Growth / Tooth Development Flashcards
Average ERUPTION Time for PERMANENT TEETH 🦷 in YEARS
@YEAR ERUPTION 🌋 PERMANENT TEETH
C L Cn 1p 2p 1 2 3 Max: 7 8 11 10 10.5 6 12 17 Mand: 6 7 9 10 11 6 11 17
“MAIN” pattern
General Rules:
- Mandibular before Max (same tooth in arch)
- Females before Males
- 2-3 rule
- Teeth begin erupting when Root is 2/3 developed
- Root take 2-3 years to complete after initial eruption.
What is the FIRST STAGE of tooth development?
What happens?
I = EC➡️M
INITIATION
ECTODERM induces the MESENCHYMAL tissue in order to initiate the process.
I = EC➡️M
Calcification timing for all primary / permanent teeth.
🕙🗓🦷
🤰🦷
👼🦷
- On average PRIMARY teeth take 10 MONTHS for completion of calcification. 🕙🗓🦷
- The PRIMARY teeth BEGIN to form in UTERO at about SIX weeks.
Hard tissue formation occurs in ALL primary teeth by the 18TH week in utero. (4th fetal month)
6-18W🤰
- The PERMANENT teeth begin to develop at approximately FOUR months of age in UTERO. Maxillary and mandibular FIRST molars begin to CALCIFY at BIRTH. They are the first to begin calcification. The mandibular THIRD molars are generally the last teeth to begin calcifying. This happens at about 8-10 years of age.
👼🦷
What are the components of a tooth bud/germ?
“Bud is a pos”
TOOTH BUD - GERM - POS
These cells are derived from
- ECTODERM of the FIRST BRACHIAL ARCH
- ECTOMESENCHYME of the NEURAL CREST
- Dental Papilla
- Enamel Organ
- Dental Sac/Follicle
Where do NEURAL CREST cells originate?
What to they differentiate into?
CREST - ECTODERM - DENTIN - CARTILEDGE
Temporary group of cells that arise from the embryonic ectoderm cell layer along the LATERAL margins of the NEURAL PLATE.
Responsible for many SKELETAL and CONNECTIVE tissue.
- Bone 🦴
- Cartilage
- DENTIN
- Dermis
Not Enamal
Dental LAMINA
INITIATION
DL6 - TOOTH BUDS - CAP 🧢 - SERRES
FIRST evidence of tooth DEVELOPMENT and begins at the SIXTH week in utero = DL6
It is formed when cells of the oral ectoderm PROLIFERATE FASTER than cells of other areas.
This dividing tissue is surrounded by and stimulated by ECTOMESENCHYMAL growth.
The DL CONNECTS the developing tooth BUD to the EPITHELIUM of the oral cavity.
T (epithelium + dl)
n (tooth bud)
Responsible for the dental PAPILLA and later ODONTOBLASTS
“Papillamina”
Eventually, the DL DISINTEGRATES into small CLUSTERS of EPITHELIUM and is RESORBED.
This is responsible for the CAP 🧢 like structure of the enamel organ.
In situations when the clusters are not resorbed, (Glands/Rests of SERRES) eruption CYSTS are formed OVER the DEVELOPING TOOTH and delay its eruption into the oral cavity.
Rests of Serres?
What can develop from them?
🦴
Ok…LGg
-REMNANTS of dental LAMINA epithelium entrapped within the GINGIVA.
OK…LGG
- Odontogenic Keratocyst
- Lateral Periodontal cyst
- Gingival cyst
- Glandular Odontogenic cyst
Average ERUPTION 🌋Time for PRIMARY 👶 TEETH 🦷 in MONTHS
@MONTH ERUPTION PRIMARY TEETH
Cent - Lat - Canine - 1st M - 2nd M
Max:
8 9 16 13 26
Mand:
6 10 17 14 23
First: lower central
Last: upper 2nd
“nxi” pattern
Rests of Malassez?
What can develop from them?
EPITHELIAL cell RESTS of MALASSEZ (ERM)
Part of the PERIODONTAL LIGAMENT cells around a tooth. They are discrete clusters of RESIDUAL cells from HERTWIG’S epithelial root sheath (HERS) that didn’t completely disappear.
A specialized form of epithelium (Hertwig epithelial root sheath) directs ROOT FORMATION, and once complete, it degenerates, leaving epithelial rests of Malassez
These rests are not isolated but form vague net-like structures around root of tooth within periodontal ligament (fibrous tissue connection between tooth root and bone of jaw)
It is considered that these cell rests proliferate to form epithelial lining of various odontogenic cysts such as RADICULAR cyst under the influence of various stimuli.
Hyperactivity of Dental Lamina can result in what?
HYPERDONTIA
Hyperactivity or over growth of dental lamina can give rise to conditions such as Hyperdontia.
On completion of the dentition, the dental lamina is usually destroyed and reabsorbed, but when REMNANTS FAIL to RESORB. it can continue to PROLIFERATE ABNORMALLY. This abnormal proliferation can form the EXTRA tooth BUD leading to supernumerary teeth.
What Pathologies are associated with Neural Crest Cell defects?
wtf hd
FETAL ALCOHOL SYNDROME DISORDER 🍷
-impair neural crest migration
TREACHER-COLLINS SYNDROME
-mutation which causes ncc apoptosis
DiGEORGE SYNDROME
-chromosome 22 deletion disrupt ncc migration
HIRSCHSPRUNG’S DISEASE
-lack of ncc migration to gut
WAARDENBURG’S SYNDROME
-defective ncc migration: deafness piebald
WTF HD?
Enamel Organ
ENAMEL ORGAN
Periphery: low Columnar cells
Central: Polygonal cells
Composed of:
- Outer enamel epithelium
- Inner enamel epithelium
- Stellate reticulum
- Stratum intermedium.
These cells give rise to AMELOBLASTS, which produce enamel and the reduced enamel epithelium.
The location where the OUTER enamel epithelium and INNER enamel epithelium JOIN is called the CERVICAL LOOP.
n
^^ (points to cervical loop on bud)
The GROWTH of cervical loop cells into the deeper tissues forms HERTWIG’S Epithelial Root Sheath, which determines the ROOT SHAPE of the tooth.
n
⬇️
Hertwig epithelial root sheath (HERS)
IEE - OEE - 🚫- DENTIN - MALASSEZ
- is derived from the INNER and OUTER enamel epithelium of the enamel organ.
- without 🚫 Stratum intermedium and Stellate reticulum.
n
⬇️
I I
- A PROLIFERATION of EPITHELIAL cells located at the cervical loop of the enamel organ in a developing tooth.
- INITIATES the formation of DENTIN in the ROOT of a tooth by causing the differentiation of ODONTOBLASTS from the dental papilla.
Odont l l Dent Pap
^
HERS
The root sheath eventually DISINTEGRATES with the periodontal ligament, but RESIDUAL pieces that do not completely disappear are seen as epithelial cell rests of MALASSEZ (ERM).
These rests can become CYSTIC, presenting future periodontal infections.
- Radicular Cysts
- Cementicles
Dental Papilla
🧢
DENTAL PAPILLA 🧢
→ The ectomesenchymal cells which are lying deep to the enamel organ
→ will develop to become the dental PULP and the DENTIN
Formation of dental papilla occurs in the CAP 🧢 stage of Odontogenesis.
The cap stage is the third stage of tooth development and occurs during the NINTH/TENTH week of prenatal development
A section of the ECTOMESENCHYME (a group of tissue made up of neurocrest cells which are present in the initial development of an embryo) CONDENSES into a MASS within the CONCAVITY of the cap of the enamel organ. This mass is now considered the DENTAL PAPILLA.
n
^ (in middle)
dp
Meckel’s Cartilage
MECKEL’S CARTILAGE
- the cartilaginous bar of the MANDIBULAR arch is formed by what are known as Meckel’s cartilages
- above this the INCUS and MALLEUS are developed.
- Meckel’s cartilage arises from the FIRST PHARYNGEAL arch.
- Meckel’s cartilage forms in the MESODERM of the mandibular process
the cartilaginous bar of the embryonic mandibular arch of which the distal end ossifies to form the malleus and most of the rest disappears in development, with the part adjacent to the malleus being replaced by fibrous membrane comprising the sphenomandibular ligament and the connective tissue covering most of the remaining part ossifying to form much of the mandible
Stellate Reticulum
🌟💧☎️
STELLATE RETICULUM 🌟💧☎️
The stellate reticulum is a group of cells located in the CENTER of the ENAMEL ORGAN of a developing tooth.
These cells are STAR 🌟 -SHAPED and synthesize GLYCOAMINOGLYCANS
. As glycosaminoglycans are produced, WATER 💧 is drawn in from the ECTOMESENCHYME cells, stretching them apart. As they are moved further away from one another, the stellate reticular cells maintain contact with one another through DESMOSOMES ☎️ , resulting in their unique appearance.
SUPPORTS and PROTECTS AMELOBLASTS
The stellate reticulum is LOST AFTER the first layer of ENAMEL is laid down. This brings cells in the inner enamel epithelium closer to blood vessels at the periphery.
Cap Stage
🧢🧢🧢
Proliferation
Morphodifferentiation
Histodifferation
CAP STAGE 🧢🧢🧢
9 weeks in utero
Placodes proliferate into ENAMEL ORGAN
3 CELL types of EO:
- OUTER enamel epithelium (CUBOIDAL ▪️▪️)
- INNER enamel epithelium (LOW ➿ Columnar)
- STELLATE reticulum (STAR 🌟 shaped)
UNEQUAL proliferation of cells, RAPIDLY dividing at the LATERAL area of the tooth BUD, giving rise to a CAP shape, pushing the lateral ends more into the ectomesenchyme leading to a CONCAVITY or infolding creating the INNER epithelium area.
(n - iee, inside border)
Stellate reticulum: - layer between the IEE and the OEE
Condensed MESENCHYME becomes dental PAPILLA.
The Papilla essentially is wearing the Enamel Organ as a “cap”
Dental FOLLICLE is the surrounding SAC that surrounds the entire Papilla + Enamel Organ
Defects during Cap Stage:
(Cyst, Odontoma, Gemination, Fusion, Dens in Dente)
What are Placodes?
PLACODES
The term placode refers to ECTODERM THICKENINGS in the cranial region that have important roles in development of special sensory and other systems.
Dental placode is the main EPITHELIAL structure participating in tooth formation. The dentla placode FORMS ALONG the dental LAMINA, rapidly INVADES the underlying MESENCHYME and gives rise to enamel-producing ameloblasts.
DENTAL LAMINA ⬇️ DENTAL PLACODES (20 in #, primary teeth) ⬇️ MESENCHYME
***PERMANENT teeth 🦷 FORM from a LINGUAL EXTENSION of the dental lamina called SUCCESSIONAL LAMINA.
***Except Permanent MOLARS, which are from the LAMINA itself.
Bell Stage 🛎 🔔
Proliferation
Morphodifferentiation
Histodifferation
BELL STAGE 🛎🔔
11 weeks in Utero
Marked by BOTH happening simultaneously:
- MORPHODIFFERENTIATION
- establishment of the SHAPE of the CROWN - HISTODIFFERENTIATION
- Dental Papilla cells ➡️ Odontoblasts
- Inner Enamel Epithelium cells ➡️ Ameloblasts
The junction where Odontoblasts and Ameloblasts meet becomes the DEJ
Ameloblast Cells = TALL ➰➰columnar
iee ➿ ➡️ ➰ a
- EARLY BELL 🛎 STAGE
FRAGMENTATION of the Dental LAMINA.
-separating the tooth germ from the oral epithelium
STRATUM INTERMEDIUM (straddles)
-cells BETWEEN iee and stellate reticulum
-SPINDLE shaped
➿l l🌟
^
SI
- speculated to work in TANDOM with the IEE to form ENAMEL
- CUSP TIP begins to form FIRST making its way sloping down to the CERVICAL region by differing rates of CELL DIVISION giving it its SHAPE.
- ADVANCED BELL STAGE 🔔
Marked by MINERALIZATION of ENAMEL and DENTIN
- Stellate Reticulum collapses
- AMELOBLASTS finally FUSE with OUTER enamel epithelium forming REDUCED enamel epithelium surrounding the entire crown.
- once ENTIRE crown is formed, the CERVICAL LOOP gives rise to HERTWIGS
- Hertwig’s bends in towards the pulp at 45 DEGREES constricting the cervical opening creating the EPITHELIAL DIAPHRAGM.
DEFECTS IN BELL STAGE:
Histo: (Amelogenesis-Dentogenesis Imperfecta)
Morpho: (size and sharp anomalies, peg laterals, example)
Odontoblasts
ODONTOBLASTS
- derived from the DENTAL PAPILLA cells
- DIFFERENTIATE under the INFLUENCE of the INNER enamel epithelium
- starting at CUSP TIP simultaneously with the ameloblasts forming the enamel.
List the Morphological Tooth Stages in Order.
MORPHOLOGIC TOOTH STAGES
- Dental Lamina
- Bud Stage
- Cap Stage
- Early Bell Stage
- Advanced Bell Stage
Initiation Development Phase
“Downloading”
Morphological Stage?
Deficient Development?
Excessive Development.
INITIATION PHASE
-Dental Lamina morphological phase
DL (DownLoading
6 weeks in utero
Effects # of Teeth (Downloading issues)
DEFICIENT Development
- Anodontia
- Hypodontia
- Oligodontia
EXCESSIVE Development
-Hyperdontia
Proliferation Development Phase
Morphological Stage?
Deficient Development?
Excessive Development.
PROLIFERATION
Bud, Cap, Early and Advanced Bell Morphological Stage.
Effects # of Teeth and Structure
DEFICIENT Development
- Hypodontia
- Oligodontia
EXCESSIVE Development
- Hyperdontia
- Odontoma
- Epithelial Rests
Histodifferentiation Development Phase
Morphological Stage?
Deficient Development?
Excessive Development?
HISTODIFFERENTIATION
Cap, Early and Advanced Morphological Stage
Effects Enamel and Dentin Structure
DEFICIENT development
- Amelogenesis Imperfecta type 1 (hypoplastic)
- Amelogenesis Imperfecta type 4 (hypomature)
- Dentinogenesis Imperfecta
**NO EXCESSIVE development
Morphodifferentiation Development Phase
Morphological Stage?
Deficient Development?
Excessive Development?
MORPHODIFFERENTIATION
Bud, Cap, Early and Advanced Bell
Effects Size and Shape
DEFICIENT Development
- Microdontia
- Peg Lateral
- Mulberry Molar
- Hutchinson Incisors
- Absence of cusp or root
EXCESSIVE Development
- Macrodontia
- Tuberculated Cusp
- Carabelli’s Cusp
- Taurodontism
- Dens in Dente
- Dens Evainatus
- Dilaceration
- Gemination
- Fusion
- Concresence
Apposition Development Phase
Morphological Stage?
Deficient Development?
Excessive Development?
APPOSITION
Deposition of enamel and dentin matrices
Effects Enamel, Dentin, and Cementum
DEFICIENT DEVELOPMENT
- Amelogenesis Imperfecta type 2 and 4 (hypomaturation)
- Enamel Hypoplasia
- Dentin Dysplasia
- Regional Odontodyplasia
“Appoplasia”
EXCESSIVE DEVELOPMENT
- Enamel Pearls
- Hypercementosis
- Odontoma
What are the Brachial Arches?
The branchial arch system begins to form in the FOURTH WEEK and consists of SIX PAIRED ARCHES that decrease in size from cranial to caudal.
Each branchial arch consists of four essential tissue components (CARTILAGE , AORTIC ARCH ARTERY, NERVE, MUSCLE)
building blocks for the FACE, NECK, and OROPHARYNX.
Growth of Facial components
Endochondral vs. Intramembranous
Ossification?
Cranial Vault
Cranial Base
Maxilla
Mandible
ENDOCHONDRAL:
Cranial Bass: SPHENO-OCCIPITAL
- principle growth cartilage of cranial base
- only one that remains ACTIVE during childhood
Mandible: CONDYLE
INTRAMEMBRANOUS:
Cranial vault: APPOSITION at SUTURES
Maxilla: APPOSITION SUPERIOR/POSTERIOR
- growth occurs UP⬆️ and Back➡️ against cranial base making the Maxilla express downward/forward ⬅️⬇️
- Resorption on anterior
Mandible: RAMUS/BODY
- Apposition on Posterior border against GLENOID FOSSA
- remodeling resorption on anterior border
What does REICHART’S Cartilage form?
REICHART’S cartilage has been described as a continuous cartilaginous formation in the SECOND pharyngeal ARCH and is the origin of several structures such as the STYLOID PROCESS of the temporal bone, the STYLOHYOID LIGAMENT and the lesser horns of the hyoid bone.
“SECOND / STYLOID”
What branchial arches form the tongue?
The first, second, third, and fourth pharyngeal arches contribute to the development of the various portions of the tongue.
The development BEGINS with the growth of a medial swelling from the FIRST pharyngeal arch, known as TUBERCULUM IMPAR.
What does the FIRST brachial arch form?
What happens if it is deficient?
The first branchial arch forms the MANDIBLE and contributes to the maxillary process of the upper jaw.
Abnormal development of the first branchial arch results in a host of facial deformities, including CLEFT LIP and PALATE, abnormal shape or contour of the EXTERNAL EAR, and malformed internal OSSICLES.
Onset of puberty is signaled by what secretion of what?
Gonadotropin-releasing hormones
A hormone made by a part of the brain called the HYPOTHALAMUS. Gonadotropin-releasing hormone causes the pituitary gland in the brain to make and secrete the hormones luteinizing hormone (LH) and (FSH)
Gonadotropin-releasing hormone causes the ANTERIOR PITUITARY GLAND in the brain to make and secrete the hormones luteinizing hormone (LH) and follicle-stimulating hormone (FSH).
In men, these hormones cause the testicles to make testosterone. In women, they cause the ovaries to make estrogen and progesterone.
T/F?
The Mandible shows greater prognathism than Maxilla because of of the circumpubertal growth spurt, which has more effect on mandible than on maxilla, especially in MALES
True
Prognathism
MANDIBLE/MALES
Cleft Lip and Palate are from the lack of fusion between?
The nose and mouth of a baby develop between the 5th and 12th WEEKS of life inside the mother’s womb.
CLEFT LIP:
results from the failure of the MEDAL NASAL and MAXILLARY PROCESSES to fuse.
CLEFT PALATE:
results from the failure of the fusion of the PALATAL PROCESSES of the MAXILLA
Central or Frontal Nasal Prominence:
- normally grows to become the forehead, nose, middle portion of the upper lip (philtrum or Cupid’s bow) and the primary palate (part of the upper jaw that holds the middle four teeth)
Left and Right Maxillary Prominences:
grow and become the lower face, lower lip and jaw, all but the middle portion of upper lip and jaw, and the secondary palate (behind the four upper middle teeth to back of mouth.
Syndromes associated with Cleft Lip / Palate
AED
DM
GP
ST
“Someone get the AED at the DM concert for Gary Perkins and his Suicidal Tendencies”
Common Syndromes:
Apert Edwards (Trisomy 18) DiGeorge Downs (Trisomy 21) Goldenhar Pierre Robin Stickler Treacher Collins
What is considered Low Birth Weight?
Infants weighing less than 2500 grams / 5.5 pounds
Prenatal
Perinatal/Neonatal
Infant
Toddler
Age classifications
Prenatal:
-Before birth, (mean duration of pregnancy / 280 days)
Perinatal/Neonatal:
-referring to mother and/or fetus from 20th week of gestation through four weeks post-partum / 28 days of extra-uterine life.
Infant:
-Child ages one month through 12 months
Toddler:
-Child from one year through 36 months
Decreased Birth Weight
Growth Restriction
Preterm delivery
Preeclampsia
Are all associated with what?
Poor Oral Health
Women are more susceptible to oral disease secondary to endocrinological fluctuations of pregnancy.
T/F
Folic Acid during pregnancy is protective for orofacial clefts
True
CODIENE during pregnancy possesses a small risk for what in the growing fetus?
💔
Small risk for heart defects 💔
Benefits of breast feeding 🤱
Maternal antibodies
Decreased risk ⬇️ :
Upper/lower respiratory tract infections
Otitis Media
GI infections
Layers in Tooth Development
- Oral Epithelium
- outer layer
- has both upper and lower arch form - Dental Lamina
- thickening of the oral epithelium
- individual teeth will eventually pinch off from
Both 1 and 2 are derived from ECTODERM
- Ectomesenchyme
- signals overlying oral epithelium to proliferate into Dental Lamina.
Derived from Neural Crest tissue
Bud Stage
Proliferation
Morphodifferentiation
8 weeks in utero
Dental Placodes / proliferating buds pinch off Dental Lamina and invades into the underlying mesenchyme.
ALL primary teeth and permanent molars derive DIRECTLY from this Dental Lamina
In Addition, the Mesenchyme itself begins to condense under the tooth bud.
What is the Enamel Knot?
What does it turn into?
What stage does it appear?
Focal areas of thickened Inner Epithelium (IEE) that turns into CUSP TIPS during the CAP Stage
Signaling centers to the remainder of tooth development.
Apposition
14 weeks in Utero
Odontoblasts deposit Dentin Matrix (Collagen)
Ameloblasts develop Enamal Matrix (Amelogenin)
Collagen secretion stimulates Ameloblasts to secrete Amelogenin
Cervical Loop:
- where IEE and OEE meet
- grows downwards forming extension (HERS)
- Hertwigs Epithelial Root Sheath
**HERS stimulates Odontoblasts to secrete Radicular Dentin
IEE + OEE = REE (Reduced Enamel Epithelium)
DEFECTS in APPOSITION
(Hypoplasia, Enamel Pearls, Concrescence)
Maturation / Mineralization
14+ weeks
Deposition of Enamel and Dentin
moves from matrices of structure to laying down of actual structure
Calcification begins at cusps tips / Incisor edges
2 YEARS for a PRIMARY tooth to complete a crown
4-5 YEARS for a PERMANENT tooth to complete a crown
explains why these defects are a lot more common, the length of this time period is much greater
DEFECTS of MINERALIZATION
(Enamel hypomineralization, Fluorosis, Tetracycline staining)
Tooth Germ Cells and what they produce?
ENAMEL ORGAN
Ameloblasts -> Enamel
DENTAL PAPILLA
Odontoblasts -> Dentin
Central Cells -> Pulp
DENTAL FOLLICLE
Cementoblasts -> Cementum
Osteoblasts -> Alveolar Bone
Fibroblasts -> PDL
Calcification dates for PRIMARY TEETH
PRIMARY TEETH
14-18th week in Utero
Central Incisor = 14th wk 1st Molar = 15th wk Lateral Incisor = 16th wk Canines = 17th wk 2nd Molars = 18th wk
ADBCE
roots completed by 3-4 years of age
Calcification dates for PERMANENT teeth
PERMANENT
First Molars - Birth / 0 months
All Incisors except Max Lat - 6 months
Maxillary Laterals - 12 months
First Premolars - 18 months
Second Premolars - 24 months
Second molars - 30 months
SUPERNUMERARY TEETH
MMM
Initiation phase / Bud phase
MALES 2:1 ratio.
3% of population (“3rd” tooth in mesiodens)
- highest in blacks/asians
- PRIMARY teeth; .3-.8%
- Permanent teeth 5x more common
Most common is MESIODENS
-95% of all supernumerary teeth in Maxilla.
(Males, Maxilla, Mesiodens - MMM)
May block normal eruption of permanent teeth.
Congenitally Missing Teeth
🎃🎃🎃🎃
Initiation / Proliferation / Bud phase
🎃
FEMALES 1.5:1 ratio “Jacqueline-lantern”
Permanent teeth 1-10%
Primary teeth < 1%
3/⬇️2/L/⬆️2
Third Molar > Mand 2PM > Max Lat > Max PM
Primary teeth; most common CM Tooth is Max Lateral
correlation between missing 3rd Molars / Max Laterals 3L
What MONTH is the PRIMARY CROWN ENAMEL FORMATION completed for all teeth?
Primary 1st Incisors: 1.5 Months
Primary 2nd Incisors: 2.5 Months
Primary Canines: 9 Months
Primary 1st Molars: 6 Months
Primary 2 Molars: 11 Months
What is Cortical Drift?
Most bones grow by interplay of bone deposition & resorption .
- A combination of bone deposition & resorption resulting in a growth movement towards the deposition surface is called “Cortical Drift”.
- If bone deposition & resorption on either side of a bone are equal - the thickness of the bone remains constant.
- If in case more bone is deposited on one side & less bone resorbed on the opposite side – The thickness of the bone increases.
How long does it take for permanent tooth to come into full occlusion?
5 years
Morphological Development Stages
DBCB
DENTAL LAMINA - BUD - CAP - BELL
