Final Exam Flashcards

(232 cards)

1
Q

What are the three main cytoskeletal components?

A
  1. Microfilaments
  2. Intermediate Filaments
  3. Microtubules
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2
Q

Microfilaments:

A

Composed of Actin, 6-8 nm in diameter, structural function, gives shapes to cells, and forms tracks for myosin, giving contractility.

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3
Q

Intermediate Filaments:

A

Vimentin (mesenchymal origin) and cytokeratin (epithelial origin). They are around 10 nm in diameter, and they anchor and help with structure, but are non-contractile. Tonofilaments are another word for intermediate filaments in epithelial cells, and they insert into desmosomes and around the peripheries of cells.

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4
Q

Microtubules:

A

Around 25 nm in diameter. Made of tubulin. They compose the monorail system (kinesins) and cilia and flagella (dynein). They help form the motor protein complex around the tubulin.

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5
Q

What are the 6 types of cell attachments?

A
  1. Tight junctions
  2. Zonula Adherens
  3. Focal Adhesion
  4. Desmosomes
  5. Hemidesmosomes
  6. Gap Junctions
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6
Q

Tight Junctions:

A

Made up of claudins, occludin, JAM, and they bind to actin microfilaments and serve as very narrow gaps between cells to control movement of stuff.

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7
Q

Zonula Adherens:

A

These hold cells together, remember that. Made up of cadherins on the outside and cantinins on the inside. The cadherins are Calcium dependent. They have vinculin and actinin attachments to actin filaments. Remember that zonula adherens bind to actin filaments, not intermediate filaments. Gaps of 20 nm.

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8
Q

Focal Adhesion Junctions:

A

These hold cells to extracellular matrix, and are similar to Cell-Cell adhesions. So here the cells are sticking to the matrix, as opposed to another cell (or actin). Integrins replace cadherins here and interact with many ECM proteins like collagen.

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9
Q

Desmosomes:

A

These are Cell-Cell adhesion. Cadherins are on the outside, and are called desmoglein and desmocollin. Catinins are on the inside and start with plako or desmoplakin. They attach to intermediate filaments, remember that. They have gaps of 25 nm, and hep resist shearing forces.

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10
Q

Hemidesmosomes:

A

These are cell to matrix adhesion, similar to focal adhesions, but they look more like desmosomes. These attach to intermediate filaments like desmosomes. They tightly attach to basal lamina by integrin-laminin and collagen XVII. They help resist shear as well.

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11
Q

Gap Junctions:

A

These are cell-cell aqueous pores. 6x connexins = 1x connexon. They form a 2nm pore, and have 2-3nms between cells. Ions and small molecules pass through but nucleic acids, sugars, and proteins are too large.

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12
Q

Basal Lamina:

A

ECM sheet attaching epithelium to connective tissue. Hemidesmosomes are here. It is 50-100nm thick. It has three zones. From top to bottom: Lamina Lucida (laminin, integrins), Lamina densa (collagen IV), and Lamina fibroreticularis (collagen III).

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13
Q

Fibroblasts:

A

They are the main cell in connective tissue. Highly motile, involved in tissue repair. Rarely have cell to cell connections, only exception is PDL. They often have cytoskeletal (actin) connections from integrins to fibronectin. Dental pulp is mostly collagen 3, and there are mainly fibroblasts there.

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14
Q

Collagen:

A

It is a triple helical structure, and is the most abundant protein in the body. It is rich in proline and lysine. Dentin is mostly type I collagen, some type II. Pulp is a mixture of collagen type I and collagen type III, and Cartilage is type II collagen. It is stacked with 5 microfibrils and a 1/4 stagger. In bone/dentin, mineral is deposited in the gap regions. Scurvy has to do with Vitamin C, specifically, prolylhydroxylase.

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15
Q

Elastin:

A

Is a fibroblast product. Assembled into sheets or fibers. Fibrillin-1 and fibirillin-2 which are glycoproteins form a microfibril scaffold onto which elastin fibers accumulate. Marfan’s syndrome is a fibrillin-1 mutation.

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16
Q

Connective Tissue Ground Substance:

A

Made up of mainly proteoglycans and glycoproteins. It is the “non fibrillar” stuff that makes up the rest of ECM. It is highly hydrated, sequesters fluid, gives compressive strength to tissues.

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17
Q

Proteoglycans:

A

Is made by fibroblasts, and is a main component of ground substance. They are protein cores with glycosaminoglycan chains (GAG). And GAGs are disaccharide units. But proteoglycans have relatively strong negative charges and are hydrophilic. Hyaluronic acid is an example. Perlecan and syndecan are examples of non-aggregating proteoglycans. But proteoglycans serve to sequester growth factors in ECM and can help activate GF receptors.

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18
Q

Glycoproteins:

A

These are proteins with carbohydrate side chains attached. They are found everywhere, but also in ground substance. Fibronectin, thrombospondin are both examples. Proteoglycans are technically specialized glycoproteins, and proteoglycans generally have a larger carbohydrate component than protein.

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19
Q

How is ECM digested?

A

With MMPs. As well as intracellular matrix.

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20
Q

What guides organogenesis?

A

Epithelial-mesenchymal interactions.

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21
Q

Which interactions dictate morphogenesis and differentiation? Cell-Cell or Cell-Matrix.

A

Cell-Matrix

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22
Q

What is ectomesenchyme?

A

It is embryonic connective tissue. Neural crest cells generate ectomesenchymal derivates like bone, dentin, cementum, periodontal ligament.

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23
Q

What is the stomatodeum covered with?

A

Primitive epithelium

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24
Q

What are the primary epithelial bands?

A

They are layers of thin ectoderm that become denser over time.

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25
What forms the dental lamina?
In oral epithelium, cell proliferation causes thickening, invaginates into the basement membrane, and becomes dental lamina. Mesenchyme is found underneath the tooth bud/dental lamina. The primary epithelial band and the dental lamina represent where the teeth start growing.
26
What are the six stages of Crown development?
1. Initiation - induction 2. Bud stage - proliferation 3. Cap stage - proliferation, differentiation, morphogenesis 4. Bell stage - proliferation, differentiation, morphogenesis 5. Apposition stage - induction and proliferation 6. Maturation stage - maturation
27
Initiation Stage:
Induction is the process whereby one tissue changes the development of surrounding tissues.
28
Bud Stage:
At ten locations along each dental lamina, proliferation of epithelium produces buds. Each bud is the precursor of the enamel organ for each deciduous tooth.
29
What are the layers of a developing tooth in the bell stage from outside in?
Dental epithelium, Outer dental epithelium, enamel organ, stellate reticulum (rich in GAGs, supports enamel production), stratum intermedium (which is rich in alkaline phosphatase, and important in mineralization), inner dental epithelium (which gives rise to ameloblasts), dental papilla, dental follicle.
30
Cap stage:
Ectomesenchymal cells condense around developing cap, and these become the dental papilla and dental sac. The tooth germ = enamel organ + dental papilla + dental sac. Successional dental lamina forms on lingual side of dental lamina.
31
What is the dental sac?
It is made up of the dental papilla and all of the mesenchyme.
32
What is the enamel knot?
It is found just north of the dental papilla, on the other side of the inner enamel epithelium. We believe that the enamel knot is the signaling center, has many genes that control the shape of the tooth, growth factors play a role as well.
33
At what stage are the four distinct layers of the developing tooth formed?
The bell stage. Continued differentiation of enamel organ produces four distinct layers with different functions: • Outer enamel epithelium. • Stellate reticulum. • Stratum intermedium. • Inner enamel epithelium. Also, during the bell stage, the cervical loop is formed, which is the junction of the OEE and IEE, and it is epithelium that will determine the shape and size of the roots of the tooth, and will become future CEJ.
34
Apposition stage:
This is the stage when the organic matrix of enamel and dentin are laid down followed by initial calcification. The order goes like this: IEE cells differentiate into preameloblasts, so these cells become polarized. Then preameloblasts induce outer dental papilla cells to differentiate into preodontoblasts which continue differentiating into odontoblasts. So IEE becomes ameloblasts, and outer dental papilla cells become odontoblasts. Enamel secretes down and dentin secretes up, both towards the DEJ. The first layer of dentin is produced and that sends signals to the ameloblasts to form more and secrete enamel. The DEJ forms after disintegration of the basement membrane. Prismless enamel is formed by early secretory ameloblasts. Enamel prisms are formed by Tomes processes of late secretory ameloblasts. Odontoblasts begin to secrete organic matrix of dentin- predentin. Predentin induces differentiation of preameloblasts into ameloblasts. Ameloblasts begin secreting enamel matrix which immediately calcifies to 25% of full mineralization.
35
Where is Tome's process found?
It is the part on the ameloblast that sticks out toward the dentin. And the odontoblasts has a odontoblastic pocess that sticks into the enamel matrix that gives the tooth vitality in the future.
36
Where does the dental lamina come from?
It comes from the ectoderm lining.
37
What two things come from the ectoderm of the arch?
Tooth germ and ectomesenchyme from neural crest.
38
What three things come from the tooth germ?
Enamel organ, dental papilla, dental follicle/sac.
39
What gives rise to the root form of a tooth.
Hertwig's root sheath, which came from cervical loop, which came from enamel organ.
40
What gives rise to enamel?
Ameloblasts, which came from the inner enamel epithelium, which came from the enamel organ.
41
What gives rise to dentin?
Odontoblasts, which came from dental papilla.
42
What gives rise to pulp?
Undifferentiated mesenchyme cells and fibroblasts, which came from dental papilla.
43
What three things does the dental follicle/sac give rise to?
Cementum (cementoblasts), PDL (fibroblasts), Alveolar bone (osteoblasts).
44
What are the seven stages of an ameloblast life cycle?
1. Inner enamel epithelial cells 2. Pre-ameloblast 3. Initial secretory ameloblasts (no tomes process, prismless enamel) 4. Secretory ameloblast (tomes process, emamel prisms) 5. Smooth ended maturation ameloblast (removal of protein and water 6. Ruffled ended maturation ameloblast (introduction of inorganic material 7. Protective ameloblasts (enamel cuticle)
45
Maturation stage:
– After deposition and initial mineralization of enamel, secretory ameloblasts lose Tomes process. – Maturation ameloblasts differentiate and remove some enamel proteins and water, and pump additional Ca++ into the matrix. – Final differentiation of ameloblasts into protective ameloblasts. – Basal lamina type material (enamel cuticle) secreted and ameloblasts attach to enamel surface via hemidesmosomes. – This will become the epithelial attachment after eruption. – Reduced enamel epithelium (REE) forms after enamel is fully matured. – REE consists of OEE, IEE and intervening remnants of the other two layers of the enamel organ (stellate and stratum).
46
What is mantle dentin?
It is the initial layer of dentin next to DEJ. It has higher mineral content and its collagen fibers are perpendicular to the DEJ. The remaining dentin around pulp is called circumpulpal dentin, and this has lower mineral content with fibers parallel to DEJ.
47
What is root dentin and epithelial rests of Malassez?
The REE grows apically and eventually becomes HERS. HERS then induces dental papilla outer cells to become root odontoblasts, which then secrete predentin. HERS then detaches from root dentin and disintegrates, and remnants are considered epithelial rests of Malassez. Also, remember that roots are not complete until after the tooth has erupted and is in function.
48
How is cementum formed?
Dental sac cells migrate in and contact new root dentin surface and there is induction of dental sac cells to differentiate into cementoblasts, which secrete organic matrix called cementoid on new dentin surface, which eventually mineralizes into cementoid. In the apical 1/2 to 2/3 of root, cementoblasts become entrapped in lacunae as cementocytes.
49
Where does the PDL come from?
Dental sac ectomesenchyme cells differentiate into fibroblasts, which secrete collagen fibers, which become anchored in cementum as it is deposited by cementoblasts.
50
Where does alveolar bone come from?
Dental sac ectomesenchyme cells differentiate into osteoprogenitor cells then osteoblasts and lay down bone. And developing collagen fibers of the PDL become anchored in alveolar bone.
51
What are the four classes of signaling factors with tooth development signaling?
Oral ectoderm, dental placode, enamel knot, and secondary enamel knots. Some of these transcription factors stay inside, while the other ones are called growth factors and they can leave the nucleus. Transcription factors are found in all cells.
52
What are the two theories of tooth development?
1. Field Theory (the cells migrate down and they don't know what they are yet and they are influenced by molecules in the field or transcription factors) 2. Clone Theory (the cells migrate down and they know where to go, molar, cuspid, incisor, and all have their own clones. The bicuspid is a hybrid. - And the zone of inhibition just makes sure that we don't have extra teeth popping out all over our jaw, it makes a boundary of where teeth can form.
53
Table of when epithelium and stages are inductive and will grow teeth:
With the lamina and bud stage, dental epithelium is the inductive one. So if you have tooth epithelium from the lamina or bud stage and combine it with other mesenchyme, you will grow a tooth. And during the cap and bell stage, dental papilla mesenchyme is the inductive one. So if you have tooth mesenchyme and combine it with other epithelium, you will grow a tooth.
54
What is the nerve, artery, muscles, and bones associated with the 1st arch?
Nerve - Mandibular Nerve Artery - Maxillary Muscles - Mastication (temp, mass, pterys), Mylohoid, anterior belly of digastric, tensor palati and tympani Bones - Maxilla, Mandible, Malleus, temporal bone, zygoma, incus
55
What is the nerve, artery, muscles, and bones associated with the 2nd arch?
Nerve - Facial Nerve Artery - Corticotympanic Muscles - Facial expression, posterior belly of digastric, Stapedius, Stylohyoid Bones - Stapes, Styloid process, upper half and lesser horns of hyoid
56
At what week does central face development happen?
At week 4. This is when nasal placodes start to develop and thicken, and you get a proliferation of ectomesenchyme on both sides of each placode resulting in the medial and lateral nasal processes.
57
How is the upper lip formed?
It is formed at 6 weeks and the medial nasal processes merge with each other as well as the maxillary processes of the first brachial arches to form the upper lip.
58
What are the primary and secondary palates formed from?
Primary - merger of the medial nasal processes | Secondary - formed from the maxillary processes of the first branchial arches
59
What is cleft lip and what causes it?
It is defective fusion of the medial nasal processes with the maxillary process. 80% of cases are unilateral.
60
What is cleft palate and what causes it?
It is a failure of the palatal shelves to fuse, and the minimal manifestation of it is a bifid uvula. The majority of cases are Cleft Lip + Cleft Palate together, and then Cleft palate alone, and finally Cleft lip alone.
61
Syndromic clefts:
There are more than 350 syndromes that can causes orofacial clefts. 30% of patients have CL + CP, while 50% of patients have Cleft Palate only. So with syndromes, it is more common to just have Cleft palate rather than both. Pierre Robin sequence is an example of cleft palate only syndromic problem, with mandibular micrognathia and downward discplacement. Nonsyndromic clefts can happen from folic acid deficiency, maternal alcohol or cigarette, corticosteroid use, etc.
62
What is lateral facial cleft?
Lack of fusion of the maxillary and mandibular processes.
63
What is oblique facial cleft?
Failure of fusion of the lateral nasal processes with the maxillary process. Upper lip to the eye, and almost always associated with CP.
64
What is a median cleft of the upper lip?
Failure of fusion of the medial nasal processes, very rare.
65
What type of race gets Cleft Palate the most?
Native Americans, then Asians, then Caucasians. CL + CP is more common in males, while CPO is more common in females.
66
What is it called when an indent appears in the very middle on the posterior hard palate margin, appears as a bluish midline discoloration, and the surface appears intact?
A submucous palatal cleft.
67
To treat cleft lip, what three things must you pass?
Rule of 10. 10 weeks old, 10 lbs, and 10gm %HM.
68
What are lip pits most commonly associated with?
Syndromes, they are usually bilateral. van der Woude syndrome is the most common cause of paramedian lip pits., also has CL + CP and is most common form of syndromic clefting.
69
What is microglossia?
Abnormally small tongue. Frequently associated with hypoplasia of the mandible. Lower incisors may be missing. Usually syndromic.
70
What is it called when the tongue has a short, thick lingual frenum resulting in limitation of tongue movement?
Ankyloglossia. Happens four times more in males, may cause problem with speech and breastfeeding, no treatment if asymptomatic. Frenuloplasty, wait until age 4-5.
71
What is a lingual thyroid?
Thyroid gland begins as epithelial proliferation in the floor of pharyngeal gut during week 3-4, and during 7, the thyroid bud descends into the neck, and forms foramen cecum in tongue, just next to terminal sulcus, but if it doesn't descend ectopic thyroid can be found there. Seven times more common in females, symptoms arise during puberty, pregnancy.
72
What is a thyroglossal duct cyst?
From epithelial remnants of the thyroglossal tract.
73
Which part of tooth does not have a mesenchymal origin?
Enamel. It has an ectodermal origin and is a product of the enamel organ.
74
Properties of Mature Enamel:
Acellular, Non-vital, non-vascular, 2.5mm at crown, 94% inorganic, 1% organic, and 3% water. No collagen in enamel. Inorganic component is Hydroxyapatite (HA).
75
Major enamel proteins:
Amelogenins, ameloblastins, enamelin, tuftelin.
76
Enamel Crystals:
Hydroxyapatite, but lots of enamel crystals are actually carbonatoapatite, when CO32- substitutes for either PO43- and OH-. Carbonate and magnesium incorporate into the inner enamel, while fluoride in the outer enamel. The enamel crystals are very long, run the entire length of the enamel layer. Hexagonal symmetry increases as crystals mature, but fully mature crystals lose their shape.
77
Enamel Rods:
They do not reach dentin. They are cylindrical accumulations of enamel crystals lined up along the long axis of the rod. They run perpendicular to the DEJ. Often called prisms. 1 ameloblast = 1 rod. At the center of the rod, they run completely parallel, and then flares out towards the bottom because the rod sheath only goes 3/4th the way around and ends.
78
Rod Sheath:
A space that fills with proteins and organic material and surrounds the rods. Ameloblastins and amelogenins are found here.
79
Interrod Enamel:
Same basic composition of rods, fills the gaps between the rods, it is all continuous with itself. It is 1 ameloblast per 1 rod, but 1 rod has four other ameloblasts contributing to it. The crystal orientation is different and opposite between rod and interrod enamel area. Caries are thought to penetrate through the higher protein rod sheath areas, thus between rod and interrod enamel.
80
Formation of Enamel:
Inner Enamel Epithelium, formation of first pre-dentin by odontoblasts, and ameloblasts are activated and deposition of enamel takes place. Initial deposition only around 30% mineralized, and as it matures, organic component reduced, and mineralization increases. Ameloblast maturation occurs in three phases: 1. Pre-secretory = mature from pre-ameloblasts to ameloblasts. 2. Secretory = deposition of enamel. 3. Maturation = reduction of organic matrix, increase mineralization via ion transport. Longest phase of enamel growth.
81
Deposition of Enamel:
Ameloblasts deposit organic matrix via secretory vesicles, which exit the cell apically. Tomes process is the site of much secretory activity. Ameloblasts are bound together by junctional complexes. Initial enamel in apposition to dentin does not have a rod arrangement, it is uniform. Tomes process forms the enamel rod structure, the distal of it towards the forming enamel, and the proximal is towards the stratum intermedium. Interrod enamel forms first, and forms a groove into which rods are formed. Eventually, tomes process retracts and outer rods are straighter and the final enamel is formed without rods. Thus Tomes process kind of equals rods.
82
Maturation of Enamel:
The loss of stellate reticulum and fusion of the OEE and IEE result in Reduced Enamel Epithelium (REE). Maturing the enamel is getting rid of the protein content and water, increasing mineralization, pumping in calcium ions to build HA crystals for mineralization. Can take up to 5 years for some permanent teeth. Modulation is the name by which water and proteins are removed. We have ruffled cells and smooth cells with enamel maturation. Ruffled cells is secreting things into enamel, secretes proteoltyci enzymes like MMP to chop up the proteins, and lowered pH favors mineralization. Smooth cells is letting things out of ameloblasts, allowing diffusion of protein fragments out of enamel, which leak in between cells and laterally diffuse through cell layer.
83
What is the fate of the enamel organ?
Fuses to form REE. So enamel organ remnants have fused with the oral eptihelium, forming a covering over the tooth. Nasmyth's membrane is the debris that remains on crown after eruption. The primary enamel cuticle is the last secretory product of the ameloblasts and is a mineralized coating. The secondary enamel cuticle or dental cuticle is formed from the remains of the REE merged with the oral epithelium and is removed due to the mechanical forces, it can be removed by toothbrushing.
84
Which rods are staighter? Outer or Inner enamel rods?
Outer 1/3rd are much straighter, the inner are somewhat interwoven.
85
Tomes process is present on maturation stage of ameloblasts. True or False?
False. While only its proximal portion is present on presecretory ameloblasts, and distal portion changes shape when the last third of enamel layer is being formed.
86
Interrod enamel forms before rod enamel. True or False?
True. It makes a pit into which the enamel rod is synthesized.
87
What are the main three proteins for enamel deposition?
1. Amelogenins - main protein, only expressed while enamel is being produced (stop during maturation). Restricts lateral HA crystal growth. Loss of function = no enamel rods, very disorganized structures. 2. Ameloblastin - Expressed at all times. Ameloblasts adhesion to developing enamel. Loss of function = ameloblasts fall off, no enamel. 3. Enamelin - Least abundant protein (but largest). Only present at leading edge of enamel deposition. Loss of function = no enamel.
88
What are the two proteins of organic component degradation of enamel?
1. Enamelysin - Is an MMP, chops up ameloblastin and enamelin. Loss of function = thin immature enamel. Critical for removal of organic component to allow for increased mineralization. 2. Enamel Matrix Serine Protease - Degrades amelogenins. Loss of function = immature enamel.
89
What are the two proteins of basal lamina during enamel maturation?
1. Amelotin 2. ODAM - The basal lamina with enamel doesn't have any collagen IV (chicken wire), just ODAM and amelotin mainly.
90
What does enamel acid etching do?
It provides a better bonding surface by increasing the porosity of enamel surface, removing crap clinging to the enamel surface, and dissolving enamel crystals. Carbonated apatite is more vulnerable to acid attack than calcium and fluoride apatite, so the core is more vulnerable, acid etching dissolves from inside out.
91
What are the three types of enamel etching that can happen?
Type 1 = most common, removal of rods. (they are usually attacked first because they are sticking out and are more vulnerable, they are perpendicular to enamel surface. Type 2 = Reverse of type I, removal of interrods. Type 3 = Irregular and indiscriminate pattern.
92
Definition of enamel abrasion:
Removal of enamel by abrasive forces, like aggressive brushing.
93
Definition of enamel abfraction:
Notch like cervical lesions caused by cyclic loading of teeth which places stress on interrod-interface, causing rods to separate.
94
Definition of enamel erosion:
Removal of enamel by break down of crystals.
95
Mineralization decreases with age. True or False?
False. Mineralization increases with age, even though enamel gets darker and thins out. Water content decreases with age as crystals enlarge and decrease pore size. Brittleness increases with age, permeability decreases with age, because of less space between individual crystals. Overall decreased incidence of caries as we age because we get an increased fluoride ion content.
96
What are the two periodic features of enamel?
1. Striae of Retzius/Perikymata - appear as stripes on ground sections running from DEJ to enamel surface, like rings of a tree, may indicate weekly rhythm enamel deposition, they have increased organic content. The darkest line here is the neonatal line which indicates significant physiological disturbances, and is found in all primary teeth. Perikymata is visible on enamel surface, and are surface manifestations of Striae of Retzius, look like orange stippling. 2. Cross Striations - these are visible bands or lines in ground sections that run perpendicular to the rod direction and to Striae of Retzius, that follow the enamel growth rate of about 4 micrometers per day, which is the distance between them.
97
What are the two optical features of enamel?
1. Hunter-Schreger Bands - optical phenomenons due to differential light scattering when adjacent groups of rods alternate direction, appear as light/dark bands, extend 2/3 distance from DEJ to surface. 2. Gnarled Enamel - Seen around the DEJ under the cusps/incisal area, form from a complex twisting of rods as they proceed vertically away from the DEJ.
98
What are the three histological features of enamel?
1. Enamel Tufts - Project from about 1/3 to 1/2 into the enamel from DEJ, do not reach the surface, similar to hunter-schreger bands. They contain more enamel proteins and are hypocalcified. Essentially branch structures found at DEJ. Help prevent fractures by giving some 'give.' 2. Enamel Lamellae - appear as cracks in ground sections which traverse the whole length of enamel, contain organic material proteins to give support to teeth like fault lines. 3. Enamel Spindles - Proceed only a very short distance into enamel, similar to enamel tufts, result from odontoblastic processes that traverse the DEJ and penetrate the enamel. They are not enamel, may have dentin/collagen associated with them.
99
How does Tetracycline staining work?
It can become incorporated into all mineralizing tissues (enamel, dentin, cementum, bone). Brown, yellow, or gray band of pigmentation, severity is proportional to dose and duration. Basically just a cosmetic issue, tooth is fine.
100
What is fluorosis?
It is when excess fluoride interferes with amelogenesis. You get hypermineralized enamel, chalk white or brown in color. Tooth form is normal.
101
What is the composition of dentin?
70% inorganic material 20% organic material 10% water
102
Dentin is harder than enamel. True or False?
False. Bone = 50, Dentin = 68, Enamel = 343.
103
What is the 20% organic material made of in dentin?
90% collagen (mostly I, with III and IV) and 10% non-collagenous protein.
104
What are the non-collagenous proteins in dentin?
``` In common with bone = Bone Sialoprotein, Osteopontin, Osteocalcin, Osteonectin. Dentin specific (found in bone, just at lower proportion) = Dentin Matrix Protein-1, Dentin Sialophosphoprotein (which is then cleaved into Dentin Sialoprotein, Dentin Phosphoprotein, and Dentin Glycoprotein, DSP, DPP, and DGP). ```
105
How is DSPP cleaved into DSP, DGP, and DPP?
By BMP-1.
106
What is DSP?
Dentin Sialoprotein = it is a proteoglycan that may act to prevent mineralization, and is found in tubules
107
What is DPP?
Dentin Phosphoprotein = Binds to Calcium and initiates HA formation and mineralization
108
What is DGP?
Dentin Glycoprotein = Is a glycoprotein with unknown function
109
What is dentinogenesis imperfecta type I?
Results from osteogenesis imperfecta (defect in collagen I), pulp chambers are filled with abnormal dentin
110
What is dentinogenesis imperfecta type II?
Is from a defect in DSPP, pulp chambers are filled with abnormal dentin
111
What is dentinogenesis imperfecta type III?
Is from a defect in DSPP, enlarged pulp chambers, hypo-mineralization
112
What does the dentin-pulp complex arise from?
The dental papilla. Odontoblasts differentiate and fill the acellular zone between the IEE and dental papilla.
113
Why is the shape of the DEJ critical? Two reasons:
1) It defines the shape of the crown and 2) keeps dentin directly attached to enamel during loading (no sheering)
114
What is the name of the first layer of dentin formed?
Mantle dentin, it is atubular. Von Korff's fibers are .1-.1mm collagen III fibrils with fibronectin, and they are not found in enamel and provide the initial framework for mantle dentin. Developing odontoblasts begin extending processes (Tomes' fibers) into the developing matrix and secreting dentin matrix components in matrix vesicles. When they penetrate the IEE, they are called enamel spindles. This is all to assemble a dentin protein scaffold, ready for mineralization. Odontoblasts produce matrix moving away from the DEJ, leaving behind Tomes Fibers (which are future odontoblastic processes). Dentin starts as non-mineralized organic matrix (predentin). Mineralization starts within odontoblast secreted matrix vesicles that are deposited alongside von Korff's fibers and future DEJ. Remember the von korff fibers provide a framework.
115
How is dentin formed?
Secreted matrix vesicles rupture, releasing mineralized matrix crystals that forms non-tubular mantle dentin. Non-collagenous matrix proteins (DMP, DSPP) regulate subsequent dentin formation, resulting in tubular primary dentin which is first called 'circumpulpal,', and this is after the DEJ formation.
116
What does HERS do?
Hertwig's Root Sheath initiates odontoblast differentiation, eventually breaks into cell rests of Malassez, is derived from the enamel organ, and is essential for root dentin and root formation.
117
What is primary dentin?
It is the first dentin formed, and comprises mantle dentin and the initial deposition of circumpulpal dentin.
118
What is secondary dentin?
It is tubular dentin laid down SUBSEQUENT to root formation and is produced throughout life. It is continuous with primary dentin but histologically distinct.
119
What is tertiary dentin?
It is dentin produced in response to an insult or trauma, can have tubules but often does not. Acts to seal off dentinal tubules or to form bridges between dentin and restorations. It can either be reactionary (trauma does not damage odontoblasts) or reparative (damages odontoblasts, requires the formation of new odontoblasts from mesenchymal cells, and brings in non-collagenous proteins that are more common with bone than being dentin specific).
120
Pre-Dentin is mineralized. True or False?
False
121
What are the three main structures in dentin?
Dentin tubules, Peritubular dentin, and Intertubular dentin
122
What are characteristics of dentin tubules?
They are fluid filled, they are surrounded by a collar of highly calcified peritubular dentin, and separated by intertubular dentin which is largely collagen I fibrils arranged perpendicularly to tubules.
123
What happens when caries enter the tubules?
Mineralized matrix is liquefied and protein scaffold is eroded. And then you get a response of the formation of tertiary dentin to occlude tubules, and then get dead tracts which is trapped air in empty tubules, sealed off after odontoblast death.
124
What is sclerotic dentin?
It is a collective term for tubules that have become occluded. It occurs naturally with age as peritubular dentin is deposited. Starts apically, goes coronally.
125
What is interglobular dentin?
It is areas of hypomineralized dentin. It is formed when fusion of mineral containing vesicles fail, can be associated with vitamin D deficiency or fluoride exposure during initial dentin formation. The tubules can still run through the interglobular dentin because the matrix still there and that is all the tubule needs.
126
What are the cyclic characteristics of deposited primary dentin?
Dentin matrix is deposited continually about 4 micro meters per day, and every 5 days or so a line of Von Ebner (similar to cross striations in enamel!) is formed, so at about 20 micro meter intervals. Secondary dentin is assymetrically deposited, and happens more slowly. The contour lines of owen are the equivalent to striae of Retzis in the enamel (where there is also a neonatal line).
127
What is the granular layer of Tomes?
It is funny looking dots around the roots of ground sections. Not sure what causes it. But if you see it, you know you are in root dentin.
128
What are the four zones of the dental pulp from outer to inner?
1. Odontoblast layer 2. Cell free zone of Wil 3. Cell rich zone 4. Pulp core
129
What does dental pulp arise from?
Dental papilla, ectomesenchymal tissue, same origins as dentin. Pulp is mainly fibroblasts, then odontoblasts.
130
What is the ECM of dental pulp made of?
Mostly collagen III and some collagen I, along with numerous non collagenous proteoglycans and glycoproteins along with water form the ground substance. The proteoglycans act to prevent mineralization. Some of the proteoglycans found in dental pulp are Chondroitins, Hyaluronic acids, and different sulfates.
131
What are the components inside of an odontoblast?
They are polarized cells with an elongated nucleus at the pulpal side and secretory components (golgi bodies) toward the dentinal side. They are held together by adherens junctions (zonula adherens). Odontoblasts can form direct communication via gap junctions with pulpal fibroblasts as well. Also, the vasculature and plexi are found in the cell-free zone of the pulp. Remember that.
132
What are characteristics of aged odontoblasts?
Fewer organelles, less secretory activity, nucleus more central.
133
How do odontoblasts differ from the function of the odontoblastic process?
Odontoblasts secrete protein and produce it, but OD process releases the secretory vesicles.
134
What is the predominant cell type found in dentin-pulp complex?
Fibroblasts. Found in pulp core and cell rich zone, and they produce and maintain the supportive matrix of pulpal tissue, which supports progenitor cells, immune cells, vasculature, lymph, and nervous tissue.
135
What is a main function of dental pulp progenitor cells?
Mesenchymal progenitor cells are in pulp to react to a strong stimulus with enamel, which communicates with dentin, and they respond to damage to recruit to form new odontoblast-like cells called reparative dentin, that is poor in collagen, not well organized, and rich in BSP.
136
Where are dendritic cells found in the pulp?
They are found under the odontoblast layer.
137
What arteries provide blood supply to pulp?
External carotid and superior/inferior alveolar arteries. 4-8 arterioles per root go up into coronal pulp. The capillary network is found in the free cell zone, but during primary dentin formation, it is found in odontoblast layer.
138
What are characteristics of the lymphatic vessels in pulp?
They have thinner walls, an epithelial lining, and a thin smooth muscle layer.
139
What is the innervation of dental pulp?
We have sympathetic, but no parasympathetic innervation in the pulp. Nerve fibers branch to form the plexus of raschkow in coronal pulp. In root pulp, there is no plexus of raschkow. Fibers come from trigeminal and sympathetic branches from superior cervical ganglion. There are myelinated (sensory) and unmyelinated axons (sympathetic, blood pressure control) in pulp as well. The myelination decreases as fibers proceed towards coronal. Some unmyelinated axons pass into dentine tubules.
140
What are the three proposed models of dentine sensitivity?
1. Direct innervation 2. Odontoblast nociception (OD's are neural crest derived) 3. Tubule fluid conductance
141
What is a pulp stone?
Mineralized tissue formed inappropriately in the pulp, occurs around collagen fibers, can grow large enough to compress pulp chamber.
142
What happens with our pulp as we age?
We get recession of pulp due to secondary dentin formation taking up the space in our teeth, we get decreased pulp permeability, loss of nerve axons, and decreases in sensitivity.
143
What are the five types of physiologic tooth movements?
1. Preeruptive = positioning of tooth germs prior to eruption. 2. Eruptive = the movement of teeth into functional occlusion. 3. Posteruptive = movements in compensation for the growth of the jaws. 4. Shedding = the programmed loss of primary teeth. 5. Avulsion = extreme example of non physiologic tooth movement. - These are all aimed at getting the teeth in occlusion.
144
Permanent teeth develop facially to primary tooth germs. True or False?
False. They develop lingually.
145
Maxillary molar occlusal surfaces face outwards (distally) while mandibular molars have a more medial inclination. True or False?
True.
146
What are the two ways in which tooth germs move?
Either with bodily movement (ostoeoblasts and osteoblacts helping the tooth move laterally or wherever) or with directional growth (which is like the enamel knot, where one part of tooth stops growing and the other keeps growing).
147
What is the gubernacular canal?
It forms along the remnants of the dental lamina attached to the lamina propria and is a channel that develops between the alveolar bone around the primary tooth and the permanent tooth as it erupts. This is how permanent teeth erupt, through this canal, and it goes pretty fast that way, but primary teeth fuse with the oral epithelium and the REE to emerge.
148
Eruptive tooth movements are axial/occlusal. True or False?
True.
149
What is thought to be the main driving force for tooth eruption?
The periodontal ligament. Remember that the dental follicle and HERS help develop the PDL, and that these are critical to tooth eruption, as they initiate bone resorption and the breakdown of soft tissues.
150
What are some of the mediators of tooth eruption, specifically for tissue resorption and tissue formation?
Tissue resorption - CSF-1, IL-6, IL-1alpha | Tissue formation - BMP-2, BMP-6
151
Name the levels of bone surrounding teeth starting with facial side:
``` Outer cortical Plate Spongy bone and marrow Cribriform plate Cribriform plate Spongy bone and marrow Inner cortical plate (With the alveolar crest at the top of the bone) ```
152
What is the difference between tension, compression, and hyalinization when it comes to ortho tooth movement?
Tension: remodeling of PDL fibers and bone deposition Compression: remodeling of PDL fibers and bone resorption Hyalinization: damage to cells in the PDL = no remodeling -Ortho tooth movement involves tissue damage and bone resorption and is not physiological. -Initial compression happens first, then hyalinization period for 10-20 days, then further tooth movement. The tooth moves in the direction the compression is on.
153
What ligament helps keep the tooth in occlusion?
The PDL.
154
Teeth tend to move in a distal direction. True or false?
False. They move in a mesial direction, and bite force in an anterior direction tends to push them against each other.
155
When do primary incisors and canines shed?
When their roots on the lingual surface are resorbed.
156
When do primary molars shed?
When the interradicular dentin and root hvae been resorbed. Regardless, all primary teeth shed at contact points.
157
How are the hard tissues of teeth including dentin and cementum resorbed?
By the action of odontoblasts. PDL and soft tissues are resorbed by cells/enzymes.
158
Order of primary teeth eruption:
``` 8 months - lower central incisors 10 months - upper central incisors 11 months - upper lateral incisors 13 months - lower lateral incisors 16 months - all four 1st molars 19 months - upper canines 20 months - lower canines 28 months - all four 2nd molars -So happens from 8 months to 28 months ```
159
Order of permanent teeth eruption:
6-7 years - lower central incisors, lower and upper 1st molars 7-8 years - lower lateral incisors, upper central incisors 8-9 years - upper lateral incisors 9-10 - lower canines 10-12 - lower 1st premolars, upper 1st premolars and 2nd premolars 11-13 - lower 2nd premolars and 2nd molars, upper canines 12-13 - upper 2nd molars 17-21 - upper and lower 3rd molars -So happens from 6 years to 18 years
160
What are the three components of periodontium?
1. Alveolar process 2. Cementum 3. Periodontal ligament
161
What is the name of a fibrous peg-in-socket joint?
Gomphosis
162
What are the four main groups of cells in periodontium?
1. osteoblasts 2. cementoblasts 3. PDL fibroblasts 4. Odontoblasts
163
What type of ossification is the alveolar process formed by?
Intramembranous ossification. Begins during the 8th week of uterine life.
164
What is alveolar bone proper vs. supporting alveolar bone?
Alveolar bone proper is compact bone, and examples are cribriform plate, lamina dura, and bundle bone (sharpey's fibers embedded in bone). Supporting alveolar bone is both compact and trabecular bone, and examples are cortical plates for compact and central spongiosa for trabecular. The alveolar bone proper is what actually forms the actual tooth socket.
165
Difference between inner and outer alveolar bone proper:
Inner remodeling rate is higher, and consists mainly of woven bone. Outer is continuous with the supporting alveolar bone, and is mainly lamellar.
166
The supporting alveolar bone is thicker in the maxilla and thinner in the molar region of mandible. True or False?
False. It is thinner in the maxilla and thickest in the molar region of the mandible. At the same time, the maxilla has more spongiosa bone than mandible.
167
What two things combine and junction to form alveolar crest?
Cortical plate and alveolar bone proper.
168
What bone divides roots of teeth?
Interradicular septum
169
What bone divides teeth?
Interalveolar septum
170
How is the PDL originally developed?
It develops after detachment of HERS, starts off as fibrillar short connective tissue, so it develops after root formation is initiated. It is composed of fibroblasts, mesenchymal cells, epithelial cells, and macrophages. It decreases in width as we age. The PDL is largely collagen fibers, collagen type I, III, and XII. Individual fibers can be remodeled while the overall bundle is not changed.
171
What is the main elastic fiber of the PDL?
Oxytalan, which is largely associated with vasculature. The PDL receives blood from superior/inferior alveolar arteries. Nerves arrive both apically and through the cribriform plate, and the concentration of nerve endings is greatest at the tooth apex.
172
What are the 4 types of nerve endings in the PDL?
1. Free nerve endings - nociceptive/mechanoreceptive 2. Ruffini's corpuscles - bulbous dendritic endings 3. Coiled nerve endings around mid-region of PDL 4. Spindle nerve endings
173
What are the 5 main histological groups of PDL fibers, based on their orientation?
1. Alveolar crest group 2. Horizontal group 3. Oblique group 4. Apical group 5. Interradicular group - These bundles terminate in cementum or alveolar bone and are attached via Sharpey's fibers.
174
What are the 5 groups of gingival ligament fibers?
1. Dentinogingival group 2. Alveologingival group 3. Circular group 4. Dentoperiosteal group 5. Transseptal fibers
175
What are the origins of cementum?
HERS or dentin induces cells in the dental follicle to become cementoblasts, which secrete cementoid, and then we get mineralized cementum. Remember that HERS cells that break off become rests of malassez, and those that remain on root can form enamel pearls.
176
What is the composition of cementum?
Very similar to bone, organic component is around 90% collagen type I, and it is 50% in organic and 50% inorganic (which is just HA). The main non-collagenous proteins with it are BSP, osteopontin, osteocalcin, and osteonectin, similar to others.
177
What are the two types of cementum and their characteristics?
1. Acellular Extrinsic Fiber Cementum (AEFC), Primary cementum = Found on coronal 2/3 of root. Is acellular with extrinsic collagen fibers produced by the PDL. No cementoid, more mineralized, and it attaches PDL to cementum. It is formed when predentin that is formed in the roots is hit by cementoblasts which send processes into the predentin and produce collagen fibers, termed the 'fibrous fringe.' PDL fibroblasts merge with the 'fibrous firinge' and form Sharpey's fibers. Cementoblasts end up only on the surface of cementum here, hence, acellular. 2. Cellular Intrinsic Fiber Cementum (CIFC), Secondary cementum = Found on apical 1/3 of root. Is cellular with intrinsic collagen fibers directly from cementoblasts. Cementoid visible, cells encapsulated, and helps with attachment and wear. Cementoblasts become trapped in this cementum causing it to be cellular and cementocytes. And the collagen fibers here are produced by cementoblasts, not PDL fibroblasts, that is why they are intrinsic.
178
Where is intermediate cementum found?
In between the granular layer of Tomes and dental cementum proper. Has high mineralization and may help seal surface of root dentin to reduce sensitivity.
179
What is hypercementosis?
Abnormal thickening of cementum. Tooth can become ankylosed. Can affect just one or all teeth.
180
Cementum is more resistant to resorption than alveolar bone. True or False?
True. This is why bone tends to be remodeled first.
181
What are the 5 types of tooth movement?
1. Tipping - top goes left, bottom goes right, vice versa. Tooth moves in direction of compression = dark area. 2. Bodily movement - unilateral shift 3. Extrusive movement - tooth moves out of socket, has tension marks only. 4. Intrusive movement - tooth is compressed into socket, has compression marks only. 5. Rotational movement - you got this. Think bird's eye view.
182
What are the three factors that determine the degree of the effect applied force?
1. Transduction - efficiency of conversion of physical force into biologic response. 2. Time 3. Magnitude of force - TTM, TTM, TTM, TTM
183
What is hyalinization and undermining resorption?
Hyalinization is from too great or too rapid a compression, braces movement, you get loss of cell activity. The hyalinized tissue must be removed for tooth movement to occur. This occurs by a process termed undermining resorption, where osteoclasts present within the adjacent bone marrow spaces begin bone resorption on the underside opposite the cell free area.
184
What is the composition of bone?
67% Inorganic and 33% organic. The inorganic is HA again and the organic is almost all collagen, with some non-collagenous proteins, the same ones as always.
185
What do calcitonin and parathyroid hormone do to bones?
Calcitonin inhibits bone breakdown of calcium (decreases blood calcium) and helps excrete the calcium while parathyroid hormone does the opposite (increases blood calcium).
186
What type of cell populations are found in bone marrow?
Both hematopoietic and mesenchymal progenitor cell populations.
187
What are the two main layers of bone?
Compact/Cortical bone as well as Spongy/Trabecular/Cancellous bone.
188
What two things make up the concentric lamellae?
Haversian canal with an osteon.
189
What are osteons? And how are they linked together?
They are the basic functional unit of compact bone, and are linked through Volkmann canals connecting to their Haversian canals.
190
What are the three types of lamellae?
Concentric (surrounds osteon), Interstitial, and Circumferential.
191
Where is cancellous/spongy/trabecular bone found?
It is found at the ends of long bones, in apposition to joints, and in marrow spaces. It is highly vascular.
192
How many layers does the periosteum have?
It has two layers. Outer fibrous layer and inner fibrous layer, that is highly cellular and vascularized. The periosteum is a connective tissue layer attached to bone by Sharpey's fibers.
193
What is the endosteum?
Loose connective tissue covering the inner surface of both cancellous and compact bone. It separates the marrow form the bone.
194
What are the origins of osteoblasts and osteoclasts?
Osteoblasts have a mesenchymal origin, and they are post-mitotic cells. Osteoblasts have a hematopoietic origin and they break down bone tissue.
195
What do osteoblasts synthesize?
They synthesize osteoid matrix. And they arise from mesenchyme, ectomesenchyme in the head. They communicate with one another through gap junctions. They also produce and secrete collagen, and non-collagenous proteins via vesicles. Also secrete growth factors into the osteoid matrix, where theya re sequestered. After bone formation, osteoblasts flatten and become 'bone lining cells.'
196
What do osteocytes form when they are bunched together?
They form interconnected lacunae in bone tissue. Osteocytes are also responsible for mechano-transduction or mechanoreception, and they coordinate osteoclast/osteoblast activity.
197
What are characteristics of osteoclasts?
They are large multi-nucleated cells and are from monocytes. They are activated with IL-1beta and TNF-alpha, inflammation. A key marker with these is Tartrate Resistant Acid Phosphatase (TRAP). They attache to surface via integrin, and their cytoplasm is rich in talin, actin, and vinculin. They form a ruffled border in apposition to bone, and they form resorption pits (Howships' Lacunae) in bone when they secrete hydrogen ions and matrix degrading enzymes. 'Lamina limitans' is the zone between the Howship's lacunae and intact bone. Hydrogen ions and everything leave the opposite way from whence they came.
198
How is bone formation controlled?
Interaction between osteoblasts and osteoclasts. Osteoblasts are what trigger osteoclasts to go to work and resorb bone. And PTH is what causes osteoblasts to do this when we need higher calcium in blood for signaling purposes. But RankL is expressed on Osteoblasts and Rank is expressed on Osteoclasts. They bind to one another when osteoblasts are trying to tell osteoclasts to resorb. Osteoprotegerin is a protein produced by osteoblasts that binds RankL (on its own surface) and prevents it from activating osteoclasts to go to work and resorb. OPG is a negative regulator in that sense. - Osteoclasts don’t really have receptors for parathyroid hormone, which increases resorption, to increase blood calcium, so osteoclasts are stimulated like this - In an inflammatory process, there are other ways and cytokines to trigger osteoclasts and resorption to get them going, other ways than this.
199
What type of bone development takes place in long bones and some parts of the mandible?
Endochondral bone formation
200
What type of bone development takes place with bones of the skull mostly?
Intramembranous bone formation
201
Endochondral formation characteristics:
Bone is formed on a hyaline cartilage pattern. Mesenchymal cells are condensed into chondrocytes. Collagen is secreted, mineralized, and is broken down by chondroclasts, allowing penetration of vasculature. And mesenchymal cells come in this vasculature and differentiate into osteoblasts. Mixed spicules are associated here in the developing of long bones and endochondral formation which is simply bone matrix surrounding remaining mineralized collagen, these make up primary spongiosa. Osteoclasts gradually remove mineralized cartilage and develop marrow cavity.
202
Intramembranous formation characteristics:
Mesenchymal cells here condense in fibrous connective tissue, differentiating into osteoblasts and forming an ossification center. Osteoid is secreted into the connective tissue matrix and is penetrated by blood vessels, and we get rapid formation of mineralized 'woven bone,' remodeled into mature trabecular bone with a collar of cortical bone around it.
203
What are sutures in the skull?
Fibrous connective tissue bands between plates allowing for internal expansion of organs. There is an inner cambian layer associated with periosteum, and an outer capsular layer that meet to join sutures together.
204
How much does bone turnover in different age groups?
30-100% of total bone per year in children. | 5% cortical, 15% trabecular per year in adults.
205
Where is most bone formed and where is most bone resorbed?
Most bone is formed around the periosteum and resorbed around the endosteum, allowing marrow cavity to get bigger. Cortical bone has primary, then secondary, and then tertiary osteons, allowing for bone growth.
206
What is the cutting vs filling cone thing in cortical bone osteon formation?
Bone needs to be structurally functioning and growing at the same time. If we are remodeling, and we are in a fully developed bone, we don’t want to do it all at once. We are gradually replacing little bits of bone. In order to remodel, you need to break something down, so osteoclasts are activating, removing part of bone that needs to be remodeled, that is the cutting cone. This is always accompanied by filling cone, that is depositing new bone right behind the osteoclasts. These are all associated with blood vessels.
207
What is the cement line that osteoblasts leave made up of?
Non collagenous proteins like osteopontin, osteocalcin, osteonectin. Osteoblasts make this line and lay new bone onto it.
208
What are the 5 stages of salivary gland development?
1. Prebud 2. Initial bud 3. Pseudoglandular (you get acini) 4. Canalicular (you get a lumen) 5. Termina Bud (you get ducts, final stage) - Salivary glands can only be made from salivary mesenchyme.
209
What are the names of the granules that are deeply stained granules in the cytoplasm of cells in granular layer of oral mucosa?
Keratohyaline granules.
210
Where is the keratinized epithelium in the mouth?
Gingiva and hard palate. The masticatory mucosa. The rest is non-keratinized lining or specialized (dorsal surface of tongue).
211
What type of epithelium is sulcular epithelium?
It is nonkeratinized in the gingival sulcus, and lacks rete ridges.
212
What is the epithelium type of interdental papilla and the col?
Interdental papilla is keratinized stratified squamous epithelium and the Col is nonkeratinized stratified squamous epithelium.
213
What is the junctional epithelium derived from?
From the REE. It forms the floor of the gingival sulcus. It along with the epithelial attachment for the dentogingival junction. It is all non-keratinized here. Should not have rete pegs. Cells joined together by desmosomes.
214
What are the 4 main phases of tissue repair?
1. Hemostasis: clot formation. Fibrin provides a scaffold for future cell migration and repair. 2. Inflammatory: infiltration of immune cells 3. Reparative/Proliferative phase: migration of cells, formulation of granulation tissue 4. Wound contraction and scarring
215
Hemostasis phase characteristics:
Initiated by exposure of collagen to circulating von Willebrand Factor, which causes platelet aggregation, and platelets can help dump out stuff to help like fibrinogen and factor V and XIII. Fibrinogen anchors platelets together. This is all primary hemostasis, and for secondary hemostasis, we will have either extrinsic (it requires tissue factor which is not normally found in blood) or intrinsic (involves factors found in blood). The main point of all of this is to convert Prothrombin into Thrombin, and thrombin helps convert fibrinogen into fibrin, and fibrin is what cross-links and forms a mesh, trapping cells, resulting in a blood clot. Then we have the inflammation phase, then granulation tissue forms, and then the wound is contracted when myofibroblasts align around the wound, form cell junctions, and hehlp form scar. But oral mucosa generally doesn't scar because fewer fibers are located in this area, neural crest cell derivation.
216
What are the three primary zones of dental caries?
1. Surface and Body - surface can remineralize, while body is the primary zone of demineralization. 2. Dark zone - zone of increasing demineralization 3. Translucent zone - caused by micro-pores.
217
What nerve innervates the temporalis, masseter, medial and lateral pterygoid?
The mandibular nerve.
218
Which arteries provide blood supply to TMJ muscles of mastication?
Maxillary, facial, and external carotid artery.
219
What are the movements associated with the upper and lower joint compartments?
``` Upper = translation Lower = rotation ```
220
What type of cartilage covers the condyle and the articular eminence?
Fibrocartilage
221
What is another name for the retrodiscal tissue?
Bilaminar zone, is where majority of nerve endings and vascularization occurs. It is right behiind the condyle and disk, while the lateral pterygoid muscle is anterior the disc.
222
What are the two types of cells in synovial fluid?
Type A cells: are macrophage like and help with phagocytosis. Type B cells: make hylauronate found in the fluid. -Synovial fluid can also help serve as a nutrient source for the avascular tissues.
223
What are the three types of displacement that the TMJ ligament restricts?
Lateral/medial, Inferior, and posterior displacement. If you get loud clicking but no pain, probably due to miscplaced ligament.
224
What is the articular disk made up of?
Coarse collagen fibers with fibroblastic cells. Has no cartilage.
225
What are the layers, in order, from the two histo slides from the TMJ lecture?
1. Fibrous articular covering 2. Proliferative layer 3. Hypertrophic zone 4. Calcified cartilage 5. Mixed bone spicules And the other one.... 1. articular disk 2. articular zone 3. proliferative zone 4. fibrocartilaginous zone 5. Calcified cartilage 6. Subarticular zone
226
What does tongue look like with scarlet fever?
First 2 days - white strawberry tongue | Days 4-5 - red strawberry tongue
227
What is the name of the type of necrosis that occurs with syphilis?
Gumma. It is scattered foci of granulomatous inflammation.
228
Where in body does actinomycosis usually take place?
Tonsillar crypts, plaque, carious dentin. Can get sulfur granules.
229
What is cat stratch disease organism name?
Baronella henselae
230
What is unique about yeast?
It is dimorphic.
231
What is the name of the gum problem with HSV?
Gingivostomatitis in young people, and pharyngotonsillitis in older. The less common HSV presentations are herpetic whitlow (thumb), herpes gladiatorum (wrestlers) and herpes barbae (bearded people).
232
Most common oral manifestations associated with HIV infection?
Candidiasis, Hairy Leukoplakia (EBV), KSHV, periodontal disease.