Operative: MIDTERM

The neurovascular supply into/out of the pulp; locate it at the root apex on the diagram. [Lecture: Biological Basis of Operative Dentistry | PDF page 3 | C0544]

What does the apical foramen transmit?

Coronal projections of pulp toward cusps; avoid them during preparation. [Lecture: Biological Basis of Operative Dentistry | PDF page 3 | C0545]

Where are pulp horns relative to cusps?

Hard, durable outer surface; protection of dentin/pulp; tooth color, contour, texture, and translucency. [Lecture: Biological Basis of Operative Dentistry | PDF page 5 | C0004]

What are enamel's structural and esthetic roles?

About 96% by weight; 90–92% by volume. Do not interchange the two. [Lecture: Biological Basis of Operative Dentistry | PDF page 6 | C0001]

What is enamel's inorganic content by weight versus volume?

Ca10(PO4)6(OH)2. [Lecture: Biological Basis of Operative Dentistry | PDF page 6 | C0002]

What is the formula of hydroxyapatite?

Organic matrix 1–2%; water 4–12%, in intercrystalline spaces and micropores. [Lecture: Biological Basis of Operative Dentistry | PDF page 6 | C0003]

What organic and water fractions does the enamel lecture list by volume?

It decreases. [Lecture: Biological Basis of Operative Dentistry | PDF page 7 | C0005]

How does enamel permeability change with age?

Thinner or more translucent enamel, accumulated trace elements, and sclerosis of mature dentin. [Lecture: Biological Basis of Operative Dentistry | PDF page 7 | C0006]

Why can teeth look more yellow with age?

Remineralization produces less acid-soluble fluorohydroxyapatite; calcium and phosphate must be available. [Lecture: Biological Basis of Operative Dentistry | PDF page 8 | C0007]

How does fluoride make enamel more acid resistant?

Ameloblasts; ectodermal mineralized tissue. [Lecture: Biological Basis of Operative Dentistry | PDF page 10 | C0008]

Which cells form enamel, and what is its developmental origin?

Calcium-containing mineral seeds in the secreted organic matrix act as crystallization nidi. [Lecture: Biological Basis of Operative Dentistry | PDF page 10 | C0009]

What initiates hydroxyapatite crystal growth during enamel formation?

Secretes enamel matrix and directs mineralization and crystal orientation into rods and interrod enamel. [Lecture: Biological Basis of Operative Dentistry | PDF page 11 | C0010]

What is the role of Tomes' process?

Primarily in crystal orientation; interrod crystals are nearly perpendicular to rod crystals. [Lecture: Biological Basis of Operative Dentistry | PDF page 12 | C0011]

How do rod and interrod enamel differ?

An optical light/dark banding effect from variation in light reflection by differently oriented enamel rods. [Lecture: Biological Basis of Operative Dentistry | PDF page 12 | C0012]

What produces Hunter–Schreger bands?

Low tensile strength between rods and natural cleavage planes; loss of dentinal support weakens fracture resistance. [Lecture: Biological Basis of Operative Dentistry | PDF page 13 | C0013]

Why is unsupported enamel vulnerable to fracture?

Its elastic foundation relieves stress and supports enamel; dentin also provides color and protects the pulp. [Lecture: Biological Basis of Operative Dentistry | PDF page 15 | C0014]

Why is dentin important beneath brittle enamel?

Bodies at the pulp periphery; processes extend into dentinal tubules. [Lecture: Biological Basis of Operative Dentistry | PDF page 16 | C0015]

Where are odontoblast cell bodies and processes located?

Organic dentin matrix and its mineralization. [Lecture: Biological Basis of Operative Dentistry | PDF page 16 | C0016]

What do odontoblasts secrete and regulate?

Approximately 3.5 nm near the DEJ and 2 nm near the pulp. [Lecture: Biological Basis of Operative Dentistry | PDF page 16 | C0017]

What apatite crystal thicknesses are listed near the DEJ and pulp?

Dentin approximately 3–3.5 mm thick; tubules comprise about 10% of dentin volume. [Lecture: Biological Basis of Operative Dentistry | PDF page 17 | C0018]

What dentin thickness and tubule volume are listed?

Near the pulp. [Lecture: Biological Basis of Operative Dentistry | PDF page 17 | C0019]

Where are dentinal tubules wider: near the DEJ or pulp?

About 45–50% inorganic apatite, 30% organic matrix, and 25% water; approximate values. [Lecture: Biological Basis of Operative Dentistry | PDF page 18 | C0020]

What is dentin's composition by volume in this lecture?

About 90% type I collagen and 10% noncollagenous proteins. [Lecture: Biological Basis of Operative Dentistry | PDF page 18 | C0021]

What is the composition of dentin's organic matrix?

Pale yellow; slightly harder than bone. [Lecture: Biological Basis of Operative Dentistry | PDF page 18 | C0022]

What are dentin's typical color and relative hardness?

Hydroxyapatite-containing collagen matrix forming the bulk between tubules. [Lecture: Biological Basis of Operative Dentistry | PDF page 19 | C0023]

What is intertubular dentin?

The highly mineralized tubule lining, with little organic matrix. [Lecture: Biological Basis of Operative Dentistry | PDF page 19 | C0024]

What is peritubular dentin?

During development until root completion; approximately 4–8 μm/day. [Lecture: Biological Basis of Operative Dentistry | PDF page 20 | C0025]

When is primary dentin formed, and at what listed rate?

First-formed dentin near the DEJ; the lecture lists an approximately 150-μm layer with larger collagen fibers. [Lecture: Biological Basis of Operative Dentistry | PDF page 20 | C0026]

What is mantle dentin?

Dentin surrounding the pulp chamber that makes up the bulk of dentin. [Lecture: Biological Basis of Operative Dentistry | PDF page 20 | C0027]

What is circumpulpal dentin?

Unmineralized collagen/protein matrix adjacent to pulp; approximately 10–50 μm. [Lecture: Biological Basis of Operative Dentistry | PDF page 20 | C0028]

What is predentin, and what width is listed?

After complete tooth formation; gradual, asymmetric reduction in pulp-chamber volume. [Lecture: Biological Basis of Operative Dentistry | PDF page 21 | C0029]

When is secondary dentin produced, and what happens to the pulp chamber?

1–2 μm/day. [Lecture: Biological Basis of Operative Dentistry | PDF page 21 | C0030]

What rate of secondary dentin formation does this lecture list?

Caries or other injury/loss of peripheral dentin. [Lecture: Biological Basis of Operative Dentistry | PDF page 22 | C0031]

What triggers tertiary dentin formation?

Mineral deposition narrows or blocks tubules as a defensive or age-related response; common in exposed roots of older people. [Lecture: Biological Basis of Operative Dentistry | PDF page 24 | C0035]

What is sclerotic dentin and why does it form?

Caries, erosion, and cavity preparation; aging also contributes. [Lecture: Biological Basis of Operative Dentistry | PDF page 24 | C0036]

Which stimuli are listed for dentinal sclerosis?

Caries, attrition, abrasion, erosion, and cavity preparation. [Lecture: Biological Basis of Operative Dentistry | PDF page 25 | C0032]

Name the five listed stimuli for tertiary dentin.

Reactionary: surviving original odontoblasts. Reparative: newly differentiated odontoblast-like cells. [Lecture: Biological Basis of Operative Dentistry | PDF page 27 | C0033]

Which cells produce reactionary versus reparative dentin?

On the pulpal surface beneath the affected area; intensity and duration of the stimulus matter. [Lecture: Biological Basis of Operative Dentistry | PDF page 27 | C0034]

Where is tertiary dentin deposited, and what determines its quantity/quality?

Outer dentin near DEJ/cementum has fewer tubules per area; inner dentin near pulp has more. [Lecture: Biological Basis of Operative Dentistry | PDF page 28 | C0037]

How does outer dentin differ from inner dentin in tubule density?

Outer dentin: no processes; inner dentin: processes present. Treat this as the lecture's simplified description. [Lecture: Biological Basis of Operative Dentistry | PDF page 28 | C0038]

What does this lecture state about odontoblast processes in outer versus inner dentin?

75% water and 25% organic material. [Lecture: Biological Basis of Operative Dentistry | PDF page 31 | C0039]

What is the pulp's water/organic composition?

Formative, nutritive, sensory, and protective. [Lecture: Biological Basis of Operative Dentistry | PDF page 32 | C0040]

What are the four functions of dental pulp?

Primary, secondary, and tertiary dentin. [Lecture: Biological Basis of Operative Dentistry | PDF page 32 | C0041]

What does the pulp's formative function produce?

Afferent pain transmission (nociception). [Lecture: Biological Basis of Operative Dentistry | PDF page 32 | C0042]

What is the pulp's sensory function?

Softer than dentin; 45–50% inorganic and 50–55% organic material/water. [Lecture: Biological Basis of Operative Dentistry | PDF page 35 | C0043]

How does cementum compare with dentin in hardness and composition?

Embedded portions of principal PDL collagen fibers in cementum and alveolar bone. [Lecture: Biological Basis of Operative Dentistry | PDF page 35 | C0044]

What are Sharpey's fibers?

Coronal root: acellular; apical root: cellular. [Lecture: Biological Basis of Operative Dentistry | PDF page 35 | C0045]

Where is cementum predominantly acellular versus cellular?

Free and attached gingiva, gingival margin and sulcus, free gingival groove, interdental papilla, mucogingival junction, and alveolar mucosa. [Lecture: Biological Basis of Operative Dentistry | PDF page 37 | C0046]

Which gingival landmarks should you identify on the slide?

Approximately 1 mm junctional epithelium plus 1 mm connective tissue attachment; sulcus is not included in this sum. [Lecture: Biological Basis of Operative Dentistry | PDF page 38 | C0047]

What two components make up the approximately 2-mm biologic width shown?

Ages 2–11: 42% primary-tooth caries and 23% untreated caries; dentate adults 20–64: 91% have had permanent-tooth caries. These are the lecture's older cited data, not current estimates. [Lecture: Dental Caries — The Agent | PDF page 2 | C0048]

What historical prevalence figures does the lecture quote?

Plaque bacteria ferment dietary carbohydrates, producing acids that cause localized loss of tooth mineral over time. [Lecture: Dental Caries — The Agent | PDF page 3 | C0049]

What is the basic mechanism of dental caries?

Reduce sugar frequency, remove plaque mechanically, and use fluoride to support remineralization/acid resistance. [Lecture: Dental Caries — The Agent | PDF page 5 | C0590]

What three prevention priorities are emphasized?

Acidogenic means acid-producing; aciduric means able to grow/survive in an acidic environment. [Lecture: Dental Caries — The Agent | PDF page 7 | C0586]

How do acidogenic and aciduric differ?

Living without free oxygen. [Lecture: Dental Caries — The Agent | PDF page 7 | C0587]

What does anaerobic mean?

From genetically different individuals of the same species. [Lecture: Dental Caries — The Agent | PDF page 7 | C0588]

What does allogenic mean?

Their extracellular matrix and interdependent communities provide protection; higher antimicrobial concentrations may be required. [Lecture: Dental Caries — The Agent | PDF page 7 | C0589]

Why can biofilms resist antimicrobials better than free-floating bacteria?

Capable of contributing to dental caries; bacteria or sugar alone are insufficient without the other required factors. [Lecture: Dental Caries — The Agent | PDF page 8 | C0058]

What does cariogenic mean?

The degree to which a solution resists pH change. [Lecture: Dental Caries — The Agent | PDF page 8 | C0059]

What is buffering capacity?

Loss of mineral from enamel, dentin, or cementum through chemical dissolution. [Lecture: Dental Caries — The Agent | PDF page 8 | C0060]

What is demineralization?

Plaque is an organized microbial biofilm requiring mechanical removal; food debris may rinse away. [Lecture: Dental Caries — The Agent | PDF page 9 | C0062]

How does plaque differ from food debris?

A carbohydrate yielding two monosaccharides upon hydrolysis, such as sucrose or lactose. [Lecture: Dental Caries — The Agent | PDF page 9 | C0573]

What is a disaccharide?

Hydrolyzes sucrose into glucose and fructose. [Lecture: Dental Caries — The Agent | PDF page 10 | C0089]

What does invertase do?

Metabolism of sugars to pyruvate with energy release. [Lecture: Dental Caries — The Agent | PDF page 10 | C0090]

What is glycolysis?

A protein with a carbohydrate component. [Lecture: Dental Caries — The Agent | PDF page 10 | C0571]

What is a glycoprotein?

A thin acellular salivary film adsorbed onto enamel or cementum. [Lecture: Dental Caries — The Agent | PDF page 11 | C0063]

What is acquired pellicle?

Hair-like bacterial appendages involved in attachment. [Lecture: Dental Caries — The Agent | PDF page 11 | C0091]

What are pili?

A protein with phosphate groups esterified to residues such as serine, threonine, or tyrosine. [Lecture: Dental Caries — The Agent | PDF page 11 | C0092]

What is a phosphoprotein?

Professional removal of plaque, calculus, and stain. [Lecture: Dental Caries — The Agent | PDF page 11 | C0093]

What is prophylaxis?

A chain of sugar units connected by glycosidic bonds. [Lecture: Dental Caries — The Agent | PDF page 11 | C0572]

What is a polysaccharide?

Calcium/phosphate supersaturation and adequate buffering; fluoride enhances the process. [Lecture: Dental Caries — The Agent | PDF page 12 | C0061]

What conditions favor remineralization?

Material metabolized by plaque bacteria to produce acids, usually fermentable sugars. [Lecture: Dental Caries — The Agent | PDF page 12 | C0094]

What is a cariogenic substrate?

Remineralization can replace lost mineral before sufficient destruction and cavitation occur. [Lecture: Dental Caries — The Agent | PDF page 13 | C0050]

Why can early caries be reversible?

No. The lecture emphasizes an ecological shift toward acid-producing/acid-tolerant organisms; bacterial transmission alone does not equal developing caries. [Lecture: Dental Caries — The Agent | PDF page 14 | C0051]

Is caries explained simply by catching one infectious organism?

Ancient “tooth-worm” belief; Aristotle's association with sweets; Parmly's surface/bacterial account. [Lecture: Dental Caries — The Agent | PDF page 15 | C0569]

What early caries theories are described?

Miles/Underwood: acid plus germs; Miller: local carbohydrate-retention/acidogenic-bacteria theory; Dean: fluoride–caries reduction link. [Lecture: Dental Caries — The Agent | PDF page 16 | C0570]

What contributions are attributed to Miles/Underwood, Miller, and Dean?

Susceptible host/tooth surface, substrate/food, oral bacteria, and time. [Lecture: Dental Caries — The Agent | PDF page 17 | C0052]

What four primary factors must interact for caries development?

Age, fluoride, tooth morphology, exposed roots, nutrition, and salivary flow/buffering. [Lecture: Dental Caries — The Agent | PDF page 19 | C0053]

What host factors influence caries risk?

Oral clearance and retention, hygiene, eating frequency, food detergency, carbohydrate intake, and carbohydrate cariogenicity. [Lecture: Dental Caries — The Agent | PDF page 20 | C0054]

What substrate factors influence caries risk?

Repeated fermentation keeps plaque acidic and reduces time available for recovery/remineralization. [Lecture: Dental Caries — The Agent | PDF page 20 | C0055]

Why does frequent sugar exposure matter?

Microbial load, plaque composition, acidogenicity, hygiene, and fluoride in plaque. [Lecture: Dental Caries — The Agent | PDF page 21 | C0056]

What bacterial/plaque factors affect caries risk?

A single acid-production episode does not instantly create a cavity; repeated net mineral loss must accumulate. [Lecture: Dental Caries — The Agent | PDF page 22 | C0057]

Why is time necessary for caries development?

Calcified plaque; bacteria can continue living in association with it. [Lecture: Dental Caries — The Agent | PDF page 24 | C0064]

What is calculus?

An aggregate of microorganisms attached to each other and/or a solid surface in an aqueous environment. [Lecture: Dental Caries — The Agent | PDF page 25 | C0065]

What is a biofilm?

Approximately 90%; the gel-like extracellular polysaccharide matrix helps hold the biofilm together. [Lecture: Dental Caries — The Agent | PDF page 25 | C0066]

What proportion of plaque biofilm volume does this lecture attribute to extracellular matrix?

Mutans streptococci, especially S. mutans, and lactobacilli. [Lecture: Dental Caries — The Agent | PDF page 26 | C0067]

Which two bacterial groups are most associated with caries in the lecture?

Gram-positive cocci in chains. [Lecture: Dental Caries — The Agent | PDF page 27 | C0068]

What morphology and Gram reaction do streptococci have?

Approximately 30–40%. [Lecture: Dental Caries — The Agent | PDF page 27 | C0069]

What proportion of plaque does the lecture attribute to streptococci?

Efficient sugar uptake/storage, acid production, and sucrose-derived sticky glucans/dextran that aid adhesion. [Lecture: Dental Caries — The Agent | PDF page 27 | C0070]

Why is S. mutans effective in cariogenic plaque?

Dextransucrase (spelled “dextransucranase” on the slide). [Lecture: Dental Caries — The Agent | PDF page 27 | C0071]

Which enzyme name is used in the lecture for sucrose-to-dextran production?

Gram-positive rods; strongly aciduric and able to thrive at low pH. [Lecture: Dental Caries — The Agent | PDF page 28 | C0072]

What morphology and acid tolerance characterize lactobacilli?

Pellicle formation → initial attachment → irreversible attachment → early maturation → late maturation → dispersion. [Lecture: Dental Caries — The Agent | PDF page 29 | C0073]

What are the six biofilm-development stages in order?

Salivary glycoproteins, phosphoproteins, and lipids; initially acellular, without bacteria. [Lecture: Dental Caries — The Agent | PDF page 30 | C0074]

What composes the initial pellicle, and does it contain bacteria?

S. sanguinis; weak, reversible van der Waals forces, followed by more secure attachment using structures such as pili. [Lecture: Dental Caries — The Agent | PDF page 31 | C0075]

Which early colonizer and initial attachment force are named?

Additional organisms attach to early colonizers via specific adhesin–receptor interactions and form matrix-embedded microcolonies. [Lecture: Dental Caries — The Agent | PDF page 32 | C0076]

What happens in irreversible attachment?

Oxygen consumption produces anaerobic zones; food chains, attachment sites, and bacterial numbers increase. [Lecture: Dental Caries — The Agent | PDF page 33 | C0077]

What changes during early biofilm maturation?

Greater diversity, pH/oxygen microenvironments, a steady-state community, and a three-dimensional biofilm. [Lecture: Dental Caries — The Agent | PDF page 34 | C0078]

What characterizes late biofilm maturation?

Enzymes degrade matrix, allowing cells to detach and colonize new surfaces. [Lecture: Dental Caries — The Agent | PDF page 35 | C0079]

How do bacteria disperse from a mature biofilm?

24 h: monolayer/microcolonies; 48 h: larger three-dimensional microcolonies; 96 h: entire surface covered. [Lecture: Dental Caries — The Agent | PDF page 36 | C0080]

What timing does the lecture's laboratory biofilm image show?

About 800 possible oral species, with roughly 50–100 in a healthy individual at a time; communities vary between people and sites. [Lecture: Dental Caries — The Agent | PDF page 37 | C0081]

What species-diversity figures does the lecture quote?

Acid-sensitive organisms such as S. sanguinis decline; acid-tolerant S. mutans/lactobacilli thrive, encouraging further mineral loss. [Lecture: Dental Caries — The Agent | PDF page 38 | C0082]

How does low plaque pH change microbial ecology?