DEVELOPMENT OF THE HEAD & NECK1. Pharyngeal Arches

a. Each arch (pharyngeal membrane) has:i. Ectoderm (clefts)

ii. Endoderm (pouches)iii. Mesenchyme—from neural crest cells

b. Each arch consists of cartilage, artery—has its own blood supply (arches), and cranial nerve

c. Neural crest cells form:i. Bones of face/skull

1. mandible, maxilla, alveolar boneii. Hyoid cartilage

iii. Cartilage, bone, dentin, teeth, dermis etc.d. Neural crest cells arise from:

i. Rhombomeres—derived from Hoxb5 genes, which are regulated by Sonic HH and retinoic acid and can have implications for the potential regrowth of teeth

2. Pharyngeal Arches at 5 weeksa. Stomadeum is present—is the opening into the pharynx (future oral

cavity)b. Surrounded by 1st archc. Ectoderm surrounds the stomadeum near the tonsillar fossa

3.

Development of the Pituitary

a. Fusion of:i. Rathke’s pouch—invagination of ectoderm

1. Gives rise to pars intermedia, distalis, and tuberalisii. Infundibulum—diverticulum from forebrain

1. Gives rise to infundibular stalk and pars nervosa

DEVELOPMENT OF THE FACE1. Neural Crest Cells

a. Migrate to pharyngeal arches and form:

i. Maxilla, mandible, frontonasal prominence, hyoid cartilage, bone, dentin, dermis, etc.

2. Face Developmenta. Week 5:

i. 5 facial prominences: 2 mandible, 2 maxilla, frontonasalii. 2 nasal placodes—ectoderm induced by ventral forebrain to

invaginate inwards to form nasal pitsiii. Lateral and medial nasal prominences surround nasal pits

b. Next 2 Weeks:i. Upper Lip—Maxillary prominences and medial nasal prominences

increase in size and move toward midline where they fuseii. Maxillary prominence and lateral nasal prominence separated by

nasolacrimal grooveiii. Nasolacrimal groove invaginates to form nasolacrimal duct and

the lacrimal saciv. Lower Lip—Mandibular prominences merge in the midlinev. Cheeks—Develop from maxillary prominences (neural crest)

vi. Nose—1. Frontal prominence=bridge2. Medial nasal prominences=crest and tip3. Lateral Nasal Prominences=alae

3. Palate—intermaxillary segment (primary) and palatine shelves (secondary)a. Primary palate (Intermaxillary Segment)—formed by 2 medial nasal

prominencesi. Gives rise to:

1. Labial component—philtrum of upper lip2. Upper jaw—4 incisor teeth3. Palatal—primary palate

ii. Fuses with nasal septum from frontal prominenceb. Secondary palate—formed from 2 outgrowths of the maxillary

processes and the palatine shelves.

i. 2 pieces of secondary palate fuse together after first fusing to primary palate, creating a junction called the incisive foramen

c. Nasal Septum fuses with primary and secondary palate to separate the nasal and oral cavity

4. Tongue—Develops at the junction of the stomadeum and the pharynx

5. Nasal Cavities—separated from oral cavity by oronasal membrane, which breaks down to form the primitive choanae

a. As secondary palate forms, the definitive choanae forms, covered by the soft palate.

6. Teetha. Maxillary incisors—nasomedial prominencesb. Maxillary canines—maxillary prominencec. Maxillary premolars—maxillary prominenced. Maxillary molars—maxillary prominencee. Mandibular incisors—mandibular prominence-1st archf. Mandibular canines—mandibular prominenceg. Mandibular premolars—mandibular prominenceh. Mandibular molars—mandibular prominence

TOOTH DEVELOPMENT1. Teeth—develop from ectoderm and ectomesenchyme (neural crest)2. Intermaxillary segment/nasomedial prominences—4 maxillary incisors

a. Rest of teeth are from either the mandibular or maxillary prominences.3. Early tooth development

a. Primary epithelial band—forms as a result of mitosis and the change in orientation of the cells

i. Causes an indentation/invagination, which is the dental lamina w/ 20 tooth buds

b. Ectomesenchyme—condenses and becomes the dental papillac. First—Ectoderm epithelium directs tooth development

i. Any type of neural crest cell that associates with maxillary or mandibular epithelium will result in a tooth, meaning you need the appropriate epithelium to form a tooth.

d. Second—Neural crest cells take over the direction of tooth development

4. Tooth Development Pathwaya. 1st arch ectoderm influences ectomesenchyme

i. Requires FGF8—inactivation leads to arrest of tooth developmentb. Ectomesenchyme upregulates SHH and downregulates BMP 2&4.

i. SHH—inactivation leads to arrest of tooth development.ii. BMP—overexpression leads to arrest of tooth development

c. 1st arch ectoderm influences tooth bud formation, which results in the formation of the dental organ.

d. The dental organ further influences the ectomesenchyme by upregulating Lhx-6&7, and Pax9

e. WNT-7B is required in non-tooth areas to prevent formation of teeth. Overexpression of WNT leads to supernumerary teeth.

5. Models of Crown Shape Determinationa. Clone Model

i. Different areas of ectomesenchyme are programmed to form different teeth by the epithelium, and coax the dental lamina to form a tooth bud

b. Odontogenic homeobox code Modeli. Each area of ectomesenchyme has components for the type of

teeth it will eventually form.ii. Different genes cause different types to form

6. Stages of Tooth Developmenta. Bud Stage

i. Cell proliferation of tooth bud (invagination of dental lamina) and ectomesenchyme (forming dental papilla)

ii. The tooth bud influences the ectomesenchyme to condense

b. Cap Stage—Beginning of Histodifferentiationi. The enamel/dental organ invaginates to make a “cap” over the

aggregating ectomesenchyme (dental papilla).1. The stellate reticulum forms within the dental organ due to

accumulation of GAGs (hydrophilic) and the drawing in of water

a. The inner and outer enamel epithelium also differentiate

i. Basement membranes are present between the outer layer and the dental follicle and between the inner layer and the dental papilla

2. Ectomesenchymal cells surrounding the dental organ and the dental papilla make up the dental follicle

c. Bell Stage—Morphodifferentiation i. Tooth assumes its final shape

ii. The dental lamina breaks up so the tooth is no longer connected to the oral ectoderm, which may cause cysts

d. Crown Stage—Successional laminai. Successional lamina arises from the dental lamina and gives rise

to incisors, canines, and premolarsii. Dental lamina gives rise to molars

e. Root Formationi. Cervical loop gives rise to Hertwig’s root sheath

ii. Inner epithelial cells of the root sheath induce odontoblasts to form from the denal papilla, which forms the dentin of the root

iii. The root sheath stretches during growth and fragments, forming the rests of Malassez

7. Important Tooth Structures/Definitionsa. Enamel Organ—The organ overlying the dental papilla

i. Forms enamel/crownb. Dental Papilla—The area under the dental organ

i. Forms dentin and pulpc. Dental Follicle—The area surrounding the enamel organ and dental

papillai. Forms cementum, periodontal ligament, & alveolar bone

d. Enamel Knot—clusters of non-dividing epithelial cells within the enamel organ

e. Enamel Niche—produced as a result of cutting curved cellsfd1

ENAMEL

1. Compositiona. Inorganic Material

i. Calcium phosphate hydroxyapatite (96%)b. Organic Material

i. Water (3%)ii. Tyrosine rich amelogenin

1. Hydrophobic, regulate crystal growthiii. Nonamelogenins

1. Ameloblastina. Promotes mineral formation

2. Enamelina. Crystal nucleation and growth

3. Tuftelina. Function unclear

2. Structurea. Enamel rod—basic unit of enamel, long crystals that run parallel to long

axis of rodi. As they mature, they get larger, and lose water and organic

material. They get pushed together.b. Interrod enamel—areas where rods are not surrounded by rod sheath

and crystals run in various directionsi. Ions can be incorporated—F, Mg, Sr, Pb

c. Rod Sheath—area between rod and interrod (surrounds rod)i. Most organic material is here

3. Amelogenesis—REQUIRES DENTIN (forms first)!a. Reciprocal induction

i. Inner enamel epithelium induces dental papilla to become odontoblasts (make dentin)

ii. Dentin induces inner enamel epithelium to become ameloblasts

b. Phases/Stages of Amelogenesisi. Morphogenetic stage—cells commit to ameloblast lineage

1. Cells of internal dental lamina have centrally located nuclei

ii. Histodifferentiation stage1. Nuclei shift toward stratum intermedium, which is in

between the inner enamel epithelium and the stellate reticulum

2. Prominent Golgi and RER3. Terminal webs hold cells together as enamel is produced by

ameloblasts

iii. Presecretory Phase

1. Cells differentiate and become protein secreting2. Rods not formed, but immediate mineralization

iv. Secretory Phase: 30% mineralized enamel1. Ameloblasts make and organize enamel

a. Small dots—ameloblastinb. Large dots—amelogenin

2. Extensive Golgi and RER3. Tomes’ Processes

a. Proximal Process—forms interrod enameli. Initially, there’s only a proximal process and

enamel is structurelessb. Distal Process—forms rods

i. As ameloblasts move away from dentin, distal process forms and secretes rods while the cell junctions (proximal) secrete interrod enamel

ii. Sits into a pit and forms rods

v. Maturation Phase: addition of mineral and removal of water and organic materials

1. Ameloblasts get smaller and absorb/remove water but still some enamel secretion

2. 2 Types of Ameloblastsa. Ruffle ended—Tight junctions are tight

i. Add inorganic materialii. Undergo modulation and become smooth ended

b. Smooth Ended—tight junctions are leakyi. Remove water and organic material

3. Apoptosis occurs (50% of ameloblasts die)4. Basement membrane present

vi. Protective stage1. Basal lamina is

secreted2. Hemidesmosomes

are formed with ameloblasts

4. Mineralization Stagesa. Stage 1—formation of partially mineralized enamel in secretory stageb. Stage 2—mineralization from surface to deeper layersc. Stage 3—mineralization from inner later to surfaced. Stage 4—heavy mineralization of outer layer

5. Organization of Enamela. Rods run perpendicular to dentinb. Stria of Retzius—incremental growth lines that represent weekly

changes in enamel formationi. Neonatal line is an enlarged stria, representing change in nutrition

from umbilical to breast milk

c. Hunter-Schrager Bands—optical pattern resulting from changes

in rod direction i. Alternating light and dark bands

d. Gnarled enamel—the cuspal region of the crown where enamel rods twist and are irregular

e. Enamel tufts—abrupt changes in enamel rods at DEJ

f. Enamel lamellae—run from enamel surface and are filled with enamel protein or organic debris

g. Enamel spindles—newly formed odontoblast processes that get caught between enamel formed by ameloblasts

DENTIN1. Composition

a. Inorganic (70%)—hydroxyapatite crystalsb. Organic (20%)—Type I collagen and proteins form scaffold for the

mineral depositsc. Water (10%)

2. Typesa. Predentin—unmineralized, like osteoid (newly laid down)b. Mantle Dentin—thin dentin, just below the DEJc. Primary—circumpulpal and mantle dentin

i. Bulk of dentin is primary, and is well organized into tubulesd. Secondary—deposited after root formatione. Tertiary—reparative dentin, formed in reaction to stimulus

i. Has no organization

3. Organizationa. Dentin is organized into tubules, that are surrounded by peritubular

dentini. The odontoblast processes sit inside the tubules, which is what

leaves the space as they move down.b. In between the tubule/peritubule complex is intertubular dentinc. Cannaliculi are also

present in between tubules

4. Dentinogenesisa. Odontoblasts (from neural crest/neuralectoderm)—form dentin

i. Inner enamel epithelium induces dental papillary cells to differentiate into odontoblasts

b. Dentinogenesis begins in the cuspal region (coronal dentin)c. Continues later in the root, induced by Hertwig’s root sheath.

i. Deciduous teeth—dentin at root finished forming 18 mo. after eruption

ii. Permanent teeth—dentin at root finished forming 2-3 years after eruption

iii. No dentinal tubules in cementum, unlike coronal dentin, which have tubules that project into enamel (spindles).

d. Presecretory odontoblasts—cells are larger, with more organelles and polarized nucleus (away from inner enamel epithelium)

e. Secretory odontoblasts—tall columnar cellsi. Secrete Type I collagen and ground substance (like fibroblasts) to

make predentin

f. Mineralization—occurs in small, round areas called calcospherites, which coalesce to form a solid mass

i. Interglobular dentin—uncalcified regions of dentin

5. Definitionsa. Enamel spindle—Odontoblastic process that becomes embedded in

enamel, and gets longer as the odontoblasts lay down dentin and move towards the pulp

b. Von Korff’s fibers—Type I collagen secreted by odontoblasts in predentin

c. Tomes’ granular layer—special arrangements of collagen and proteins at the CEJ

d. Lines of von Ebner—incremental growth linese. Lines of Owen—larger, more pronounced incremental line that

indicates change in nutrition status after birth

CLINICAL CORRELATION ON INTEGUMENT1. Skin and Mucosa

a. Skin Layersi. St. Basale

ii. St. Spinosum1. Cells adhering via

a. Hemidesmosomes—integrinsi. Attach cells to the basal layer

b. Desmosomes—cadherinsi. Attach cells to neighboring cells with the help of

desmogleins, which attach tonofiliamentsiii. St. Granulosaiv. St. Lucidumv. St. Corneum

b. Mucosa—lose keratinization2. Types of Skin Cancers—they usually present as abnormalities in the dermis,

as the cells have broken through the basal lamina protective barrier separating the epidermis from the dermis.

a. Basal cellb. Squamous cell

i. Can occur in the mouth, especially is tobacco userc. Melanoma—melanocytes

i. A (asymmetry) B (border) C (color) D (diameter) E (evolving) 3. Other Skin Conditions

a. Psoriasis—a pruritic (itchy) condition causing patches of flaky, red, blistering skin all over the body including the mouth

i. Skin is red due to an overgrowth of blood vesselsii. Dentritic cells affected

b. Pemphigus—autoimmune disease to desmosomesi. Pemphigus foliaceus—mild form (skin only)

1. Caused by the knockout of Dsg1 (IgG antibodies)a. Dsg1 present in high quantity in the stratum corneum,

resulting in detachment of St. corneum, causing light pink, superficial lesions/blisters

b. Very little Dsg1 in the mouth, so lesions are only present in skin

ii. Pemphigus vulgaris—more severe (skin and mouth)1. Caused by knockout of Dsg3 (IgG antibodies)

a. Dsg3 present in high quantity in the stratum basale, resulting in a complete separation of the upper layers from the basal layer, causing angry, deep red blisters

b. High quantity of Dsg3 in the mouth, so lesions are present in the oral mucosa

c. Can have both Dsg3 and Dsg1 knocked out, resulting in lesions in both the skin and mouth

iii. In both types, the basal layer is still attached because they are attached to the basal lamina via hemidesmosomes, which don’t have Dsg1 or Dsg3 and are unaffected.

iv. Nikolsky’s Sign—a test to diagnose pemphigus (and other issues)1. Is either positive or negative

a. Positive results are those with loose skin that slips free from underlying layers when rubbed

b. Doctor uses the eraser of a pencil and twists it against the skin. If positive, a blister will form there in minutes.

v. Generally has a good prognosis with topical steroidsvi. Risk factors are Myesthenia Gravis, Cancer, sun exposure, and

travel to Brazil (mosquito bite initiates).c. Bollous Pemphigoid—auto immune disease of hemidesmosomes)

i. Causes disruption of adhesion between the St. basale and the basal lamina, resulting in complete detachment of the epidermis from the dermis causing angry red blisters.

THE PULP COMPLEX1. Zones of the Pulp

a. Odontoblast Layeri. Odontoblasts—produce

Type I collagenb. Cell free zone

i. Nerve plexus of Raschkowc. Cell Rich zone

i. Fibroblasts—make pulp matrix

ii. Ectomesenchymal cells—give rise to odontoblasts/fibroblasts

d. Core zone

i. Blood supply Arterioles enter the pulp

from the apical and accessory foramen

1. Main capillary bed is near the odontoblast layer

2. Shunts are present throughout the pulp

ii. Nerves Sensory and Sympathetic

nerve bundles also enter through the apical and accessory foramen and regulate the vasculature.

Myelinated and Unmyelinated Nerves (surrounded by Schwann)o Myelinated—detect pressure and vibrationo Unmyelinated—detect pain

1. Major nerve plexus of Raschkow present in cell free zone

2. Nerve growth factor is present in dentinal tubules, meaning that stimulation of dentin may cause pain sensation. All sensations within the dentin/pulp complex cause pain.

iii. Lymphatics Begin in coronal region and exit through the apical foramen

1. Macrophage—from monocytes2. Lymphocytes—mostly T cells3. Dendritic cells—Antigen presenting cells that can project

processes into dentinal tubules2. Collagen of the Pulp

a. Types I and III (TMJ=Type II)i. Greatest concentration of collagen is in the most apical portion of

the pulp3. Pain in the Dentin/Pulp Complex

a. All sensations cause pain (ex. Heat, air, cold, water, etc.) due to presence of nerves in the dentinal tubules

b. Theories of Pain—none are proveni. Dentin is directly innervated

ii. Odontoblasts act as receptors for neurons1. No synapses have ever been found

iii. Fluid movement through tubules stimulates receptors in pulp1. Fluid movement influences the pulp and is sensed by nerve

endings4. Age-Related Changes to Pulp

a. Decrease in volume of chamber due to continued dentin productionb. Reduction of vasculaturec. Cell density reduced with increase of fibrous bundlesd. Loss of axons and pulp sensitivitye. Calcifications/Pulp Stones

5. Age-Related Changes to Dentina. Gradual reduction in diameter of dentinal tubuleb. Closure of dentinal tubule, resulting in sclerotic dentinc. Increased brittlenessd. Dead tracts found near the root apex due to the death of odontoblasts

THE PERIODONTIUM1. Parts

a. Gingiva—support teethb. Alveolar Processes—bone that supports teethc. Periodontal ligament—fibers that connect cementum/roots to bone

i. Inserts into cementum (Sharpey’s fibers) between cementocytesii. Made of Type XII collagen

d. Cementum—covers root of teethe. Composition

1. Matrix (50%)a. Mostly collagen Type I, III, XII (also V, VI, XIV)b. Proteins

2. Mineral (50%)a. Hydroxyapatite

2. Types of Cementuma. Primary

i. Aceullar extrinsic fiber cementum1. No cementocytes embedded2. Provides tooth attachment 3. Found at cervical crown4. Cementoblasts align along predentin and initially produce

collagen that intermingles with dentin collagena. PDL fibers sit between cementoblasts and insert into

the primary cementum, resulting in Sharpey’s fibers that get trapped in the mineralized cementum

b. Secondaryi. Cellular intrinsic fiber cementum

1. Has cementocytes in lacunae embedded in mineralized cementum

2. Adaptive role to tooth wear, movement, repair3. Found at the apical root4. Formed after tooth is in occlusion

3. Cementogenesis—not clear which cells actually produce cementuma. Initiated at Hertwig’s Root Sheath (HERS)b. After odontoblasts produce predentin, it comes in contact with

ectomesenchymal cells from dental folliclec. 2 Theories about what happens next

i. Dental follicle cells receive signal from HERS or dentin and differentiate into cementoblasts

ii. HERS cells differentiate into Cementoblastsiii. BMP and Runx2 may cause differentiation

d. During these processes, some cementoblasts undergo apoptosis, forming the cell rests of Malassez, which are present in the PDL and contribute to maintenance/regeneration of the PDL

4. CEJa. Types of junctions

i. Overlap of Cementum and Enamelii. Gap between Cementum and Enamel

iii. Perfect meeting/opposition of Cementum and Enamel5. Alveloar Process aka Lamina Dura aka Alveolar Bone Proper

a. Made up of spongy bone which sits between cortical bone and the lamina dura (closest to PDL)

b. Derived from ectomesenchymec. Bundle bone—directly lines the socket where teeth sit

i. Collagen fibers of the PDL insert/attach via Sharpey’s fibersd. Tooth movement causes constant remodeling (resorption and

deposition) of bone

6. PDL—made of Type I, III, and XII collagena. Development

i. Derived from ectomesenchyme (neural crest)1. Gives rise to fibroblasts, which produce collagen of PDL

ii. Early on the PDL fibers are unorganizediii. Later becomes

organized1. Alveolar crest

fibers2. Horizontal fibers3. Oblique fibers4. Apical fibers5. Interradicular

fibersb. Has significant nerve supply

i. Free nerve endings—pain

ii. Ruffini endings—

pressurec. Blood supply is extensive

7. Important Definitionsa. Sharpey’s (extrinsic acellular) fibers—Collagen fibers of the PDL that

become embedded in the ingoranic cementum matrixb. Cementoid—newly laid unmineralized cementum made up of collagen

fibers which intermingle with dentin collagenc. Cell rests of Malassez—remnants of the epithelial sheath (Hertwig) that

are part of the PDL and maintain/regernate it.

SALIVARY GLANDS1. Salivary Glands—Tubuloalveolar exocrine glands

a. Glands form from epithelium and differentiate to be ducts or secretory cells

b. They are surrounded by CT, which invaginates to form lobulesi. Acini are in the lobules in bunches

ii. Product moves from the acini, to an intercalated duct (simple cuboidal), to a striated duct (simple columnar), to an intralobular duct, to an interlobular duct, to a lobar duct, and out to the main duct

1. Striated ducts—have basal infoldings w/Na+ ion pumps, which help produce a hypo-osmotic saliva

c. Tubules—are mucous producingi. Have myoepithelial cells at the base, which are filled with

actin filaments and contract to move secretions through the ducts

ii. Can have serous demi-lunes, which will produce a serous secretion that mixes with the mucous secreting tubule

d. Alveolus/Acinus—Serous secretingi. Have myoepithelial cells as well

2. Types of Glandsa. Parotid—serous acini

i. Stains intensely because acini are making lots of proteinsii. Produce a watery saliva w/ amylase, lysozyme, IgA, and

lactoferrin

b. Submandibular—mixed, mostly serous (w/demilunes)

c. Sublingual—mixed, mostly mucous due to mucin (pale staining cells)

d. Minor glands—labial, palatal, buccal, linguali. Mixture of serous and mucous

3. Innervation (unmyelinated w/ Schwann cells)a. Parasympathetic (most common)—evokes fluid secretion during

eating, etc.i. Fluid and electrolyte secretion

1. Acetylcholine (parasympathetic) binds to cholinergic receptor

2. Sets off a cascade, leading to excretion of fluids/electrolytes

b. Sympathetic (more intermittent)—do not mobilize fluid secretion due to fight or flight response

i. Protein secretion1. Norepinephrine (sympathetic) binds to B adrenergic

receptor, setting off a cascade and ultimately releasing proteins

ORAL MUCOSA1. Masticatory Mucosa/Oral Mucoperiosteum (hard palate, gums)

a. Epithelium—stratified squamous wetb. Lamina Propria—lots of CT fibers that hold the mucosa tightly bound

against the bone along with vessels, nerves, etc.i. Has many papillary ridges, which increase area for a secure

attachment to the overlying epitheliumii. Held to epithelium via hemidesmosomes, tonofibrils, and carious

other components that work in concert to form tight connectionsiii. Cells include fibroblasts (Type I, III), mast cells (heparin),

macrophages and other immune cells (Plasma, neutrophils, lymphocytes)

c. Bone2. Lining Mucosa (lips, posterior palate, cheek, etc.)

a. Epithelium—stratified squamous wetb. Lamina Propria—fine CT

i. Has papillary ridges to attach to epithelium and all the same features as oral mucoperiosteum (see above)

ii. Sometimes has skeletal muscle depending on function of areac. Submucosa—loose CT, vessels, nerves, etc.

3. Epithelium Types

a. Ker

atinized—tough, resists abrasioni. St. Basale—divides and has tonofilaments

ii. Prickle cell layer—tonofibrils, membrane coating granules, desmosomes

iii. Granular layer—keratohyaline granules, tonofibrils, membrane coating granules

iv. St. corneum is highly keratinized and cells have no nucleus/organelles

v. Found in hard palate, gingivab. Para-keratinized

i. St. corneum is highly keratinized but some cells still have nucleic. Non-keratinized—thick but flexible

i. St. Basale—divides and has tonofilamentsii. Prickle cell layer—tonofilaments, membrane coating granules,

desmosomesiii. Intermediate layer—tonofilaments, glycogeniv. St. corneum cells have nucleiv. Found in lips, cheek, soft palate, floor of the mouth, underside of

tongue

1. Floor of mouth is thinnest stratified squamous epithelium and is often used as a site for administering drugs directly into the bloodstream as they dissolve easily

4. Turnover Ratea. Cheek—15-25 daysb. Gingiva—40-50 daysc. Influenced by cytokines, which are produces by epithelium cells,

fibroblasts, and inflammatory cellsi. Inflammation can either stimulate (slight) or slow (severe) mitosis

5. Nerve supplya. Better anteriorly to detect temperature and taste (buds on tongue)

TONGUE/TASTE BUDS

2. Anterior 2/3a. Filliform—highly

keratinized

b. Fungiform—non-keratinized, mushroom-like and occasionally have taste buds

3. Posterior 1/3 (sulcus terminalis—junction of anterior 2/3)

a. Circumvallate—non-keratinized w/ many taste budsi. Have crypts, which is where the taste buds are located

ii. Have von Ebner’s glands, which are serous secreting and dump into the crypts

4. Taste Budsa. Function

i. Microvilli on taste pores bind ligands which turns on G-coupled protein receptor pathways

ii. This activates channels allowing NaCl in, which depolarizes the neuroepithelial cells and releases neurotransmitters to the brain about taste (sweet, sour, salty, umami, bitter).

PALATES1. Hard Palate—masticatory mucosa

a. Stratified squamous epithelium w/ different composition based on area. Gets more keratinized at the midline, and keratinization decreases as you more laterally and posteriorly.

i. Anterior Hard palate—keratinized

ii. Anterolateral—para-keratinized

iii. Posterolateral—non-keratinized

2. Soft Palate—extension of hard palate (back of mouth to pharynx) that has both a respiratory and oral epithelium surface

a. Respiratory surface w/ respiratory epithelium (pseudostratified ciliated columnar) and skeletal muscle

b. Oral surface—wet stratified squamous w/ mucous glands and lymphatic nodules

GINGIVA—masticatory mucosa1. Alveolar mucosa—non-keratinized

a. Meets with attached gingiva at the mucogingival junction2. Attached gingiva—para-keratinized3. Free gingiva—keratinized

a. >3 mm sulcus means periodontal diseaseb. Has junctional epithelium where the free gingiva attaches to the

enameli. Enamel is separated from epithelium by a basal lamina

ii. Epithelium is separated from lamina propria by a basal lamina

TOOTH ERUPTION1. Stages of Tooth Eruption

a. Pre-eruptive stagei. Tooth changes location during Bell Stage

b. Eruptive Stagei. Upward movement of the tooth that begins with root formation

and ends when the tooth reaches the occlusal planeii. There is an intraosseous and extraosseous phase as the teeth

move through the bonec. Post-eruptive Stage

i. Normal growth of jaw up until age 20, with readjustment between 14 and 18

1. Teeth move occlusally with root formation and jaw growth2. Occlusion causes PDL to become organized and causes the

alveolar bone to increase in density2. Teeth movement

a. Teeth move in 2 ways in relation to the growing jawi. Total Bodily movement

1. Entire tooth shifts and involves bone reabsorption and formation

ii. Eccentric growth1. One part of the tooth grows (ex. Root elongates but crown

doesn’t grow)

3. Mechanisms of Tooth Eruptiona. Little is actually known about tooth eruption, but there are 4 factors to

be consideredi. Root Formation

1. Occurs after amelogenesis is complete

2. Teeth without roots can eruptii. Bony remodeling—CSF1 and RANKL are

important

1. CSF-1 is needed. It stimulates monocytes to enter during tooth eruption, which become osteoclasts

a. Coronal region of the dental follicle regulates osteoclasts and RANKL expression increases (parathyroid hormone upregulates RANKL)

2. Basal region of dental follicle regulates osteoblast activity and BMP expression increases to create alveolar bone

a. Controlled by Runx2iii. Forces generated by the PDL

1. The PDL forms after root formation starts and must be remodeled as eruption occurs

2. It is thought that the PDL helps pull the tooth through the bony socket

a. BUT with osteopetrosis, there is a PDL but teeth don’t erupt and teeth with no roots and without a PDL do erupt, so we aren’t really sure.

iv. Molecular changes in the dental follicle1. The dental follicle is attached to the lamina propria of the

oral mucosa via the gubernacular cord, which travels through the gubernacular canal

a. The canal is widened by osteoclasts and teeth travel up through it

2. Eruption may be dependent in part on the presence of the dental follicle

a. Even without a tooth or with a replica, the gubernacular cord develops and the tooth will erupt, suggesting programmed bony remodeling and a reliance on the dental follicle

3. Dental follicle regulates:a. Eruption pathway:

i. Bone, CT, and epithelium reabsorptionb. Moving tooth into eruption pathway:

i. Interradicular bone formation, root growth, and PDL growth

4. Tooth weara. Occlusal

i. As teeth wear down they erupt furtherb. Interproximal

i. Teeth have a tendency to move anteriorly (“mesial drift”)1. Involves continued bone remodeling. Bone resorption on

mesial and apposition on distal2. Transeptal fibers play a role in the mesial drift along with

occlusal forces5. Tooth exfoliation

a. Some of pulp cavity is lost when tooth is lost, but root and dentin are reabsorbed by odontoclasts (from monocytes)

b. Caused by pressure from tooth underneath and increased forces from mastication and jaw

c. Mandibular lost before maxillary and girls before boys