Developmeent of dentition (reading note)

DEVELOPMENT OF DENTITION

December 2016

By

Dr. Mohammed Almuzian (Mo)

For inquires please email me at: [email protected]

Table of Content

M. Almuzian, 2016 John Radcliffe Hospital/ Oxford 0

s

EMBRYOLOGY OF TEETH .......................................................................................... 2

GENETIC CONTROL OF THE TOOTH DEVELOPMENT .................................. 2

PRENATAL TOOTH FORMATION ............................................................................ 3

POSTNATAL DEVELOPMENT OF THE DENTITION ......................................... 4

EDENTULOUS AND PRE-ERUPTIVE STAGES ...................................................... 7

ERUPTION OF DECIDUOUS DENTITION (EARLY PRIMARY

DENTITION) ..................................................................................................................... 10

FULL AND FUNCTIONAL PRIMARY DENTITION ........................................... 11

MIXED DENTITION ...................................................................................................... 13

FUNCTIONAL PERMANENT DENTITION (FULL PERMANENT

DENTITION) ..................................................................................................................... 15

CHANGES IN THE PERMANENT DENTITION INTO ADULTHOOD .......... 18

POST-ERUPTIVE MOVEMENT ................................................................................ 20

DENTAL MATURATION OR DENTAL DEVELOPMENTAL AGE ............................ 21

APPLICATION OF DENTAL MATURATION ............................................................... 22

DEMIRJIAN METHOD ..................................................................................................... 23


Embryology of teeth

The prenatal development of the dentition starts at 4-6 week of IU life. Upper

anterior teeth form from the frontonasal process; maxillary posterior teeth develop

from maxillary process of the first pharyngeal arch while all mandibular teeth

originate from mandibular processes of the first pharyngeal arch, these include

primary and permanent teeth. The basic histology of tooth development suggests that

dental tissues derive from two principle cell types: the oral ectoderm gives rise to

enaml, and the neural ectomesenchymal cells of the first branchial arch contributes to

the formation of of all remaining tooth structures including dentine, pulp tissue,

cementum and periodontal ligament (Sadler, 2011, Sperber et al., 2001).

Genetic control of the tooth development

There are two main types of genes that participate in tooth formation. Firstly, the

signaling genes, which initiate tooth development such as s Pax; Msx; Barx and Axin

which present in the oral ectoderm cells. Secondly, the morpho-genes, which

determine tooth morphology such as SHH, fibroblast growth factors and bone

morphogenetic protein, which present in the neural crest cells. Some genes might be

present in both ecto-mesenchymal and oral epithelial layers and provide a signaling

and morphogenetic control (Maas and Bei, 1997, Ruch, 1995, Sarkar et al., 2000,

Cobourne and Sharpe, 2003). But what is the evidence?

The genetic interaction was proven by a series of recombination experiments that

carried out by Prof. Lumsden at Guys Dental Hospital in the 1988 (Lumsden, 1988).

Prof. Lumsden demonstrated that: tooth development occurs when the oral epithelium

was combined with caudal ectomesnchymal cells (neural crest explanted from the

trunk level) or cranial neural ectomesnchymal cells (neural crest explanted from the

cranial level) but if limb epithelium was combined with any, no teeth formed.

Recombination experiments also suggested the dominance of neural cress cells in the

specification of tooth shape. For example, recombining incisor neural crest cells with

molar epithelium results in the formation of an incisor tooth. Similarly, recombining


molar neural crest cells with incisor epithelium produces a molariform tooth. To sum

up, the recombination experiments demonstrated for the first time that oral epithelium

is essential for initiation of tooth formation while neural cress cells are essential in the

specification of tooth shape.

Prenatal tooth formation

Tooth development consists of six main phases (Fehrenbach and Popowics, 2015,

Ahmed, 2011). The cell interaction and differentiation in these stages is: (1) well-

programmed: i.e. each stage should is under the control of genetic interaction, (2)

sequential: i.e. each stage follow its ancestry stage, and (3) reciprocal: i.e. the

inductive tissue activate the target tissue which in turn activate the differentiation of

its inductive tissue and so on (Thesleff, 2000).

During the initiation stage, development of the deciduous dentition begins at around

4-6 weeks with the formation of a continuous horseshoe-shaped band of thickened

epithelium called oral epithelium, around the lateral margins of the primitive oral

cavity. The free margin of oral epithelium consists of two parts: outer process or

vestibular lamina which deepens to form the oral vestibule that demarcates the

cheeks and lips from the tooth-bearing regions, while the inner process or dental

lamina develops teeth and their supporting structures. Through the bud stage (9th

week of IU life), the dental lamina invaginates into the underlying mesenchyme to

form the tooth bud. The tooth bud give rises to enamel organ and dental lamina of

permanent teeth with the exception of the dental lamina of permanent molars that

develop directly from oral epithelium. The enamel organ consists of two layers: outer

and inner enamel epithelium. At 11th week of IU life, immediately below the inner

enamel epithelium, dental papilla is formed by localized condensation of neural

crest-derived ectomesenchymal cells, the early cap stage. Then, the dental papilla

extends laterally around the enamel organ to form the dental follicle. Enamel organ,

dental papilla and dental follicle are collectively called tooth germ which give rises

to all structures that make up the mature tooth and its associate structures. In the late


cap stage (13th week of IU life), the dental lamina of permanent teeth separates and the

tooth germ fold more (Fehrenbach and Popowics, 2015, Ahmed, 2011).

At the start of the 14th week of IU life (early bell stage), the inner enamel epithelium

grow in size and activate adjacent cells of the dental papilla which differentiate into

odontoblasts that lay down predentine. The first layer of predentine reciprocally acts

as a signal to the overlying inner enamel epithelial cells to differentiate into

ameloblasts and begin secreting the enamel matrix; enamel matrix secretion induces

the conversion of predentine into calcified dentine. This process spread along the

whole crown and result in the formation of calcified crown. Later one, tooth

development enters the late bell stage (16th week of IU life) when cells of the inner

enamel epithelium are confluent with the outer enamel epithelial cells, at the cervical

loop. Growth of these cells in an apical direction forms a skirt-like sheet called

Hertwig’s epithelial root sheath, which maps out the future root morphology of the

developing tooth. Degeneration of this sheath leads to exposure of the dental follicle

to the newly formed enamel that in turn activate the cells of the dental follicle to

produce the alveolar bone and collagen fibres of the preriodontium. At the same time,

Hertwig’s epithelial root sheath activates the underlying dental lamina to secret root

predentine that reciprocally initiates the differentiation of Hertwig’s root sheath into

cementoblasts. The latter calcify to form cementum, which again activate the

conversion of root predentine into dentine. This process continues along the root and

believed to be one of the theories for tooth eruption (Fehrenbach and Popowics, 2015,

Ahmed, 2011).

Dental Anomalies

Stages of Tooth Development and Their Relation to Dental Anomalies

1. Dental Lamina Formation

Migration neural crest cells (ectomesenchyme) into branchial arches

Anodontia (associated with ectodermal dysplasia)

Duplication of dental arches


2. Initiation and Proliferation

Induction of ectoderm by ectomesenchyme

Oligodontia

Supernumeraries

Gemination/Fusion

Compound Odontome

3. Histodifferentiation

Complex Odontome

4. Morphodifferentiation

Macro/Microdontia

Dens Invaginatus (Dens-in-dente)

Dens Evaginatus

Taurodontism

Hutchinson’s incisor / Mulberry molar

Talon cusp

5. Apposition

Organic matrix apposition and primary mineralisation stage

Dentinogenesis imperfecta

Dentinal dysplasia

Amelogenesis imperfecta (hypoplastic)

Enamel hypoplasia

6. Calcification

Amelogenesis imperfecta (hypomineralisation)

Fluorosis

7. Maturation

Removal of water and enamel proteins

Amelogenesis imperfecta (hypomineralisation)

Fluorosis

8. Eruption Stage and Root Development


Premature, delayed, ectopic eruption

Transposition

Impaction

Postnatal development of the dentition

According to Richardson (Richardson, 1999a), the postnatal development of the

dentition consists of 6 stages: Edentulous, pre-eruptive, early primary dentition, late

primary dentition, mixed dentition and full permanent dentition stage.


Edentulous and pre-eruptive stages

The normal features for edentulous stage, which occurs during the first six months

after birth, are 10 maxillary and 10 mandibular gum pads representing the teeth

forming below, well-developed grooves distal to the canine segments called lateral

sulci, and dental or gingival groove, are a horizontal groove on the palatal side

separated The alveolar processes from the palate. At this stage, there is considerable

variation in the antero-posterior relationships of the jaws but assessment is difficult,

as the temperomandibular joints are not fully formed yet. Any parental concern

regarding jaw relationships should be delayed, except if there is an airway risk as in in

Pier Robin Syndrome, as there is no way to predict future relationship (Heaf et al.,

1982). Occasionally, on the alveolar mucosa, small whitish nodules may appear and

often called Epstein’s pearls or Bohn’s nodules. They are about 2-3 mms in diameter,

contain keratin and they tend to occur on the midline of the palate or on the alveolar

gum pads. Parents should be reassured that they will spontaneously burst and resolve

(Cataldo and Berkman, 1968).

Another abnormality, that might be present in the edentulous stage, is natal and

neonatal teeth. The latter erupt during the first 30 days after birth while the former are

that group of teeth present at the birth. Some of these teeth are an actual prematurely

erupted primary teeth while other are supernumerary teeth. The prevalence is 1:2ooo-

3000 baby (Chow, 1980), more in males than counterpart, and more common in

American Indian and Amish group proposing a genetic and racial background (Cunha

et al., 2001). Ironically, in many African tribes, children born with natal teeth were

executed after birth as they were thought to bring bad luck to the tribe (Bodenhoff and

Gorlin, 1963)! Possible aetiologies are genetic factors particularly among Amish

group & association with certain syndrome and/or intra-uterine environmental factors

for example teratogen, infection, malnutrition including hypo-vitaminosis or trauma

(RTa et al., 2002).

Clinically, natal and neonatal teeth may present with swelling of the gum tissue with


an unerupted but palpable tooth, partially erupted or completely erupted with little or

no root. Neonatal teeth may develop some complications such as ainful bitten or

bleeding nipples (Cunha et al., 2001), Riga-Fede disease (trauma to the tip or

undersurface of the tongue) (Buchanan and Jenkins, 1997) or rarely associated with

risk of inhalation or swallowing (Cunha et al., 2001). If these problems develop, then

suggested management should start by consulting paedodontist and some and

palliative treatment using local analgesia. A radiographical evaluation to determine

whether the teeth are normal primary or supernumerary teeth is recommended.

Treatment options could be conservative such as grinding or smoothing sharp edges

of the tooth, composite resin over the sharp edge or changing feeding technique to

reduce nipple trauma. Topical fluoride application should be prescribed if the plan is

to maintain the tooth. Non-conservative treatment include extraction, however it is

important to provide vitamin K supplement before extraction as neonate under the age

of 10 days has very low level of clotting factors and has high risk for bleeding (Cunha

et al., 2001).

Before primary teeth erupt (Pre-eruptive phase), many signs and symptoms related to

teething, develop. A great review paper about teething was published in the British

dental journal by Dr. McIntyre from Dundee (McIntyre and McIntyre, 2002). From

this paper we can conclude that children during teething phase usually suffer general

irritability, malaise, pain, disturbed sleep, bowel upset, loss of appetite and alteration

in volume of fluid intake. Other symptoms are facial flushing (Le Feu Des Dents),

circumoral rash and sialorhoea (Drooling). Children try to rub their ear and gum with

an increase appetite to bite and suck objects. Intraorally, inflammation of the mucous

membrane overlying the tooth possibly with small bleeding might be noticed. As

treatment for teething problem, lancing, which was introduced by Dr. Paré in the 16th

century, was the historical method to treat teething. The procedure involves two

incisions of the tissue overlying the ‘erupting’ tooth.


Teething babies love to feel pressure on their gums because it helps distract their brain

from the sensation of teething pain. Applying pressure can be done using hard or

chilled objects such as:

Hard sugar-free teething rusks or bread-sticks

Teething rings (chilled)

Cucumber (peeled)

Frozen items (anything from ice cubes to frozen bagels, frozen banana, sliced fruit,

pretzels, vegetables, ice cubes or even frozen pacifier!)

Rub gums with clean finger, cool spoon, wet gauze

In sever cases, topical medication or even over-the-counter painkiller like paracetamol

is used.

At the end the pre-eruptive phase, teeth start to appear and there are many theories on

how the eruptive mechanism is generated. One of the theories is the genetic theory;

many genes were found to be in control of eruption process but are defective in

certain disorders and syndromes such as cleidocranial dysplasia leading to delay or no

eruption (impaction). Some believe that eruption’s force comes from the follicle,

which probably has many cytokines and growth factors (Follicular theory). Removal

of the dental follicle results in complete cessation of eruption but if a silicone replica

of a tooth is used to replace a normal tooth during its development, eruption still

occurs as long as the follicle remains intact (Cahill and Marks, 1980).

Other assumed that crown moves occlusally as a result of root growth, however, root

elongation cannot be expected to move a tooth in three-dimensional space (Marks and

Schroeder, 1996). Similarly, formation of bone apical to developing teeth has long

been proposed as one mechanism for eruption (alveolar bone growth theory). There is

no doubt that bone forms in these sites, but bone formation per se is not sufficient for

tooth eruption either. A good example to illustrate this is the presence of an unerupted

dentition in osteopetrotic mutations in which bone formation is nearly normal or

elevated and bone resorption greatly reduced (Marks and Schroeder, 1996).

Moreover, a good evidence suggests that periodontal ligament fibroblasts are capable


of generating contractile forces, pulling the tooth in an occlusal direction (periodontal

activity theory), however, teeth still erupt when the periodontal ligament is disrupted

(Marks and Schroeder, 1996). The last theory in the list is the Hydrostatic forces

theory. It states that forces, which are generated either within the pulp or by the apical

vasculature, are responsible for pushing the tooth in an occlusal direction.

Nevertheless, teeth still erupt when their pulp is removed, and hypertensive drugs

seem to have no effect on eruption (Sutton and Graze, 1985).

Eruption of deciduous dentition (Early primary dentition)

Generally, the first deciduous tooth erupts between the age of 6 and 12 months, still,

all deciduous teeth should be erupted at 3 years. The conventional orders of eruption

are central incisors, lateral incisors, first molars, canines and finally second molars.

Generally, mandibular teeth tend to erupt before maxillary teeth and there is no

gender dominance for eruption date but times can vary up to six months. Root

formation completes 12-18 months after eruption. During eruption the alveolar bone

becomes progressively more developed, there is a small increase in vertical

dimensions, antero-posterior and transverse dimensions as the teeth progressively

erupt, and after eruption the arches change very little until eruption of the permanent

teeth (Richardson, 1999a, Richardson, 1999b).

Prior to tooth’s eruption, a translucent bluish cyst may appear so-called eruption cyst.

There is a gender predilection; male to female ratio is 2:1; they most commonly occur

over primary molars and formed by an accumulation of tissue fluid within the dental

follicle. The cyst requires no intervention as it may spontaneously burst on eruption

but parents may concern, especially if it becomes painful and inflamed, and in this

case it might need surgical excision (Bodner et al., 2005).


Full and functional primary dentition

At 3 years of age, full primary dentition completed. The Ideal deciduous dentition has

six main features (Richardson, 1999a, Richardson, 1999b) as mentioned in table

below.

Semi-circular arch form

Incisor spacing

Positive overjet and overbite;

Class I canine relationship

Anthropoid (Primate) spaces. These spaces are located mesial to the maxillary canine

and distal to the mandibular one, they are important for the accommodation of

permanent teeth and parents should be informed of this if concerned.

Flush or medial step terminal plane molar relationship.

The question now is, does a normal deciduous dentition exist and can a future

malocclusion be predicted from the deciduous dentition?

Foster and Hamilton studied the complete deciduous dentitions of 100 children aged 3

years (Foster and Hamilton, 1969a). Their main finding was that there was not a

single child within this sample that had the six main features at one point. The greatest

variation was seen in the incisor relationship, with only a fifth of children having a

normal overbite, although, almost three-quarters having some increase in the overjet.

The presence of primate spaces was the most constant finding and approximately one-

third of the sample had spacing between all incisors. Furthermore, around one third to

half of the children had second deciduous molars that were flush in the terminal plane

and this is close to findings of other studies (Nanda et al., 1973, Baume, 1950, Arya et

al., 1973). Baume (Baume, 1950) found that 60% of terminal molar relationship in

primary teeth are distal step, 30% are flush and only 10% have mesial step

relationship, however no treatment is indicated at this stage, as growth is

unpredictable.


An answer to the second section of the question is that there is wide individual

variation in occlusal development and predicting a malocclusion in the permanent

dentition, based upon an established deciduous dentition, is difficult. Unilateral

crossbite, anterior open bite and an increased overjet associated with a digit-sucking

habit will usually spontaneously improve, if cessation of the habit occurs before the

mixed dentition is established. However, in the absence of a digit-sucking habit, a

markedly increased or reverse overjet will give a fairly accurate prognosis for the

incisor relationship in the permanent dentition (Larsson, 1994). Additionally, parents

may express concern about developmental incisor spacing in primary dentition but

they should be reassured that this feature is not only developmentally correct but also

important to accommodate the permanent teeth. Leighton 1971 (Leighton, 1970)

showed that approximately, 70% and 50% of children might develop future crowding

if the spacing is >0mm and 1-3, respectively. But, then there will be a little chance for

crowding if the spacing is equal or more than 6mm.

Once primary dentition is complete, between the ages of three and six years, three

changes occur: First, non-carious tooth losses (attrition and/or erosion), which have

the effect of shortening the heights of the incisors, followed by forward movement of

the mandible, the net result is worn teeth that occlude edge to edge. Parents may be

concerned about this but they should be reassured. The second occlusal changes that

take places is the increase in intercanine width which causes either incisor spacing or

increasing of the existent spacing (Richardson, 1999a). The last change is at radicular

level, where roots start to resorb as a first stage for exfoliation. The resorption process

involved is not constant; there are episodes of resorption alternating with periods of

repair. There are four causes of exfoliation of the primary dentition similar to the

theories for tooth eruption (Cahill and Marks, 1980, Marks and Schroeder, 1996) as

mentioned in the table below.


Cementoclastic activity

of permanent teeth

The erupting permanent teeth exert pressure on the

surrounding bone, causing the differentiation of osteoclasts.

These in turn resorb the roots of the primary teeth

Follicular effect of

permanent teeth1. Where teeth have been experimentally wired to prevent

eruption, bone resorption has continued leading to cystic

cavities. It appears therefore that resorption is the rate-

limiting step and is signalled for by the follicle of the

erupting tooth

Alveolar bone growth Continued growth of the alveolar bone results in loss of

structural support of the deciduous teeth

Force of mastication Increased masticatory forces on the weakened teeth, causes

increased compression of the periodontal ligament and

encourages resorption of primary teeth and alveolar bone

Mixed dentition

By the age of 6, primary teeth start their retirement and exfoliate. The eruption

sequence can be variable. However in the upper jaw the normal sequence of eruption

is 61243578 while in the lower jaw, it follow 16234578 sequences however variation

of 1 year in eruption timing is considered normal.

The first permanent tooth to erupt is the first permanent molar eruption and largely,

30% of First permanent molar erupt in 1/2 unit class II relationship, 10% in class I

and 60% in full unit class II molar relationship (Baume, 1950). The question now,

why classes I molar relationship in late permanent dentition is around 55%? How

these molar relationships change? There are several scenarios (Richardson, 1999a).

The first one called‘’ early mechanism’’ which states that a lower first permanent

molar pushes primary molars forward to occupy the primate space and so class I

molar relationship is generated. However, the upper first permanent molar cannot


drive upper primary molars into primate space because the latter is mesial to upper

primary canine and far away from upper first permanent molar. The second theory

called late mechanism in which normal class I relationship is achieved after

exfoliation of primary molars and via utilisation of the Leeway space. The last

scenario for the potential correction of molar relationship in permanent dentition is the

differential jaw growth mechanism. Looking at Scammon growth curve, it could be

decided that from the age of 10 or mid mixed dentition, mandibular growth rate

(growth speed) become higher than that of maxilla, this might result in correction of

molar relationship. Conversely, a recent study by Barros in 2015 states that mesial

and distal steps molar relationship produce stable relationships of the permanent first

molars as the latter are locked by occlusion (Barros et al., 2015).

As a result, the presence of mesial step molar relationship in primary dentition is

associated with 15% of class III, 5% of class II and 80% of class I molar relationship

in permanent dentition. On the other hand, the presence of flash terminal plane molar

relationship is associated with 45% of class II molar relationship in permanent

dentition (Bishara et al., 1988), while in distal step relationship, half of the cases will

develop class II molar relationship in permanents dentition Bishara et al., 1988)

(Baccetti et al., 1997). If add all these together we will find the exact prevalence of

class I, II and III in Caucasian (Foster, 1974).

The second group of permanent teeth to erupt is upper and lower incisors at

approximately 6 years. When upper and lower central incisors erupt, they essentially

use up all the spacing between the primary incisors, with the eruption of the lateral

incisors at the age of 7-8 years, there is an average of 5 mm of space deficiency in the

lower arch and 6mm in the upper arch, this developmental space deficiency called the

incisor liability. Parents should be reassured that this will improve in most of the

cases. But how? The extra space comes from three sources: transverse growth of the

arch, which can provide up to 1-2 mms of space, permanent incisors eruption in

proclined position and this gives another 1-2 mms of extra space and finally the uses

of primate space, which provide the final 2mm. However, if the primate space was

already burn by mesial movement of buccal segments, then incisor crowding might


develop (Moorrees and Chadha, 1965). Another developmental abnormality during

early mixed dentition is the physiological diastema, which is caused by pressure from

the developing permanent canines. Parents should be reassured that this situation

generally self corrects. A final common developmental abnormality during early

mixed dentition is transient anterior open bite this is mainly due to eruption of the

incisors as they approach the occlusal plane and it is spontaneously corrected without

any treatment unless sucking habit prevent full eruption of incisors.

Functional permanent dentition (Full permanent dentition)

Late mixed or early permanent dentition characterize by the eruption of canines and

premolars. Unlike the anterior teeth the permanent premolars are smaller than the

primary teeth they replace, in particular the second premolars. This extra spaces

known collectively as the leeway space or E space. The reason why it is named E-

space because most of the space is achieved via the differential mesio-distal

dimension between second permanent premolars and second primary molars, while

replacing first primary molar in fact add negligible space to the Leeway. Favorable

development of canines and premolars depends upon favorable eruption sequence,

good tooth arch size ratio, and attainment of a class I molar relationship with minimal

loss of space for canines and favorable transverse relationship between the maxillary

and mandibular alveolar processes. (Proffit et al., 2014).

The sequence of eruption of canines and premolars are variable and they tend to erupt

earlier if the deciduous molars are removed earlier, providing space loss is not so

great to have caused an impaction. In the lower buccal segment, the first tooth to erupt

is either the lower 1st premolar or canine while lower 2nd premolar usually erupts next

but occasionally its eruption is late even after the 2nd permanent molar. In the

maxillary buccal segments, the 1st premolar erupts first followed by the canine and 2nd

premolar. The maxillary canine has the longest eruption pathway and potentially has

more eruptive problems associated with it; Ericson and Kurol recommend annual

inspection and palpation of maxillary canines from the age of 8 years, in order to

intercept if necessary (Ericson and Kurol, 1986). The final stage of permanent


dentition development involves the eruption of 2nd molars between the age of 12-14

years while the third molar eruption is highly variable but is quoted to erupt between

16-20 years or even at 40s (Richardson, 1999a).

In general, the ideal features of permanent occlusion are:

Ideal static occlusion (Andrew’s six keys)

Mutually protected functional occlusion.

The upper canine occludes in the embrasure between the lower permanent canine and

the first premolar.

The lower incisors should occlude with the cingulum plateau of the upper incisors

The overbite is about a third of the height of the lower incisor crowns

The overjet is approximately 2mm.

In the full dentition the upper buccal segments are tilted slightly outwards and the

lower buccal segments slightly lingually (Curve of Monson).

The occlusal plane has a distinct upward curve anteriorly (curve of Spee).

Static occlusion is the relationship between the maxillary and mandibular teeth when

the teeth are brought to maximum intercuspation. The ideal static occlusion should

have Andrews’s six keys of occlusion. Andrews (1972) have described keys for an

ideal occlusion based on his study of 120 casts of non-orthodontics models; compared

to 1150 post-treatment study casts that were presented at the American Association of

Orthodontists (Andrews, 1972). Andrews’s six keys are:

1. Class I molar relationship which has two conditions: firstly, the distal surface of the

distal marginal ridge of the upper first molar contacts and occludes with the mesial

surface of the mesial marginal ridge of the lower second molar and secondly, the

mesiobuccal cusp of the upper first permanent molar occlude on the mesiobuccal

groove the lower first molar.

2. Crown Angulation (Tip): In normally occluded teeth the gingival portion of the long

axis of each crown is distal to the occlusal portion of that axis. The degree of tip

varies with each tooth type.


3. Crown Inclination (Torque): This means that always the roots is buccal or labial to the

crown except in upper incisors where the crown is labial to the gingival portion.

4. Rotation: Teeth should be free of undesirable rotations.

5. No spacing

6. Flat curve of Spee or no deeper tham 1.5mm

A seventh key was added by Bennett and McLaughlin (1993) which enforce the

importance of normal tooth-size discrepancies (McLaughlin and Bennett, 2003). With

regard to Dynamic occlusion, Roth stated that an ideal occlusion should function well

(Roth, 1976). His keys for ideal functional occlusion are:

ICP coincide with RCP

Presence of mutual protection occlusion:

Canine guidance or group function

Incisor guidance

Upper teeth should overlap lower teeth

Cusp/fossa lingually

Cusp/ embrasure buccally

Teeth should bite along their LA

Mutual protection occlusion is thought to be achieved in the presence of:

1. ICP (or centric occlusion, CO) coincident with the retruded contact position (RCP) (or

centric relation, CR) but with some limited freedom for the mandible to move slightly

forwards in the sagittal and horizontal planes from ICP.

2. An immediate and permanent posterior dis-occlusion in lateral and protrusive contact

with no associated non-working side interferences (tooth contacts); this is achieved by

the presence of canine guidance or group function in lateral excursion and incisal

guidance in protrusion. Thus, the anterior teeth protect the posteriors;

3. Multiple, simultaneous and bilateral contacts of the posterior teeth in intercuspal

position (ICP) with the incisor teeth slightly out of contact; thus, the posterior teeth

protect the anterior.


There are many theories behind functional occlusion similar to the Apollo Moon

Flags myth! It has frequently been proposed that the following problems can result if

Roth functional keys are absent for example:

Mandibular dysfunction and Bruxism, However a strong evidences by Egermark-

Erikson et al (1983) shows no evidence as most people have nonfunctional occlusion

but not all develop TMD or Bruxsim (Egermark-Eriksson et al., 1983).

Thirdly, it was claimed that non-functional occlusion is a source for periodontal

disease but again there is very little work to support this idea except in Thilander

study which is an experimental study on dogs and can not rely on it (Ericsson and

Thilander, 1978).

The last claim is that in non-functional occlusion, teeth positions are unstable and they

are subjected to high risk of relapse however there is weak supporting evidence.

Changes in the permanent dentition into adulthood

These changes include:

1. Slight increase in mandibular prognathism.

2. Reduction of the overbite with age.

3. Increase in the interincisal angle.

4. Arch width (KNOTT, 1972, Carter and McNamara Jr, 1998): The arch width at

intercanine increased after eruption of primary teeth (1-2mm) followed by a period of

little changes then another increase during mixed dentition (3mm) followed by small

increase in intercanine width during permanent dentition. Growth posteriorly provides

space for the permanent molars, and considerable appositional vertical growth occurs

to maintain the relationship of the arches during vertical facial growth. However

regarding the arch width measured at intermolar are, between the ages of 3 and 18

years an increase of 2 in LA and 4 in UA mm takes place but for clinical purposes

arch width is largely established by the late mixed dentition.

5. Arch circumference: It is determined by measuring around the buccal cusps and

incisal edges of the teeth to the distal aspect of the second deciduous molars or second


premolars. There is little change in the maxillary arch with growth. The mandibular

circumference decreases by about 4mm because of the Leeway space utilisation

(Bishara et al., 1996).

6. Late lower incisor crowding (tertiary crowding) (Richardson, 1999b, Bishara et al.,

1996, Richardson, 1994): Apart from third molar development the most noticeable

change is an increase in crowding between the ages of 15 - 20 years. This is most

noticeable in the lower incisors possibly as a result of a change in interincisal angle

under the influence of soft tissue maturation and differential growth of the mandible

and maxilla with a tendency to prognathism and forward mandibular rotation. The

other factors often discussed in relation to late lower incisor crowding is mesial drift

of buccal teeth and the eruption of third molars. Many factors thought to be related to

late lower incisor crowding may include:

Mandibular growth rotations which cause trapping of lower incisors behind upper

incisor and lead to lower crowding

Anterior component of occlusal force that force the lower teeth to move mesially and

become crowded anteriorly.

Degenerative periodontal changes that allow teeth to drift under light pressures;

Change in diet and lack of interproximal wear as shown by Begg study on aboriginals

(Begg, 1954).

Lower lip maturation which exert extra pressure on the labial surface of lower incisor

leading to crowding (Richardson, 1997).

Mandibular third molars (Richardson and Orth, 1989), however a RCT by Harridan et

in 1998 (Harradine et al., 1998) showed that there is no correlation between impacted

third molars and lower incisor crowding but according to National Institute for

Clinical Excellence (NICE) guidelines, prophylactic orthodontic removal of wisdom

tooth is contraindicated.


Post-eruptive movement

Teeth continue to move in three planes of space after their full eruption at an

approximate rate of 0.4mm per annum. There is many reasons for post eruptive

movement including zompensation for occlusal and proximal wear as well as

accommodation for growth. The latter occurs to accommodate the final growth of the

jaws and usually complete by the late teens. Observing the effects of an ankylosed

tooth best sees the amount of growth occurs after eruption.


Assessment of Dental Age

The eruption times and sequences of the permanent dentition are influenced by

hereditary, environment, early tooth loss, infection, socio-economic and geographic

condition.

Moorrees & Kent (1978)233

Tooth emergence curves or “step-function” are constructed for the deciduous and

permanent dentitions. (Age in years vs. no. of teeth erupted) Validity of this method

is shown to be convenient and simple method.234,235 This method can only be

applied at ages when emergence can be expected. It is more valid in populations with

low incidence of such disturbing factors as caries. It does not depend on knowledge

of the exact emergence ages of specific teeth.

Moorrees & Fanning (1963)236

For each tooth the degree of calcification is determined according to arbitrarily

selected stages from OPG and compared to normal tables. Horizontal bars show the

chronology of tooth formation for each stage +/-1,2 SD’s. Dental development then

related to chronological age.

Three methods for estimation of chronological age based on tooth formation on

radiographs investigated by Hagg & Matsson (1985).237 The accuracy was at least

+/- 12 months for all methods in young age groups and +/-20 months in older

groups.238-240 Hence poor correlation, all methods contain subjective elements.

Dental maturation or dental Developmental age

It is an indicator of the stage of development of teeth and may reflect the

physiological growth of the person.


Application of dental maturation

1. Diagnosis and treatment planning

2. Forensic dentistry

3. Immigration purposes: it is proving valuable when birth data is lacking or doubted in

the management of immigration to help determine physiological age

There are two main methods to assess Dental maturation

1. Gingival emergence methods: This method may be influenced by local factors

(Ogodescu et al., 2011, Demirjian et al., 1973):

Ankylosis,

Early or delayed extraction of the deciduous tooth, impaction

Crowding of the permanent teeth

Genetically determined

1. Radiographic methods: In contrast to emerging method, the formation rate of the

permanent teeth is not affected by premature loss of the deciduous teeth. This can be

achieved by using panoramic radiographs or full mouth periapical radiography.

Example:

Demirjian method (Demirjian et al., 1973) 8 stage technique, 7 stage technique and 4

stage technique (French-Canadian origin. 2500 males and 2500 female). It is better to

use 4 teeth method because chronologically lower incisor is almost the same as for the

first molar, and is often missing the central incisor. Also, for practical reasons, it is

often simpler to take a radiograph of fewer than seven teeth. However 4 teeth system

has limitation of inability to use in very young and very old children in the

standardizing sample.

Nolla technique (Nolla, 1952)

Haavikko technique (Haavikko, 1970)


Demirjian method

It involve the following steps:

A. The left mandibular teeth should be chosen for their minimum variability.

B. Either OPG or Periapical is used and the stage of each tooth is determined. There are

8 stages:

Stage A: In both uniradicular and multiradicular teeth, a beginning of calcification is

seen at the superior level of the crypt in the form of an inverted cone or cones. No

fusion of these calcification points is observed.

Stage B: Fusion of calcified points forms one or several cusps which unite to give a

regularly outlined occlusal surface.

Stage C: Enamel formation is complete at the occlusal surface, dentine deposition has

started and the pulp chamber has a curved shape at the occlusal border.


Stage D: Crown formation is complete, extending down to the cemento-enamel

junction. Beginning of root formation is seen in the form of a spicule.

Stage E: The walls of the pulp chamber form straight lines. The root length is less

than the crown height. In molars the formation of the radicular bifurcation is seen like

a calcified point or a semi-lunar shape.

Stage F: The walls of the pulp chamber form an isosceles triangle. The apex ends in a

funnel shape. The root length is equal to or greater than the crown height.

Stage G: The walls of the root canal are parallel and the apical end is still partially

open.

Stage H: The apical end of the root is completely closed and the periodontal

membrane has a uniform width around the tooth apex.

C. The stage of each tooth is converted to a numerical score and the sum is called

maturation score, two table are available for both genders.

D. The maturation numerical score is traced on the line chart using the 50th centile curve

as a guide in order to determine the patient dental age. There is curve for males and

curve for females.


E. To assess wheather the patient dental age is consistent with peers, resultant dental age

from previous step is traced against patient chronological age (Chronological age for

each patient was calculated by subtracting the date of birth from the date when the

radiograph was taken.). If the points intersected in the 3rd or 97th centile curve, this

mean the person has delayed or advanced dental development in comparison to

his/her peers respectively.


Example: Let us look at this OPG and repeat step A-E

Step A: Scoring

Tooth Stage

M2 12

M1 11.2

PM1 7.3

PM1 12.6

C 11.1

I2 12.5

I1 9

Step B: By looking at the males table, it was found that the maturation score is equal

to 75.7, Chronological age 7.9 years

Step C: According to the line graph for the boy, the patient dental age is 8.2 years and

his is following the 50th centile curve.


Chronology of development of the primary dentition (Foster and Hamilton, 1969b)

Teeth Crown Complete

(months)

Calcification (weeks

IU)

Eruption

(months)

A 1.5-3 13-15 6-9

B 1.5-3 13-15 6-9

D 6 14-17 12-15

C 9 15-18 18-20

E 10-11 16-23 21-35

Root development complete 1-1.5 years after tooth eruption


Chronology of development of the permanent teeth (Foster and Hamilton, 1969b)

Teeth Calcification begins

(months)

Crown Complete

(year)

Eruption

(year)

First molars Birth 2.3-3 6

Mandibular Central Incisors 3-4 4-56-7

Mandibular Lateral Incisors 3-4 4-5 7-8

Mandibular Canine 4-5 6-7 9-10

Mandibular First premolar 21-26 5-6 11-12

Mandibular Second Premolar 27-30 15-7 12-13

Second Molars 30-36 7-8 12-13

Third Molars 7-10 year 12-16 16-21

Root development complete 3 years after eruption


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Health & Medicine

Developmeent of dentition (reading note)