Growth and DevelopmentLecture 18-24-10

Somatic growth: pattern, variability, timing, and methods of study

Growth Growth: Increase in size or number Anatomic phenomenon Hyperplasia: Increase in number of cells Hypertrophy: Increase in size of individual cells Ex: Secretion of extracellular material: increase in size independent of the number size of cells Odontoblast secretion & Ameloblast secretionDevelopment Development: Increase in organization, complexity, specialization (loss of potential) Physiologic and behavioral phenomenon Immaturemature Pattern: a changing and complex set of spatial proportionalities over time Ex: the proportion of head and limbs to body Head and face = decrease Newborn = 25% Adult = 12% Limbs = increase Reflect Proportionality Cephalocaudal gradient of growth An axis of increased growth extending from the head toward the feet The further from the head (ie the lower limb) will have more growth Size of components of craniofacial complex Post natally more facial growth than cranial growth Overall body proportions change during the normal growth and development Not all the tissue systems grow at the same rate Scammons curve Neural: cranium, brain Nearly complete by 6 or 7 Lymphoid: tonsil, adenoid Grow far beyond the adult size and then regress Around age 10 = larger than at any other time Sometimes the lymphoid tissue is so large that is interferes with the air passage General: bone, muscle, viscera S shaped curve Childhood growth rate = slow Acceleration of growth rate at puberty Genital Grow rapidly at puberty Craniofacial Depends on the distance from the brain Maxillacloser to neural Mandiblecloser to general Man and max between the neural and general tissue Growth Plots Distance curve (cumulative curve) Accumulation of data over time (longitudinal) Velocity curve (incremental curve) Amount of growth within an interval of time Velocity curve allows seeing acceleration or deceleration of growth over time. Peak velocity = 14 yrs Growth Studies Longitudinal studies: measures individuals over many years Time consuming Highlight individual variations Smaller sample size Cross-sectional studies: a large group of individuals representing all ages are measured at one time Easier and quicker Variations conceal details Larger sample size Growth variability Variability within species Timing Size Each individual tends to follow their own pattern, patterns are similar Assumption Human traits such as height and weight adhere to normal curves These curves occur at all ages There is normal variability within individuals Children outside of 97% of pop should be referred for medical evaluation Change of growth pattern (height or weight) is reason for concern Growth Spurt All children undergo growth spurts, but timing and amount can vary Depends on Sex: girls, boys Genetics: early, average, late Sexual maturation accompanies growth spurt Events that occur during growth spurt/maturation Girls Increase in weight Development of 2nd sex characteristics Breast buds Genital hair Increase in height Menses Bony change Hand-wrist Cervical Boys Increase in weight Muscle mass Development of 2nd sex characteristics Genital hair Size of genitals Facial hair: lip and chin Increase in height Bony change Hand-wrist Cervical Adolescent growth stages vs. 2nd sexual characteristics Girls: adolescent growth 3 yrs Stage 1 (beginning of adolescent growth) Appearance of breast buds Initial pubic hair Stage 2 (peak velocity in height, about 12 months later) Noticeable breast development Axillary hair Darker/more abundant pubic hair Stage 3 (growth spurt ending, 12-18 months later Menses Broadening of hips with adult fat distribution Breasts completed Boys: adolescent growth 5 yrs. Stage 1 (beginning of adolescent growth) fat spurt weight gain Feminine fat distribution Stage 2 (height spurt beginning, about 12 months later) Redistribution/reduction of fat Pubic hair Growth of penis Stage 3 (peak velocity in height, 8-12 months later) Facial hair appears on upper lip only Axillary hair Muscular growth with harder/more angular body form Stage 4 (growth spurt ending, 15-24 months later) Facial hair on chain and lip Adult distribution/color of pubic and axillary hair Adult body form Growth Spurt variability Girls mature about 2 yrs earlier than boys Orthodontic implications: growth modification Relation of Growth Spurt and Maturation If ages are removed and peak growth superimposedpeaks are similar Menses occur on downward slope Implication: only 2 years of rapidly decreasing growth remains Stages of adolescent Growth Summary Girls mature earlier than boys by about 2 yrs Total time of duration Girls3 years Boys5 yrs Boys are larger because they grow longer Orthodontic implications Growth modification for girls starts earlier Boys can outgrow orthodontic treatment more than girls Problems with determining growth spurt/maturation Difficult to check secondary sex characteristics Menses means limited growth potential Growth spurt/maturation does not correlate well with age Chronologic age vs. development (biologic) age Chronologic age is not an accurate indicator because 2 girls at the same age may be at different stages of development/growth spurt Skeletal, dental, 2nd sex characteristics Skeletal age Hand wrist radiograph Bottom: See epiphyses Top: Epiphyses ossified (older) Cervical vertebrae radiograph Look at inferior border of vertebrae As grow olderget concavity in inferior border of vertebrae When youngerslope from posterioranterior.as get older, this superior surface of vert. becomes more straight Methods of Studying Physical Growth Measurement approaches Measure living samples or skeletal remains Non-destructive Craniometry Measurements of skulls found among human remains Precise measurements Cross-sectional data, only can be measured one time Anthropometry Measurements on living individuals Longitudinal data, can be measured repeatedly Soft tissue interference Cephalometric radiology Introduced in 1934 by Hafrath in Germany and Broadbent in US Study growth pattern Evaluate malocclusion Evaluate outcome of treatment (superimposition) 2-D image represents 3-D structure Three-dimensional imaging: Computed tomography (CT) Conventional CT and cone beam CT (CBCT) Rapid scan (less than 1 minute) Less radiation exposure (3-20% of conventional CT) No distortion of image Magnetic resonance imaging (MRI) Using electromagnetic spectrum (not Xray) No radiation exposure High contrast sensitivity Experimental approaches Destructive manipulation of samples Restrict to non-human species Ex: Vital staining Alizarin red: timing of dental mineralization Tetracycline: cause dental staining Radioactive tracers Implant

Growth and DevelopmentLecture 28-26-08Craniofacial Growth

Review of Last Week Growth = increase in size or number, anatomic phenomenon Hyperplasia = increase in number of cells Hypertrophy = increase in size of individual cells Secretion of extracellular material: increase in size independent of the number or size of cells Intersistial growth = growth occurs within the tissue Characteristics of soft tissues and uncalcified cartilage Appositional growth = growth occurs on the surface of the tissue Characteristics of mineralized tissue Development = increase in organization, complexity, specialization (loss of potential), physiologic and behavioral phenomenon

Types of bone formation Endochondral bone formationinitial formation of cartilage Extremities of all long bonesepiphyseal (growth) plate Vertebrae Ribs Condyle Cranial base Intramembranous bone formationno intermediate formation of cartilageNO CARTILAGE!! Alveolar bone Calvaria Long boneCranial Structure and Characteristics Craniofacial cartilage Cranial base bones that formformed with cartilage 1st Ethmoid Sphenoid Occipital Nasal cartilage Condyle Small area at junction of right and left mandible These are Endochondral bones Nearly avascular Diffusion of oxygen and nutrients Multiple centers of ossification Only small areas of cartiage growth remain between bones after birth Eventual fusion of those bonesSynchondrosis Looks like a 2 sided epiphyseal growth plate Bidirectional growth (cranial bone) vs. unidirectional growth (long bone) Types of Synchondrosis Spheno-ethmoidal synchondrosis Between the sphenoid and the ethmoid bones Active growth prenatally Allow anterioposterior growth of cranium Fuses around 6-7 yrs of age in human Inter-sphenoid synchondrosis Between the pre-sphenoid and basissphenoid Fuses around the time of birth in human Does not contribute to postnatal growth Spheno-occipital synchondrosis Between the body of the sphenoid and occipital bones Active postnatal growth Fuses around 13-15 yrs of age Allows more vertical growth of cranium Clinical significance of synchondrosis Growth of cranial synchondrosis has direct effect on the growth of nasomaxillary complex and mandible Displaces facial bones (max and mand) inferiorly and increases facial height Disease (Achondroplasia) affects the growth of cranial base and midface. Affects fibroblast growth factor and production Growth of face is severely retarded Growth of mandible is pretty normal. Development of Meckels Cartilage Bilateral about 7-8 wk in utero From 1st pharyngeal arch Bone forming next to it becomes mandible and cartilage is removed. Distal extension forms incus and malleus. Condylar cartilage develops in separate area of mandible. Growth Center vs. Growth Site Growth Center Synchondrosis Epiphyeal plate a location at which independent, genetically controlled growth can occur Innate growth potential and cannot be influenced by environmental circumstances Growth Site Condyle All growth centers can be sites, but not all sites can be centersIntramembranous Bone Suture growth When bone grows inside there is bone formation on the 2 sides of the suture. Surface remodeling Sutures connect bones to form cranium Maxilla is connect to cranial base with suture Ossification occurs without cartilage formation Brain (neural growth causes tension and deposition of bone When neural growth slows or stops, suture fuse Periosteal growth can occur at surfaces Outer or inner surface Cranial Intramembranous Bones Newborn skull shows sutural areas with minimal bone (fontanellessoft spots) Connected by dense CT = fontanelles Close by 8 wks after birth Anterior closes after 18 months Most of the growth is at the suture Premature closure of cranial sutures leads to craniosynostosis (Crouzon, Apert syndromes) Craniofacial sutures FM = Frontmaxillary suture ZM = Zygomaticaomaxillary suture ZT = Zygomaticotemporal suture ZF = Zygomaticofrontal suture FN = Frontonasal suture Median palatine suture Increase the facial height/depth/width Transverse palatine suture Sutures become more interdigitated with increasing age. Bone Growth/Movement Shaping of surfaces with different fields of apposition and resporption. Not every bone always has one surface doing just one thing. Some parts will undergo apposition and some will undergo resorption. Drift: growth movement of bone by the combination of resportion and deposition (apposition) Displacement: movement of the whole bone as a unit Picture: The point has grown outward as a result of increase in the size of the object itself Secondary Displacment: The point has grown outward as a result of increase in the size of another object. Pictures #2! Primary + Secondary Displacement The point has grown outward as a result of both primary and secondary displacement. Maxillary Growth Intramembranous bone formation forms the maxilla Growth occurs by Apposition at the suture that connect the maxilla to the cranium and cranial base Displacement from the growth of cranial base (Secondary) Surface remodeling Disease affecting growth of suture will lead to underdevelopment of the maxilla. Surface remodeling Resorption of anterior surfacebone becomes less prominent in adult Deposition of alveolus with eruption of teeth Deposition of the maxillary tuberosity Primary and secondary displacement Surface remodeling moves maxilla backward Whole maxilla is moving forward. Palatal Vault Growth Resorption from the floor of nose and anterior surface Deposition to the roof of the mouth Drift: downward and backward Palate moves downward Displacement: downward and forward ***Size of the oral cavity does not decrease. With eruption of teeth the sides of the oral cavity increase dramatically. Maxillary + Palatal Vault Growth Bone remodeling (drift) results in Upward and backward Tension at suture causes bone to be added at sutures Resorption of anterior surface Deposition at the maxillary tuberosity Downward Eruption of teeth bring alveolus down Vertical drift of palate Nasal Septum Cartilagenous remnant of the chondrocranium that ossifies posteriorly as the vomer bone. The anterior part remains as cartilage and continues growing later than most of the rest of the face. Mandibular Growth Endochondral Growth Conversion of condylar cartilage to bone Only occurs at the condyle! Intramembranous Growth Remodeling at multiple adjacent site: Deposition/resorption Main direction of growthUpward or backward Anterior portion stays the same width Major area of mandibular growth is in posterior areasroom for posterior teeth to erupt Growth of mandible will not releive anterior crowding Measured by: Position of chin or basal bone in space Absolute increase in size Drift is the result of periosteal remodeling Deposition and resorption also occur in anterior mandible Result = definition of chin Allows: growth of ramus and room for posterior teeth to erupt Mechanism of growth: Condyle cartilage is not the major mechanism for growth of mandible Absolute growth result of: Apposition of posterior ramus Resorption on anterior ramus Condylar growth Coronoid process Dental arch perimeter growth Resorption at anterior portion of ramus Allows molars to erupt Displacement Primary Growth of mandible in posterior direction displaces mandible forward and downward Secondary Grwoth of cranium pushing mandible forward and downward Growth of maxilla pushing mandible downward Soft Tissues Lips Mixed dentition yearsshort lip height, lip incompetence and gummy smile Adolescenceelongation of lips, lip thickness reaches max then decreases Nose Growth of nasal bone is complete @ 10 yrs Nasal cartilage and soft tissue undergo adolescent spurt, which results in more prominent nose at adolescence (esp boys) Nose and chin become prominent at adolescence and post adolescence Relative decreased prominence of lips V principle An important facial skeleton grwoth mechanismsince many facity and cranial bone have a V configuration or V shaped region Outer surfaceResorption Inner surfaceDeposition V moves away from its narrow end and enlarges in overall size. Applies to the mandible and PalateSummary of Craniofacial Growth Actual growth of maxillabackward, upward When teeth are eruptingalveolar bone grows downward Actual growth of mandibleupward, backward When teeth are eruptingalveolar bone grows upward Growth of face Result of primary and secondary displacement Comparison can be made by superimposition on various cranial base structures Those structures are also remodeling (not constant)

Growth and DevelopmentLecture 39-02-08Theories of Craniofacial DevelopmentThree Theories of Craniofacial Skeletal Growth Genetic Factors Exert their influence within the cells in which they are contained Determine the characteristics of cells and tissues Chondrogenesis is affected by genetic factors Epigenetic Factors Determined genetically Are effective outside of the cells and tissues in which they are produced Only occur indirectly Ex: Sex hormones, growth hormones which are produced a long distance away Environmental Factors Regulate or modify the morphogenesis controlled by the genome Ex: muscular forces, food, oxygen Three major theories as to the location of genetic control: Bonethe primary determinant of growth Cartilagethe primary determinant of skeletal growth, while bone responds secondarily Soft tissue matrixthe primary determinant of growth Soft tissue surrounds skeletal tissue Growth Center vs. Growth Site Growth Center A location at which independent, genetically controlled growth can occur Innate growth potential Cannot be influence by environmental circumstances Growth Site Location at which growth occurs All growth centers can be sites, but not all sites can be growth centers Bone as a growth determinant Growth Centersuture, periosteum Basis of theoryobservation that overall craniofacial growth pattern is constant Examplemaxillary growth result of sutural growth Problems with theory: Lack innate growth potentialfail to grow if transplanted to another location Influenced easily by environmental circumstancesgrowth at sutures respond to mechanic forces Viability of theory Dominant theory until 1960s Currently rejected Cartilage as a growth determinant Growth Centercartilage Basis of theorycondylar cartilage and nasal cartilage are growth centers for mandible and maxilla Example: Nasal cartilage growth causes vertical maxillary growth Surgical procedures removing the nasal cartilage results in midface deficiency Problem with theory: A surgical procedure itself or the interference with blood supply can have caused the midface deficiency (not necessarily the absence of the cartilage). Not all skeletal cartilages have innate growth potential Epiphyseal plate>cranial synchondrosis>nasal cartilage>condylar cartilage Condyles regenerate after fracture in 75% of children Viability of theory Some cartilages can act as growth centers (ie epiphyseal cartilage, cranial synchondrosis, nasal septum) Condyle is not a growth center. Important for growth modification in ortho treatment. Soft tissue as a growth determinant Growth centersoft tissue Bases of theory: Proposed by Moss in the 1960s functional matrix theory Growth of face occurs in response to functional needs and neurotrophic influence. Example: Size of cranium based on growth of the brain Increase pressure of brain on cranium = bigger cranium Can cause cranium to be 2-3xs normal size Growth of mandible and maxilla is in response to nasal and oral cavities Growth of eye socket is in response to eye development Picture: Bones, cartilage, ligaments protect the functional matrix. Orofacial matrix = oral, nasal cavities and pharyngeal spaces. This one is the most important one for growth of the face. Growth of skeletal units is secondary to the growth of functiona matrix (soft tissue or functioning space). Problem Not clear how theory works Viability of theory Suggests that loss of function has considerable effect on growth of structures Modified by Moss in 1997 to incorporate more genetic background. Current consensus These are only theories Bone theory is no longer valid Probably a combo of cartilage and functional matrix theories Understanding of the influence of genetics on craniofacial structures is increasing, but have much more to learnSummary of craniofacial growthMechanisms of growth for cranium, cranial base, maxilla and mandible Growth of cranium occurs in response of growth of brain Growth of cranial base is the result of endochondral bone formation at synchondroses, which have independent growth potential, at the same time influenced by the growth of brain. Growth of maxilla and its associated structures occurs from a combo of growth at sutures and surface remodeling. The surrounding soft tissues and nasal septum cartilage may contribute to the forward repositioning of maxilla. Growth of mandible occurs by endochondral bone formation at condyle and surface remodeling. The growth of muscles and other adjacent soft tissues may contribute to the repositioning of the mandible. Distraction Osteogenesis A biologic process of new bone formation between the surfaces of bone segments that are gradually separated by incremental traction (0.51.5 mm/day). Can be divided by external or internal device. External deviceattached to bone Internal deviceattached to teeth or bone Can be bi/uni-directional. Advantages of the devices Larger distances of movement are possible than with conventional orthognathic surgery Deficient jaws can be increased in size at an earlier age. Adaptation of soft tissues, histogenesis Alveolar Distraction Augmentation of the maxillary and mandibular alveolar ridges Alveolar deformities and defects may result from: Developmental anomaliescleft palate, congenital tooth absence Maxillofacial trauma Periodontal disease leading to bone and tooth loss Ex: Bone graft. CT graft These grafts cannot provide an increase in bone volume. Alveolar distraction can provide construction of bone. This is a graft that is used to fix the bone. Can increase bone remodeling. Periodontal Ligament Distraction (AKA Rapid Canine Retraction) Used to reduce resistance when move the canine distally. Periodontal ligament is stretched. New bone is created mesially to the canine. After extraction there is surgical prep of socket. Socket is extended to same depth as canine. Widen socket and increase septum. Last step is to undermine the septum. More detail: Remove premolarattach distraction device to move the canine distally to relieve anterior crowding. Takes 3 weeks compared to 6 months with traditional methods.

Prenatal Craniofacial Development

Stages of Development

Cleavage Stages Fertilization of the egg by the sperm Distal 1/3 of fallopian/uterine tube Development of nonpermeable membrane around egg Division of cells into multicelled morula Movement through the uterine tube to reach uterine cavity4th day Implantation6th day Attachment of blastocyst to uterine wall Separation into inner embryonic cell mass (embyroblast) and outer covering (trophoblast) Trophoblast layer produces enzymes to break down uterine wall. Cells attach to the posterior wall. Release enzymes to allow deeper attachment. Blastocyst Stage Layers of ectoderm and endoderm form Ectodermal = columnar Endodermal = cuboidal Yolk sac forms and provides food source until blood vessels form. Yolk sac between endodermal and trophoblastic cells. Mesoderm migration Mesoderm migrates anteriorly and laterally between ectoderm and endoderm except at: Future area of the mouth (prochordal plate) Anus (cloacal membrane) Derivatives of Germ Layers Ectoderm Nervous system Sensory epithelium of eye, ear, nose Epidermis, hair, nails Mammary and cutaneous glands Epithelium of sinuses, oral and nasal cavities, intraoral glands Tooth enamel Mesoderm Muscles CT derivatives: bone cartilage blood dentin pulp cementum periodontal ligament Endoderm GI tract epithelium and associated glands Neural tube formation Ectodermal cells multiply and folding occurs Neural tube forms about 4 wks anteriorly and continues posteriorly Neural plates curve to form a tube. Neural Crest cells Separate Crest cells break off from neural fold area Neural crest cells migrate ventraly along the lateral wall of the neural tube. Become: Sensory ganglia Sympathetic neurons Pigment cells Cartilage of pharyngeal arches Contribute to embryonic connective tissue of the face (pulp, dentin, cementum) Neural Crest cell migration Migrate ventraly and laterally. The main point: Neural crest cells from different sources have to migrate into specific places to form the head and neck area. If adequate neural crest cells do not migrate or live, certain tissues do not develop.Teratogen Suspecptibility Congenital deformities can be hereditary. Not much can be done to reduce hereditary hazards in humans. Before 2 weeks, developing human is not susceptible to teratogens. After 2 weeks, it is most critical time periodthis stage is period of differentiation of tissues/organs. Teratogens may be highly defectivedeformities. After 8th week, the susceptibility will decrease and will only cause minor effects.

Growth and Development Lecture 4

Postnatal Craniofacial DevelopmentImportant Points Dental Development Including all primary teeth and 1st permanent molar. Begins in the 3rd month uterus. Calcification occurs around the crown A line can form in the crown if any disturbance or insult occurs. Birth--a dramatic processLeads to growth cease and weight decrease during the first 710 days after birth Almost every child has a neonatal line in the primary teeth These insult lines are more obvious in permanent teeth Picture: Cross section of enamel. See striae of retzius. Reflects apposition of growth in enamel layer. Neonatal line shows dramatic physiological change during the birth. Location of the neonatal line After birth, any disturbance in formation of teeth can be tracked by the neonatal line.

Factors affecting Postnatal Development Premature birth (low birth weight) Chronic illness Nutritional status Picture: Growth of limbs of body length and weight. See extremely rapid growth in early infancy. Growth slows down after the 1st 6 months.

Premature Birth (low birth weight) Low birth weight (LBW): fetus < 2500 g Extreme LBW: fetus < 1000g Incidence in developed country = 8%. Can be expected to be smaller the first 2 years. If survives the neonatal periodgrowth of the LBW will follow the normal pattern and gradually overcome the initial handicap.

Chronic Illness Disease or illness has negative impact on growth The severer the disease, the longer the time, the greater the cumulative impact. Chart Boy with Growth hormone deficiency. Red dot is actually growth height. Circles is height vs. skeletal development. Around 6 yrs there is a delay in growth height compared to skeleton. After treatment was started there was a dramatic increase in growth.

Nutritional Status Chronically inadequate nutrition has similar negative impact on growth. Adequate nutrition is a necessary condition for normal growth but is not a stimulus. Adequate nutritionoverweightproblem in developing countries. During the last centurymore rapid growth and earlier maturation. Better nutrition Chemicals (ie pesticidescan affect hormones and growth) Children are larger and mature more quickly these days.

Mandible Defiency at birth Relatively lack of prenatal growth of mandible makes the birth process easier. Mandible grows more than other facial structures postnatally. Eyes too far apart/small chin Prenatal growth of the mandible begins later and continues longer than the midfacial structure and orbital structure.

The mouth of the neonate At birth, the alveolar process is covered by gum pads. Although the upper and lower gum pads touch There is no precise jaw relationship. Tongue of the infant always contacts with the lower lip.

Mouth of Neonate (infantile swallow, adult swallow) Infantile swallow The jaws are apart during swallowing. The tongue is pushed forward and placed between the gum pads. The tip of the tongue protrudes. The mandible is stabilized by the contraction of the tongue and the orofacial musculature and when the tongue contacts with the lips. Position of tongue is lower in swallows than the adult/mature swallow. Adult swallow Teeth occlude momentarily during swallowing act The tip of the tongue is enclosed in the oral cavity. Mandible is stabilized by contraction of the mandibular elevator muscles (not facial muscles). Teeth occlude and the tongue is enclosed in the oral cavity. Vs. infantile where tongue protrudes onto lips. After 6 months = infants swallow is more precise in opening and closing. Transition of swallow Infantile swallow disappears during the 1st year of life. With eruption of the primary teethtransition from infantile swallow to adult swallow occurs. If sucking habits persist, there will not be a total transition to the adult swallow. 60% achieve adult swallow by age 8. Remaining 40% are still in transition.

Postnatal Facial Development Striking difference between the newborn and adult skull. Baby face is not miniature of adult face. Baby: larger eyes, tiny nose, puffy cheeks, high forehead, small mouth, wider and shorter proportions. Proportionally, more facial growth than calvarial growth after birth. Note on slide: more facial growth than temporal growth after birth. Newborn face has attained: 64% of adult width 54% of adult depth 41% of adult height. Maturation of an infants faceadult form occurs with the changes in: Size Shape Position Composition of all cranial tissues (bones, muscles, nerves, and sense organs) **Differential development process with progressing facial development. Size The oral cavity and nasal spaces, eyes, and brain increase in size, but at different rates. The adult face differs markedly from the infant face in size, proportions, structure and functions. Aging Further alters appearance as minor skeletal modification continue Skin loses elasticity Wrinkle Fat deposits under mandible and bags around the eyes. Mandible growth In postnatal period, mandible grows proportionally more than the early developing cranial base and brain. Changes in shape Infancy: Wide gonial angle No chin Small ramus Immature condyle Relatively retruded position Childhood: Teeth erupt Gonial angle (mandibular angle) decreases Chin develops Adulthood: Prominent chin Fully developed alveolus and condyle Decreased gonial angle Old age: Lose teeth and bone mass Increased gonial angle Peak growth for maxilla and mandible occur simultaneously growth slows and stops at different times. Mandible continues to increase in length when the maxilla finishes growing. Grwoth of maxilla is much less than mandible and body height. Grow in this order: maxillaheightmandible The anterior part of the nasal septum remains as cartilage and continues growing later than most of the rest of the face. The forward growth of the forehead is due to the development of brow ridges and frontal sinus (not aerated at birth). Gender differences for skeletal age may be greater than for dental age. Girls attain skeletal maturity earlier than boys Some girls may have more mature facial bones but still have primary teeth. Maxilla Result of Growth of cranial base Apposition of bone Eruption of teeth Major growth sites Sutures Alveolus (with eruption of teeth) Major growth direction Sutures: upward and backward At alveolus: downward with eruption of teeth. Resulting growth directiondownward and forward. Mandible Result of Conversion of cartilage to bone Apposition Growth of maxilla Major growth sites Ramus Alveolus Condyle Major growth direction Condyle and ramus: upward and backward At alveolus: upward with eruption of teeth Resulting growth direction Downward and forward Completion of facial growth Transverse About 4 yrs First to be completed Anterioposterior About 7 yrs in cranial base Mandible and maxilla continue into late adolescence Growth of sigmoidal and ethmoidal at cranial base Vertical Late adolescence and early adulthood Last to be completed Postnatal facial development Remove inhibitions of normal growth Promote normal function Reduce iatrogenic damage to tissues (surgical scars) Consider the effect of growth on the final result when intervention during the growth period is necessary

Variations in Facial Features Different facial type, relate to shape and form of head Changed the shape of nose to balance the shape of the midface Dolichocephalic: long, narrow head form Meoscephalic: medium, head form Brachycephalic: wide, short head form

Dolichocephalic Face: Narrow, long, and protrusive Nose: Long and protrusive with convex contour (aquiline) Slope of the nose tends to follow the same slope of the forehead. Brachycephalic Face: Wide, short Nose: Shorter with rounded tip Straight or concave contour Male and female facial differences Male Proportionaly larger nose Protrusive, longer, wider, straight or convex (aquiline) profiled Profile dropping straight downward from a protruding forehead Female Thinner and less protrusive nose Straight or concave profile More rounded noseoften tips upwarddropping downward from bulbous forhead Because of the less protrusive forehead and nose The upper jaw and cheekbone looks more prominent

Growth and DevelopmentLecture 5 (continued)9-09-08Prenatal Craniofacial Development (continued)Teratogen Susceptibility Congenital deformities can be hereditary and/or environmental. Beyond prenatal exam and parental counseling, not much can be done to reduce hereditary hazards in humans. On the other hand, to understand the noxious environmental agents, teratogen, and the time of their maximum effects on fetal development is important to prevent those deformities. From the picture, we can see before 2 weeks, developing human is not susceptible to teratogens, because at this early proliferative stage, any damage may be compensated by the remaining cells that have not become committed or differentiated. From the 3rd week to the 8th week, it is the most critical time period, because this stage is the period of differentiation of tissues and organs. Teratogens may be highly effective and result in numerous deformities. After 8th week, susceptibility to teratogens rapidly decreases and may cause only minor defects. From the picture, we can see around 7-8th week, palate and teeth are more susceptible to teratogens. Teratogens Infectious agents Radiation Deformities like cleft palate Drugs Ex: Tetracycline during 2nd/3rd trimester = hydroplasia of enamel and discoloration of dentin Should be avoided unless necessary Hormones Nutritional Disorders Ex: Folic Acid deficiency = neural tube defects Teratogenic habits: Smoking, Alcohol Ex: smoking = higher cleft palate incidence Ex: alcohol = MR = growth defiencyStages of Embryonic Craniofacial Development (5)StageTime (post-fertilization)Related syndromes

Germ layer formation and initial organization of structuresDay 17Fetal alcohol syndrome

Neural tube formationDay 18-23Anencephaly

Origin, migration, and interaction of cell populationsDay 19-28Hemifacial microsomia Treacher Collins syndromeLimb abnormalities

Formation of organ systemsPrimary palateSecondary palateDay 28-38Day 42-55Cleft lip and/or palate, other facial cleftsCleft palate

Final differentiation of tissuesDay 50-birthAchondroplasia Synostosis syndromes (Crouzons, Aperts)

Craniofacial Syndromes Fetal Alcohol Syndrome Characteristics: smooth philtrum, short nose, thin upper lip Growth deficiency, brain damage Treacher-Collins Syndrome (mandibular dysostosis) Failure of neural crest cells to migrate Possible caused secondarily by excessive cell death in the trigeminal ganglion Characteristics: Underdevelopment of jaw and zygomatic arch, downward slanting eyes, notch on eyelids, hearing loss Hemifacial microsomia Usually unilateral/assymetrical Characterisized by tissue on one side of the face is affetcted Characteristics: deformed/missing ear, ramus of mandible affected Currently thought to be caused by early loss of neural cells The farther the cells have to migrate, the more damage Midline structures (palate) no affected as much. Those cells migrating to middle of the face are ok. Back to development! Initiation of oral cavity Start in the 3rd week as a pit or invagination underlying the forebrain. Lower part of face/neck are formed by pharyngeal arches on both side s of the neck Derivatives of Pharyngeal/branchial arches Formation of the arches occurs at 5-6 weeks Only 1st and 2nd extend to the midline. Each arch is separated to adj arch by shallow grooves called pharyngeal pouches internally. Outer surface of pharyngeal arches are covered by the ectoderm and inside is lined by endoderm 1st arch is lined by the ectoderm of the oral mucosa. In each arch there is differentiation of neural crest cells Arch 1 (mandibular arch) Muscles of mastication Anterior belly of digastrics Meckels cartilage Cranial nerve V: Trigeminal Arch 2 (hyoid arch Muscles of facial expression Posterior belly of digastrics Cranial nerve VII: facial Arch 3 Cranial nerve IX: glossopharyngeal Arch 4 Cranial nerve X: vagus Face at 4 weeks Oral pit is surrounded by frontal process, two maxillary processes, and mandibular arch. Frontal processupper face First pharyngeal archmaxillary process arises from mandibular arch (later form cheek, most of upper lip) Mandibular arch grows toward midline and fusesmandible, lower part of face, and body of tongue) Face at 5 weeks Formation of nasal pits (as they deepen they form the nostrils) Face at 6 weeks As tissue around nasal pit enlarges2 medial nasal processes form intermaxillary portion of upper lip (philtrum) Maxillary and medial nasal processes fuse (externally) to form upper lip Connective tissue moves between areas of fusion and bind fused area Floor of nostril fuses front to back Failure to fusecleft lip Upper lip has 3 parts 2 max process grow inward Medial nasal process grows downward Face at 7 weeks Medial nasal processes merge at deeper levels also and form the intermaxillary segmentprimary plate Yellow colormaxillary process Blue colormandibular process Development of Palate Primary Palatepremaxilla Medial palatine process from medial nasal process Secondary Palate Develop from medial edges of the maxillary processes Fusion of medial palatine process with lateral palatine processes (lateral processes grow medially) Contain hard palate and posterior soft palate Cross-section of palatal fusion 6 week 7 weektongue is narrow, fills oralnasal cavity 8 weeklateral palatine processes slide and roll over body of tongue. Tongue lowers down and helps fusion of midline tissue 9 weekfusion of lateral palatine process and with nasal septum. Later, around 12th week, bone appears in the palate. Palatal Fusion Anterior portion of palate develops from fusion of maxillary processes and medial nasal processes Fusion occurs from frontback

Common Facial Congenital Deformities Cleft lip and palate Most common craniofacial defect CL/P occur in about 1 in 500-700 births Male > female Unilateral >bilateral Left > right CP occurs in 1 in 2000 births Female > male Cleft lip-unilateral Failure of medial and nasal process and maxillary process to fuse unilaterallyleads to nasal distortiontissues pulled toward attached side Cleft lip-bilateral Failure of medial nasal process and maxillary process to fuse bilaterally Cleft of face Width of mouth is determined by fusion of the maxillary process and mandibular process Failure of maxillary and mandibular processes to fuse produces the cleft of face. Other less common cleft Cleft of nose and upper lip Failure of fusion of medial nasal process (around 6th week) Cleft of mandible Failure of mesenchymal cells of mandibular process to merge together (around 6th week) Synostosis syndrome Crouzons Premature fusion of superior and posterior sutures of maxilla along walls of orbit Causes midface deficiency Protrusion of the eyes and wide separation of eyes. Severe mental/neurological feedbacksrelease of fused suture is a critical step in treating this. Usually requires surgical procedures along with orthodontics to correct malocclusion Aperts Premature fusion of superior and posterior sutures of maxilla along walls of orbit Causes midface deficiency Maxilla sometimes fused to sphenoid Hands and feet involvedTooth Formation Prenatally During 6th weekperipheries form dental laminant Divided into 4 stages Bud Cap Bell And something another Considerable calcification is necessary to detect tooth radiographically. Most of our info is based on radiographs. Primary teeth 20 primary teeth Centrals Laterals Canines 1st primary molars 2nd primary molars Primary tooth development timingCalcification BeginsCalcification BeginsCrown CompletedCrown Completed

ToothMaxMandMaxMand

Central14 wk iu14 wk iu1.5 mon2.5 mon

Lateral16 wk iu16 wk iu2.5 mon3 mon

Canine17 wk iu17 wk iu9 mon9 mon

1st molar15 wk iu15 wk iu6 mon5.5 mon

2nd molar19 wk iu18 wk iu11 mon10 mon

Primary Tooth Eruption Order Centralslateral1st molarcanine2nd molars In permanent dentitionOccurs earlier in boys than girls In primary dentitiongirls are earlier than boys Shaded teeth erupt earlier than opposing countpart Upper lateral = earlier than lower lateral Upper 1st = earlier than lower 1st Upper canine = earlier than lower canine Lower 2nd = earlier than upper 2nd

Important Points All primary teeth start formation prenatally. Clinically, teeth are forming before a radiograph detects them. Teratogens can affect formation of teeth. Because certain teeth start forming at different times, insults can affect teeth at different places on their crowns.

Lecture Six: Development and Eruption of the DentitionNote: my notes that I took during class are in italicsmind you, I dont really understand the guy so a lot of them dont make sense.Outline: Tooth development Sequence and timing of eruption of the primary and permanent teeth Pre-emergent eruption and its control Post-emergent eruption and the circadian rhythmTOOTH DEVELOPMENT:My notes: initiated with dental lamina; oral epithelium proliferates and goes from bud stage to cap stage. At the bell stage, the tooth has its final shape. Followed by odontogenesis mineralization of dentin and enamel. Tooth starts to erupt and reaches functional position.

Initiation

Primary teeth During the 6th week, oral epithelium proliferates and forms the dental laminae Dental laminae undergo further proliferation at sites corresponding to the positions of primary teeth During 6th and 8th week in uterus, 20 primary tooth buds form Permanent tooth buds develop lingually at later prenatal period Permanent molars develop posteriorly to the primary molars

Permanent teeth 5 months IU central incisors 10 months (IU?) premolars 4 months IU first permanent 4 years of age second molars Most of the other organ systems (i.e. digestive, CV) are all functioning completely before birth, but development of teeth continues long after birth

Bud stage (pic) Bud stage is the initial stage of definitive tooth development If initiation is stopped, dental agenesis occurs

Cap stage Early cap stage Late cap stage Cells adjacent to the dental papillae are those outside the enamel organ divide and grow around the enamel organ to form the enamel organ? Enamel organ, dental papillae, and dental follicle are developed. Enamel organ forms enamel Dental follicle forms cementum, PDL, and something else?

Differentiation/bell stage 13-14 weeks The cap continues to grow into a bell shape Appearance of specialized cells in the tooth germ The enamel organ is divided into inner and outer enamel epithelium The dental lamina of the permanent tooth appears as an extension of the primary Tooth germ of permanent molars develops the posteriorly extended dental lamina Dentinogenesis, Amelogenesis Cells of the dental papilla adjacent to inner enamel epithelium differentiate into odontoblasts Odontoblasts will produce predentin Predentin calcifies to form dentin Cells of the inner enamel epithelium differentiate into ameloblasts, which produce enamel Enamel and dentin formation begins at the tip of the tooth and progress towards the future root The inner and outer enamel epithelium come together in the neck region and form epithelial root sheath, which initiates root formation The inner cells of the dental follicle differentiate into cementoblasts which produce cementum Tooth assumes its final shape Ameloblasts and odontoblasts appear Cells from dental papilla differentiate into odontoblasts where they will form the dentin Cells of the inner enamel epithelium differentiate into ameloblasts to form enamel Two characteristics: Shape is defined Junction of inner and outer EE and dental papilla 14 weeks IU, primary teeth are in the bell stage Around 18 weeks IU, odontoblasts of primary teeth start to form dentin and then ameloblasts start to form enamel

Root Formation After clinical crown formation, the inner and outer enamel epithelial fold over at the CEJ The epithelia without the stellate reticulum is called Hertwigs epithelial root sheath Hertwigs epithelial root sheath grows away from the crown, increasing size, moving the teeth, and allowing room for additional root growth Root sheath determines number of roots and shape

Primary teeth development timing:

1) Central incisors2) Lateral incisors3) First molars4) Canines5) Second molarsTeeth tend to be delayed more than they are early; same teeth in the same arch tend to erupt at the same time.

Primary Tooth Spacing Generalized Primate 70% of children have space while 30% show no space Children with space will have decreased chance of crowding in permanent teethChronology of Permanent Tooth Development:

The first permanent molar is the only permanent tooth starting calcification before birth Crowns of most permanent teeth show radiographic evidence of calcification after birth Approximately of an incisor crown calcifies a year; longer for other teeth By 8-9 years of age, all permanent teeth except third molars should show on radiographs Only the first molar develops before birth All crowns are developed before age 8, except 3rd molar By 8, any disturbance may affect crown formation (i.e. tetracycline)

Chronology of tooth development summary Usual eruption order of permanent teeth Maxillary M1, I1, P1, P2, C, M2, M3 Mandible M1, I1, C, P1, P2, M2, M3 Root completion occurs about 2-3 years after eruption Implications: Roots of unerupted teeth should not appear closed Trauma requiring root canal therapy can be problematic

Rule of four for permanent teeth At birth, 4 first molars have initiated calcification At 4 years of age, all crowns have initiated calcification At 8 years of age, all crowns are complete At 12 years of age, all crowns emerge At 16 years, all roots are complete

Dental Ages Dental age 6 Eruption of 4 first molars and mandibular central incisors Dental age 7 Eruption of maxillary central incisors and mandibular later incisors Dental age 8 Eruption of maxillary lateral incisors A delay of 2-3 years before any further permanent teeth appear From 6-8, the first molar and incisors erupt like a group and then there is a delay of 2-3 years before any further permanent teeth appear Dental age 9 1/3 of the root of the mandibular canine, first premolar, and maxillary first premolar is complete Root development just starts on the mandibular second premolar and maxillary canine and second premolar Dental age 10 of the root of the mandibular canine, first premolar, and maxillary first premolar is completed Significant root development of mandibular second premolar and maxillary canine and second premolar Completion of roots of mandibular incisors and near completion of the roots of maxillary laterals Dental age 11 Eruption of first premolars and mandibular canine Completion of the roots of all incisors and first molars Eruption of permanent teethnone before this! Dental age 12 Eruption of remaining succedaneous teeth and all the 2nd molars Dental age 13-15 Completion of the roots of permanent teeth (except 3rd molar) By dental age 15, the 3rd molar should be seen on the radiographs

Effects of radiation on tooth development: Radiation in high doses inhibits further crown and root development Calcification of crown matrix was not inhibited If only cusp tips were calcified at the beginning of radiation, they can continue after radiation This picture shows effects of radiation, mainly on the mandible (max seems normal) For the upper teeth, the second molars have erupted and only 2 permanent canines Upper left side, first premolar didnt erupt Pt should be around dental age of 12 Mandible: four lower incisors, first molar, this means pt is at least the dental age of 7 at the time of radiation Normally at dental age 9, there should be 1/3 of root development for lower canines and lower first premolars However, they dont have root formation in this case Crown development of 2nd molar is completed and around 7.5 dental age Pt probably had radiation around dental age 8

Stages of tooth eruption Emergence is the first sign of eruptionbefore emergence, there is pre-emergent eruption which begins soon after root formation and long before the teeth are seen in the oral cavity. After emergence, they continue to erupt at a slower rate to compensate for occlusal wear and mandibular dropping Pre-emergent tooth movement Bodily movement of tooth germ Movement within the bone before root formation. During this phase, the growing tooth germ moves various directions to maintain position in expanding jaw. The primary teeth in the alveolar bone move in the facial, occlusal direction. Permanent teeth also move within the jaw (adjust positions). Change of position of permanent teeth Permanent teeth develop lingually to the primary predecessor. Gradually, the developing permanent teeth are positioned lingual near the apical 1/3 of the primary teeth. The premolars are located under the roots of the primary molar. This change of position is the result of the eruption of the primary teeth and coincident increase in the height of the supporting tissue. Not apical movement of permanent tooth germs. Pre-emergent eruption Begins after root formation Resorption of bone/primary tooth roots Eruption mechanism moves the tooth occlusally Post-emergent eruption Post-emergent spurt Juvenile occlusal equilibrium Adult occlusal equilibrium

Pre-Emergent Eruption: Resorption of bone/primary tooth roots Defective bone resorption leads to eruption failure (M-CSF, Rankl, IL-1) Heavy fibrous gingiva or multiple supernumerary teeth may mechanically block the eruption Eruption mechanism moves the tooth occlusally Resorption of bone/primary tooth roots and tooth eruption are not controlled by the same mechanism Osteoclasts are required. If mutation of genes for osteoclasts leads to defective osteoclasts no more resorption. Experiments have shown that in absorption and tooth eruption may not be controlled by the same mechanism.

Defective Osteoclast (pic) Defective gene for osteoclast maturation defective osteoclast teeth cannot erupt

Cleidocranial dysplasia (radiograph) Mutation of an important gene

Bone resorption without eruption (2 radiographs) Mandible fracture First pic canines are the same height Second pic right canine didnt erupt + bone resorption

Mechanisms for tooth eruption Root formation/elongation Root formation is the consequence, not the cause of eruption Root formation is not required for tooth eruption although it may accelerate tooth eruption Eruption of rootless teeth (pic) Radiation experiment on a monkey Left: root of teeth are missing , but can still erupt though suggesting root formation is not required for eruption Right: control without radiation Periodontal ligament Animal studies showed that substances affecting the development of cross-links in maturing collagen interfere with eruption Transaction of fibers in the dental follicle prior to the onset of eruption does not affect eruption rates or movement Different mechanisms for pre-emergent and post-emergent eruptions PDL should not be the primary mechanism of pre-emergent eruption (but may be responsible for post-emergent eruption PDL is considered a factor in tooth eruption because of traction power of the fibers More PDL fibers in post-eruption phase compared with pre-eruption phase Before emergence of the tooth, the fibers are not as well organized Suggests that there may be different mechanisms Vascular pressure Regional changes in vascular pressure have long been proposed as a force of eruption, but the evidence for this is both inconclusive and contradictory Injection of vasodilators above the root apex can cause transient increase in eruption Injection of vasoconstrictor can decrease Dental follicle Dental follicle is required for eruption Removal of the follicle from the unerupted tooth prevented the tooth from erupting Leaving the follicle intact and substituting and inert object for the tooth resulted in eruption of the inert object Clinical Application In infant, tooth eruption may be accompanied by a slight temperature increase, mild irritation of the gums, and general malaise Although some systemic disturbances at the time of the tooth may be expected, severe general symptoms should not be associated with teething

Post-Emergent Eruption Post-emergent spurt The stage of relatively rapid eruption from the time a tooth first penetrates the gingiva until it reaches the occlusal level Eruption occurs between 8pm and midnight or 1am Tooth stops erupting and often intrudes slightly during the early morning and the day The circadian rhythm is possibly related to the similar cycle of growth hormone release Juvenile occlusal equilibrium Teeth that are in function erupt at a rate that parallels the rate of vertical growth of the jaws As the mandible continues to grow and moves away from the maxilla, tooth eruption matches the jaw growth A pubertal spurt in eruption of teeth accompanies the pubertal spurt in jaw growth After a tooth is in occlusion, the rate of eruption is controlled by the forces opposing eruption from mastication or soft tissues Adult occlusal equilibrium When the pubertal growth spurt ends, teeth continue to erupt at an extremely slow rate during adult life Teeth continue to erupt at an extremely slow rate during adult life Occlusal wear of teeth is compensated by additional eruption and facial height remains constant If extremely severe wear occurs, eruption may not compensate and lead to decrease of facial height To compensate for occlusal wear increase in thickness of cementum

Eruption Teeth tend to erupt in groups First permanent molars and incisors Canines, premolars, second molars Third molars Root formation at time of eruption Incisors about formed Premolars and canines about 2/3 formed Eruption of teeth is more genetically determined than environmentally susceptible Only cases of severe malnutrition may cause delayed eruption

Development and eruption of the dentition (lecture 7)9-30-08

Outline Clinical problems related to tooth development Most commonly encountered clinical problems

Problem with tooth development Enamel hypoplasia Infection or trauma of primary tooth may interfere with matrix formation or calcification of permanent tooth Nutritional deficiencies Vit A Vit C Vit D Calcium Phosphorus Excessive fluoride intake

Fusion Results from the union of two adjacent tooth germs involving the dentin There are really 2 separated roots and pulp chambers Look at the lower right anteriors

Gemination Results from the splitting of a single tooth germ Clinically appers as a double tooth or fused tooth. Single root and single pulp canals. In less than 1% of population. Happens in the anterior region.

Peg lateral 1-2% of population. Smaller conical and tapered to a point in the incisal.

Accessory cusp/tubercle Enamel pearl Will not allow the normal CT attachment. Accessory cups in the cingular area. Remove the cups from max incisor for O purpose may require endo treatment.

Dilacerations/flexion Dilacerations (left) A severe bend or distortion of a tooth root Flexion (right) A sharp curvature or twist to a root

Congenitally missing teeth Heredity Localized inflammation or infections Systemic conditions Can be autosomal dominant, recessive or X linked Severe interuterine disturbance can lead to tooth development problems

Failure of initiation primary (general) lamina all primary teeth and permanent molar successional lamina fusion of mandibular processes or premaxilla and maxillary processes

Congenitally missing teeth Occurs most commonly at areas of Fusion of dental lamina, 77% here The weakest site, increased site of missing teeth Maxillary laterals Mandibular centrals Ends of dental lamina, 24% here Second premolars Third molars More frequently affected permanent teeth 3rd molar > 2nd molar > premolar > lateral incisor Congenital missing later incisor can be linked to opposite lateral incisor missing too Andontia congenital absence of all teeth, deficiency or absence of epidermal glands Oligodontia: absence of six or more permanent teeth Hypodontia: absence of less than six permanent teeth MSX1, PAX9, BLX are the mutations of these genes that can lead to missing teeth, but have nothing to do with the syndromes.

Supernumerary teeth (Cleidocranial dysplasia) Problem with excessive initiation, genetically determined May link to some skeletal dysplasias Most located in the anterior maxillary region, but can be anywhere Can prevent or deflect tooth eruption Location determines the extent Impacted supernumerary tooth is found on a radiograph This can cause crowding and interfere with O

Problems with teeth during eruption Number of teeth The inheritance of the number of teeth is autosomal dominant with variable penetrance Supernumerary teeth Congenitally missing teeth Lost teeth (primary and permanent) Early loss of primary teeth may result in movement of the remaining teeth, blocking out unerupted permanent teeth, tipping of neighboring teeth, extrusion of the opposing teeth This change can cause functional interference. The earlier loss of the lower right canine (primary) leads to less space for permanent of canine and shift of midline. If extraction after the permanent tooth is being to erupt, the perm tooth will reupt quicker. If extraction before eruption, the permanent tooth eruption will be delayed. Size of teeth Mismatch of size of teeth and size of basal bone leads to crowding or spacing, which can lead to malocclusion Tooth size discrepancy between maxillary and mandibular teeth Teeth are smaller there will be spacing, teeth are larger there will be crowding Eruption of teeth: location/direction/amount Usual eruption order of permanent teeth Maxillary M1, I1, I2, P1, P2, C, M2, M3 Mandible M1, I1, I2, C, P1, P2, M2, M3 Development/eruption in the wrong place or direction This can lead to esthetic problem or functional problem. The teeth can become impacted. Maxillary canine is the most common impacted one. Strong genetically components. Eruption in undesirable place can cause Premature contact and functional shift resulting in cross bite

Double row of teeth Roots of primary teeth have not resorbed Check root length with radiograph to make decision about extraction Check the x-ray to make the decision about extraction Pressure of tongue will push the permanent teeth forward

Extreme type of ectopic eruption: Transposition Most common on the maxillary In 1/300 ortho pts Generally seen in b/w Incisors and Canines or b/w Canine and Premolar

With amount of eruption: deficient or eruption failure Can be localized Can erupt to the surface, but then fail to erupt further

Types of eruption failure Physical obstruction Scar tissue Cyst Other teeth Lack of ramal remodeling Trauma

Ankylosis Usually primary molars 5-10% US children have one ankylosed primary molars Ankylosed tooth may finally resorb and exfoliate Primary molars that become ankylosed at early age can become totally submerged, and unlikely exfoliate. May delay a little bit of the eruption of the successive tooth. The primary molar is unlikely to exfoliate and the permanent is severly delayed and this can cause sever problems. Ankylosis of lower primary 2nd M. Can lead to malocclusion. Fusion of alveolar bone and cementum or dentin Fusion usually occurs in root bifurcation 20% of ankylosed teeth are associated with congenitally missing teeth Failure of Hertwigs epithelilal root sheath could cause ankylosis of teeth

Primary failure of eruption Infection of condyle can lead to severe growth deficiency There are lack of bone remodeling and lead to eruption failure An eruption defect, manifesting as a complete failure of eruption or cessation of initial eruption with no obvious local or systemic causative factor Evidence suggests that this disorder has a substantial geographic component?? Tooth forms but does not erupt Teeth may erupt into initial occlusion and then cease to erupt, or may fail to erupt entirely Predominantly affects the posterior dentition Both primary and permanent molars may be affected Involvement may be unilateral or bilateral The first and second permanent molars are the most frequently affected teeth Application of orthodontic force in an attempt to bring the affected teeth into the arch leads to ankylosis rather than normal tooth movement Strong family history of eruption failure or eruption problems in the primary dentition Accompanied with higher level of hypodontia Diagnosis relies principally upon exclusion, all possible causative factors have been considered and eliminated

In the permanent teeth Lower right 1st molar Other molars didnt erupt at all