts
2. calcium salts make it resistant to compression forces
3. collagen fibers make it resistant to tensional forces |
|
|
Term
| How does cementum help bind the tooth to the jaw? |
|
Definition
| 1. it is a bony substance that binds the tooth to the jaw and several collagen fibers from the jaw also bind the tooth to the jaw; additionally, when the tooth is exposed to excessive strain, the cementum grows thicker; it also grow thicker and stronger with age |
|
|
Term
| What is the core of the tooth composed of? What is in this layer? |
|
Definition
1. pulp
2. nerve fibers, blood vessels, and lymphatics |
|
|
Term
| What forms the dentin of the tooth? |
|
Definition
| odonoblasts that line the pulp of the tooth |
|
|
Term
| Is there any calcium, phosphate or other mineral exchange with the teeth as there is with other bones? |
|
Definition
| Yes, it occurs in the cementum at the same rate as bones, in the dentin more slowly, and in the enamel even more slowly |
|
|
Term
| How many sets of teeth do humans develop? What is the first set of teeth called, how many are there, and when do they show up? How about the second set? |
|
Definition
1. 2
2. deciduous or milk teeth, of which there are 20 and they show up within the first few years of life and fall out from ages 6-20
3. permanent teeth, of which there are 28-32 (depending on if the wisdom teeth erupt), and they show up from age 6 and later |
|
|
Term
| How is the cell layer that forms teeth formed? What part of the layer forms the ameloblasts? The odontoblasts? |
|
Definition
1. in utero, epithelium above the teeth invaginates into the dental lamina to form the tooth-producing organ
2. the upper portion of the epithelial cells
3. the lower portion of the epithelial cells |
|
|
Term
| What causes the eruption of teeth through the gums? What causes deciduous teeth to fall out? |
|
Definition
1. it is uncertain, but it is most likely the development of the bone underneath the tooth
2. as permanent teeth are pushed through the gums, they erode the root of the deciduous teeth and cause them to fall out |
|
|
Term
| What factors contribute to the development of teeth? |
|
Definition
| growth hormone, thyroid hormone, dietary calcium, phosphate, vitamin D levels, and PTH secretion |
|
|
Term
| What are caries? What cause them? |
|
Definition
1. cavities in the teeth
2. bacteria growing in the mouth release acids after the digestion of carbohydrates; the acids dissolve the enamel, causing cavities to form, after which proteolytic enzymes they secrete can aid in the destruction of dentin |
|
|
Term
| What is the most common bacteria involved in carie formation? What methods are offered to prevent carie formation? |
|
Definition
1. streptococcus mutans
2. low carbohydrate diets, which largely deprive bacteria of their food source; brushing, which removing the pplaque that forms from bacteria, saliva, and food; alcohol rinses, which can kill bacteria; fluorine, which make the teeth stronger by replacing the hydroxyl groups on hydroxyapatite crystals with fluorine and are also believed to be both toxic to bacteria and helpful in laying down calcium salts in small pits in the enamel |
|
|
Term
| What is a malocclusion? What causes this? What can it cause? |
|
Definition
1. the situation of the upper and low teeth not digitating properly
2. hereditary abnormality, usually
3. it can cause improper function of the teeth, misplacement of the lower jaw with the upper jaw, pain, and/or abnormal wear to the teeth |
|
|
Term
| How is malocclusion treated? |
|
Definition
| braces can gradually apply pressure to the teeth, shifting them into place, and gradually apply pressure to one side of the jaw, resulting in new bone on the compressed side of the jaw and bone absorption on the non-compressed side |
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|
