AAPD Handbook Chap 2 - Dental Development, Morphology, Eruption, and Related Pathologies Flashcards
syndromes with supernumerary teeth
Apert, cleidocranial dysplasia, gardner syndrome, crouzon syndrome(craniofacial dysostosis), sturge-weber, orofaciodigital syndrome I, hallermann-strieff, CLP, down syndrome
apert snydrome? aka
aka acrocephalosyndactyly. narrow, high palate, 30% cleft of soft palate, delayed or ectopic eruption, shovel shaped incisors, hypoplastic midface, supernumerary teeth
cleidocranial dysplasia
delayed development/eruption of perm teeth, supernumerary, delayed primary exfoliation, pseudoprognathism(mid-face hypoplasia), enamel hypoplasia
gardner syndrome
delayed eruption, supernumerary teeth, osteomas of the jaw
crouzon syndrome, aka
aka craniofacial dysostosis. dysostosis is a disorder affecting development of bone. hypoplastic midface, maxillary hypoplasia, inverted V shaped palate, supernumerary teeth
sturge-weber syndrome
port-wine capillary malformation, overgrowth of bony maxilla, supernumerary teeth
orofaciodigital syndrome I
multiple or hyperplastic frenula, cleft tongue, cleft alveolus(hypodontia ensues), supernumerary teeth common if no cleft alveolus, median pseudocleft of upper lip, cleft palate
hallermann-strieff snydrome A
mandibular hypoplasia, high palatal vault, premature teeth, delayed primary exfoliation, malar hypoplasia(malar is zygomatic bone so afx maxilla, eyes), supernumerary teeth
hypodontia not associated with a syndrome is thought to be passed on in an
autosomal dominant fashion
there is a relationship between the agenesis(failure of organ to develop) of what teeth?
agenesis of third molars is associated with agenesis of one or both perm maxillary laterals
what conditions can be characterized by hypodontia
ectodermal dysplasia, crouzon(craniofacial dysostosis), non syndromic CLP, achondroplasia, chondroectodermal dysplasia(ellis-van creveld), incontinentia pigmenti, orofaciodigital syndrome I, hallermann-strieff, rieger syndrome, seckel syndrome, williams syndrome
ectodermal dysplasia features
conical crowns, hypodontia to anodontia, deficient alveolar ridge
achondroplasia features
midface hypoplasia, frontal bossing(prominent forehead)
chondroectodermal dysplasia(ellis-van creveld) features
premature teeth -25%, absent maxillary sulcus, conical crowns, partial anodontia, enamel hypoplasia
incontinentia pigmenti features?
conical crowns, delayed eruption, premature teeth, CLP
reiger syndrome features?
midface hypoplasia, delayed eruption, hypodontia, usually upper incisors
seckel syndrome
microcephaly(small head), facial hypoplasia
williams syndrome
partial anodontia, prominent lips, microdontia, enamel hypoplasia
anomalies of size(micro/macro dontia) associated with what stage of development?
proliferation
what must be ruled out when macrodontia is observed?
single tooth macrodontia is rare, rule out gemination and fusion
microdontia frequency?
lateral incisors, 2nd premolars, 3rd molars
Conditions exhibiting microdontia
oligodontia, ectodermal dysplasia, chondroectodermal dysplasia(ellis-von creveld), hemifacial microsomia, down syndrome, crouzons syndrome
conditions exhibiting macrodontia
hemifacial microsomia, accelerated eruption on affected side submucous cleft, crouzon syndrome, otodental dysplasia aka globodontia(teeth and hearing abnormalities)
gemination
more common in primary dentition, 1 tooth tries to divide into 2, bifid crown, single root and pulp chamber, familial inheritance, clinical dx is made by seeing an extra crown.
twinning
complete cleavage of single bud results in supernumerary mirror image tooth
fusion
more common in primary dentition and higher frequency in japanese. is the dentinal union of two developing teeth. two separate pulp chambers, separate or fused canals, may appear as large bifid crown with one chamber. Clinical dx, bifid crown with normal complement of crowns
concresence? its etiology?
fusion that occurs after root formation(not a true developmental defect). Etiology: trauma, crowding may occur pre or post eruption
anomalies of size and shape occur during _____ and include?
morphodifferentiation. dens in dente, dens evaginatus, taurodontism
dens in dente(dens invaginatus)
maxillary lateral most affected in both dentitions, invagination of IEE. significant b/c communication b/w oral environment and invagination
dens evaginatus
afx mostly males and perm teeth, mostly maxillary incisors. characterized by evagination of enamel epithelium and focal hyperplasia of pulp mesenchyme. Pulp tissue within extra cusp may fx easy
taurodontism
failure of HERS invagination. Elongated crowns at the expense of the roots, significant b/c results in large pulps
syndromes with taurodontism
klinefelter, tricho-dento-osseous syndrome(TDO),mohr syndrome, ectodermal dysplasia, down syndrome, amelogenesis imperfecta, type IV(hypomaturation-hypoplastic type, with taurodontism), dilaceration
Klinefelter syndrome
small cranial dimension, bimaxillary prognathism, taurodontism in 30%
tricho-dento-osseous(TDO) syndrome
dolicocephalic(long narrow skull) with frontal bossing, taurodonts have PAROs and high pulp horns, delayed eruption
mohr snydrome(orofaciodigital syndrome II)
lobed tongue, upper lip midline cleft, oligodontia
dilaceration.
etiology: trauma to primary dentition, such as intrusion.
amelogenesis imperfecta general characteristics
heritable enamel defect, multiple inheritance patterns, 4 major types, differentiated from other enamel dfx as it has distinct patterns of inheritance and occurs apart from syndromic, metabolic, or systemic conditions
AI Type I
Hypoplastic, insufficient quantity of enamel, both dentitions afxed, autosomal dominant inheritance, anterior open bite seen in 45%
AI Type II
Hypomaturation
AI Type III
Hypocalcified
AI Type IV
Hypomaturation-hypoplastic with taurodontism
Dentinogenesis Imperfecta general chars?
heritable dfx of predentin matrix, normal mantle dentin, amorphic and atubular circumpulpal dentin, 3 subtypes
DI- Shields type I
occurs with OI, primary teeth affected more but perm centrals and 1st molars are often afxed, amber translucence, PARLs, autosomal dominant, rapid attrition
DI Shields Type II
occurs alone, no OI, both dentitions equally afxed, same chars as DI Type I, irregular or tubular pattern, rapid attrition, autosomal dominant
DI Shields Type III
rare, brandywine population. bell shaped crowns, shell teeth(short roots, large pulp chambers), multiple pulp exposures, regular tubules, enamel pitting, different expression for the same DI-DII gene.
Osteogenesis Imperfecta general chars
4 major types, Type I most common, Type II lethal in perinatal period(5 months before and 1 month after birth), DI more common in types III and IV.
bowing of legs, fragile bones(fxs),blue sclera, bitemporal bossing,defective collagen, hearing loss, macrocephaly, autosomal dominant
enamel hypoplasia is a potential marker for what dx?
celiac disease, predominant locations are both upper and lower primary and permanent central/lateral incisors
Dentin dysplasia type 1 aka and chars?
radicular dentin dysplasia, normal crown color, short roots or rootless in both dentitions, obliterated pulp chambers, PARLs, mobility and misalignment, autosomal dominant
dentin dysplasia type 2 aka and chars?
coronal dentin dysplasia, only primary teeth afxed, coronal and root dentin afxed, amber colored crowns, permanent teeth look normal but radiographically have thistle tube shaped pulps, pulp stones, autosomal dominant
regional odontodysplasia chars?
aka ghost teeth. tooth development arrests. See atubular tracts, irregular tubules, no odontoblastic layer, cementum can be normal or aberrant, thin enamel, both dentitions afxed, central incisor most involved, no established etiology or inheritance pattern
other conditions that exhibit dentin abnormalities?
vitamin d resistant rickets, hypoparathyroidism, pseudohypoparathyroidism, albright hereditary osteodystrophy, ehlers-danlos syndrome
Conditions that exhibit cementum anomalies?
hypophosphatasia, epidermolysis bullosa, cleidocranial dysplasia
Vitamin D resistant rickets chars?
x linked dominant or autosomal recessive, failure of distal tubule reabsorption of phosphate in kidneys, hypomineralized dentin, increased predentin width, enlarged pulp and pulp horns, enamel may be spared
hypoparathyroidism chars?
permanent teeth afxed, short roots with delayed apical closure, enamel hypoplasia,
pseudohypoparathyoridism
large pulp chambers, irregular dentinal tubules, small crowns and short roots, pitted enamel surfaces
albright hereditary osteodystrophy
inadequate H- ion clearance, hypocalcemia, hyperphosphatemia, ectopic calcifications, short stature, brachydactyly(short fingers and toes), blunted roots, small crowns, mental deficiency, x linked dominant, intrapulpal calcifications
ehlers-danlos syndrome
hyperelastic,fragile skin and mucosa, skin hemmorhages and scars, joint hypermobility, x linked, intrapulpal calcifications,
hypophosphatasia
lack of serum alkaline phosphatase, urinary phosphoethanolamine, autosomal recessive, little cementum produced, ealy exfoliation of primary dentition
epidermolysis bullosa
fibrous acellular cementum, excess cellular cementum
what type of cementum is deficient in cleidocranial dysplasia?
cellular cementum
AI Type 3, aka and chars?
aka hypocalcified. deficit in mineralization of matrix, normal thickness, soft enamel, anterior open bite in 60%, high calculus formation, delayed eruption, 2 subgroups(AD or AR)
enamel fluorosis
anomaly of mineralization of enamel. >2ppm = 10% chance of fluorosis, >6ppm = 90% chance.
AI Type 2 aka and chars?
hypomaturation. normal thickness, low radiodensity, poorly mineralized although less severe than hypocalcified type(type III),mottled brown-yellow-white color, x linked recessive, AR, and AD*
AI Type 2 subgroups
AR - pigmented
XL-R
AD - snow capped, fairly common
AI Type 4 aka and chars?
hypomaturation-hypoplastic with taurodontism, mottled yellow-brown enamel with pits, molars are taurodont,
blood borne pigments can cause intrinsic staining of teeth. name the pigments and what color they turn teeth
porphyria-porphyrin - purplish brown bile duct defects - green neonatal hepatitis, bilirubin - black, gray Rh incompatibility, blue-green, brown hemosiderin anemias - gray dental trauma - red,gray,black
Most favorable eruption sequence of primary dentition?
ABDCE
most favorable eruption sequence of permanent maxillary dentition
61245378, sequence more important than timing
most favorable eruption sequence of permanent mandibular dentition
61234578
what clinical guides are used to assess eruption stage/rate of permanent dentition
root development, overlying bone, infection, timing of primary tooth loss(before 5yo - delays premolar, after 8yo - accelerates premolar)
Premature teeth general chars? what findings associated with premature teeth?
erupt prior to 3 months of age, natal teeth(present at birth), neonatal teeth(present within 30 days of birth), natal:neonatal is 3:1, finding assoc with premature teeth is riga-fede dx(sublingual traumatic ulceration from teeth)
what structures in the newborn are often confused with premature teeth?
bohn nodules(buccal,lingual aspects of maxillary alveolar ridge, mucous gland tissue)
dental lamina cysts, found on crest of alveolar ridge, derived from remnants of dental lamina
epstein pearls, midpalatal raphe, trapped epithelial remnants, visible cysts in 80% of newborns
Teething and its associated problems? what are the problems
While teething(eruption of primary teeth), babies usually have otitis media, paroxysmal atrial tachycardia, GERD(diarrhea).
what is the differential dx when a teething baby presents with associated symptoms? Rule out what?
R/O febrile convulsions, URI, bronchitis, eczema, H. flu meningitis, fever, dehydration,
Cysts can occur during dental development and eruption, name 4 cysts that can occur?
eruption hematoma, primordial cyst, dentigerous cyst, ameloblastoma
eruption hematoma chars?
dilation of follicular space, blood or tissue fluid, form of eruption cyst
primordial cyst chars?
from stellate reticulum
dentigerous cyst?
from reduced enamel epithelium
ameloblastoma
dentigerous cyst and odontogenic cyst, epithelial rests of malassez, disturbed anemal organ
what local causes can delay primary exfoliation and permanent eruption?
trauma, impaction, ankylosis, supernumeraries
what local and systemic causes can accelerate eruption of primary and permanent teeth?
local causes are early loss of primary tooth(closer to time of perm tooth eruption only). systemic causes are hemifacial hypertrophy, precocious puberty, hyperthyroidism, sturge-weber syndrome, chondroectodermal dysplasia, OI, pachyonychia congenita, sotos syndrome(cerebral gigantism)
which dx of bone causes premature primary exfoliation
fibrous dysplasia
which dx of periodontium causes premature primary exfoliation
LAP,GAP, papillon-leferve
which dx of metabolism causes premature primary exfoliation
hypophosphatasia
which deviations in growth and development causes premature primary exfoliation
hemihypertrophy, premature teeth
which dx of blood causes premature primary exfoliation
chediak-higashi, cyclic neutropenia
which physical and chemical injuries causes premature primary exfoliation
acrodynia, facial burns
which benign and malignant tumors causes premature primary exfoliation
histiocytosis/langerhans cell group, letterer-siwe(fatal), hand-schuller-christian(better px), eosinophilic granuloma(excellent px)
which dental anomalies causes premature primary exfoliation
dentin dysplasia, odontodysplasia
etiologies for ectopic eruption of maxillary first permanent molars? how many self correct?
larger mean size of all max prim and perm teeth, larger affected Es and 6s, smaller maxilla, posterior position of maxilla in relation to cranial base(smaller SNA), abnormal angulation of erupting 6, delayed mineralization of some affected 6s
most(66% self correct), much lower in CLP
order primary teeth most often ankylosed to least often
primary mandibular 1st molar, mandibular 2nd, maxillary 1st, maxillary 2nd molar
ankylosed primary teeth often associated with
agenesis of succedaneous tooth
sequelae of ankylosis
deflected eruption path, impacted premolars, loss of arch length and alveolar bone, supraeruption of opposing teeth(esp maxilla)
Tx of ankylosed teeth?
primarily empirical(derived from experience). Observe primary mand molars, ext, restore to occlusion, luxate(for permanent teeth)
prevalence of max central diastema more common in ?
6yo(44-97%) than 9yo than 14yo.
etiologies of max central diastema
normal development of mixed dentition, excessive skeletal growth(acromegaly), pernicious habit(lip biting, digit sucking, pacifier use, infantile swallow with tongue thrust), spaced dentition, missing/peg laterals, exts, excessive OJ, excessive OB, ectopic laterals/crowded to lingual
tx of maxillary central diastema
after eruption of perm canines, based on dx of cause(bolton analysis helpful)
eliminate habit if present, mesial tipping of central incisors, bodily movement of central incisors, reduction of excessive OJ, enlargement of incisors
