Orthodontic and Peadiatric Dentistry - COLOUR GUIDE 2000
Orthodontic and Peadiatric Dentistry - COLOUR GUIDE 2000
Orthodontic and Peadiatric Dentistry - COLOUR GUIDE 2000
Primary dentition
I ncisors are usually spaced and upright. No
spacing indicates the probable crowding of
successors (Fig. 1). 'Primate' spacing may exist
distal to cs and mesial to cs. Distal surfaces of es
are flush in most cases. By 5-6 years, an edge-to-
edge occlusion with incisor attrition is common.
4.h Less extensive hypodontia requiring 2.a Increased overjet greater than 3.5mm but less
prerestorative orthodontics or orthodontic than or equal to 6mm with competent lips.
space closure to obviate the need for a 2.b Reverse overjet greater than Omm but less
prosthesis. than or equal to I mm.
4.a Increased overjet greater than 6mm but less
2.c Anterior or posterior crossbite with less than
than or equal to 9mm.
or equal to I mm discrepancy between
4.6 Reverse overjet greater than 3.5 mm with no retruded contact position and intercuspal
masticatory or speech difficulties. position.
2.d Contact point displacements greater than
4.m Reverse overjet greater than I mm but less I mm but less than or equal to 2mm.
than 3.5mm with recorded masticatory and
speech difficulties. 2.e Anterior or posterior openbite greater than
I mm but less than or equal to 2mm
4.c Anterior or posterior crossbites with greater
than 2mm discrepancy between retruded 2.f Increased overbite greater than or equal to
contact position and intercuspal position. 3.5mm without gingival contact.
4.1 Posterior lingual crossbite with no functional 2.g Pre-normal or post-normal occlusions with
occlusal contact in one or both buccal segments. no other anomalies (includes up to half a unit
discrepancy).
4.d Severe contact point displacements greater
than 4mm.
GRADE 1 (None)
4.e Extreme lateral or anterior open bites greater
than 4mm. 1. Extremely minor malocclusions including
contact point displacements less than I mm.
4.f Increased and complete overbite with
gingival or palatal trauma.
Fig. 11a Dental health component of the index of orthodontic treatment need.
Cephalometric interpretation
Aetiology
Dilaceration
Definition Sudden angular alteration in the long axis of the
crown or in the root of a tooth (Fig. 36).
Aetiology Trauma: most commonly follows the intrusion of a;
i t is often accompanied by enamel and dentine
hypoplasia.
Developmental: characteristic labial and superior
coronal deflection of the affected tooth.
Treatment
planning
principles
Treatment
Class I or mild Where overbite and retroclination of 111 or 21112 are to be
Class II skeletal accepted. Confine treatment to the relief of upper
pattern arch crowding and upper labial segment
alignment.
More marked
Class II skeletal
discrepancy
Post-treatment
stability
Incidence 3% of Caucasians.
Aetiology Skeletal pattern. Usually Class III associated with a
l ong mandible, forward placement of the glenoid
fossa positioning the mandible more anteriorly
( Fig. 58), short and/or retrognathic maxilla, short
anterior cranial base or a combination of these
( Fig. 59); it may be Class I with Class III incisor
relationship due to incisor position or inclination.
FMPA may be reduced/average/increased. There is
commonly a transverse discrepancy with a narrow
maxillary and a wider mandibular base but
worsened by a Class III skeletal pattern.
Occlusal features
Mild to moderate
Class III skeletal
pattern
Severe Class III Either align arches and accept the incisor
skeletal pattern relationship or resort to orthognathic surgery.
Definition Buccolingual malrelationship of upper and lower
teeth.
Classification Anterior or posterior (unilateral or bilateral) with or
without mandibular displacement.
Lower teeth occlude buccal to
Buccal crossbite.
corresponding upper teeth (Fig. 63).
Indications
Retention component
Some commonly used means are:
Adams clasp. Used posteriorly in the arch (Figs 74,
75, 76). Arrowheads engage about 1 mm of mesial
and distal undercuts on the tooth. 0.7mm wire is
used for molars; 0.6mm wire is advisable for
premolars and primary molars. The clasp is easily
modified to incorporate hooks for elastics, or tubes
may be soldered for extraoral anchorage (Fig. 75).
Southend clasp.Recommended anteriorly with 'u'
l oop engaging the undercut between incisors (Fig.
74).
Long labial bow. 0.7 mm wire (0.8 mm if it includes
reverse loops). This is useful in preventing buccal
drifting of teeth during mesial or distal movement
( Fig. 71; p. 58); it can also be fitted to the teeth as a
retainer.
Baseplate
This is usually made of cold-cured acrylic but may
be heat-cured. It connects the other components;
guards palatal springs; aids anchorage by contact
with the palate and with teeth intended not to
move; and transfers active component forces to
the anchorage. It may also be active.
Used to reduce overbite
Flat anterior biteplane (FABP).
( Fig. 74) or to remove occlusal interference to
allow tooth movement. FABP should contact two or
three lower incisors.
To remove occlusal
Posterior bite platform.
i nterferences and to facilitate tooth movement
when overbite reduction is unnecessary. It is
commonly used in the correction of unilateral
buccal crossbite with displacement or incisor
crossbite (Fig. 76).
Definition Resistance to the force of reaction generated by
the active components. It is best thought of in
terms of available space for intended tooth
movement.
Effects ( Fi gs 89a-d)
Surgical procedures
Maxilla Le Fort I osteotomy. This is the most common
procedure. It allows repositioning of the maxilla
superiorly, inferiorly or anteriorly.
This allows correction of marked
Le Fort II osteotomy.
maxillary retrognathism and nasal retrusion.
Used to correct Crouzon's
Le Fort III osteotomy.
syndrome. It may be combined with a Le Fort I
osteotomy.
Segmental procedures. These include Wassmund for
premaxillary prominence; they are now used rarely
since there is a risk of root damage from
i nterdental cuts.
Mandible Sagittalsplitosteotomy. I nferior dental nerve damage
i s common.
Vertical subsigmoid osteotomy. Used to correct
mandibular prognathism.
Body osteotomy. Useful if existing space or space
created by extraction orthodontically. Valuable if
there is mandibular prognathism and asymmetry.
Sub-apical osteotomy. Usually of the anterior
dentoalveolar segment only, but may involve the
entire arch. Loss of pulpal vitality is possible.
Genioplasty. Allows chin repositioning.
Fig. 99a Post-decompensation: profile. Fig. 99b 1 year post-bimaxillary
osteotomy: profile.
Fig. 102 Occlusion in a patient with left unilateral cleft lip and
palate.
Management of care
This is best coordinated in a specialised centre by
a team comprising orthodontist, speech therapist,
health visitor, plastic, ENT and maxillofacial
surgeons. Dental care should be monitored
regularly by a general dental practitioner.
Neonatal period to 18 months
Parental counselling and reassurance by the
orthodontist; feeding instruction; advice and
support from a specialised health visitor. Pre-
surgical orthopaedics may be needed to reposition
displaced cleft segments. Lip closure is usually
carried out at 3 months (usually Millard technique),
with bilateral lip repair in either one or two stages.
Palate repair is usually at 9-12 months (usually von
Langenbeck procedure).
Primary dentition
Preventive advice; regular speech and hearing
assessment; speech therapy as required. Possibly
pharynoglasty and/or lip revision at 4-5 years.
Mixed/permanent dentition
Correct incisor crossbite in early mixed dentition or
postpone until preparation for alveolar bone
grafting (8-11 years). Usually align incisors and
expand upper arch prior to bone grafting. Graft
restores arch integrity (Fig. 103a, b), allows
eruption of 3, space closure, supports alar base
and aids closure of oronasal fistulae. Once 3
erupts, correct the centreline and move buccal
segments forward so 3 replaces missing or
diminutive 2. Consider relief of crowding in the
non-cleft quadrant and in the lower arch. Delay
l ower arch extractions if orthognathic surgery is
planned.
I n late teenage years
I f there is gross midface retrusion (Fig. 104), Le
Fort I or II advancement is likely with possible
mandibular setback and/or genioplasty. Consider
rhinoplasty later.
Retention
Bonded permanent retention in the upper arch in
all cases.
Primary teeth erupt at the following times: incisors
6-9 months; first molars 12-14 months; canines
16-18 months; second molars 20-24 months.
Permanent teeth erupt at the following times:
i ncisors 6-9 years; first molars 6-7 years; lower
canines 9-10 years; first premolars 10-11 years;
second premolars 11-12 years; upper canines
11-12 years; second molars 11-13 years; third
molars 17-21 years.
Natal/neonatal teeth
Definition Natal (present at birth). Neonatal (erupt within
28 days of birth).
Incidence 1 in 700 to 1 in 6000 births.
Clinical features They are usually lower incisors (Fig. 105) of the
normal dentition (only 10% are supernumeraries).
They may cause tongue trauma, nipple trauma
(if the child is breast fed), or be a danger to the
airway if they are very mobile.
Management Retain if possible. Extract for any of above reasons.
Eruption cyst
Hypodontia
Definition Absence of one or more teeth.
Incidence and 3.5-6.5% of the population (not counting third
aetiology molars).
Multifactorial genetic inheritance, cytotoxic
drugs, radiotherapy.
Clinical features Hypodontia of genetic origin usually affects the last
tooth in a series: lateral incisors (Fig. 132); second
premolars; third molars. Microdontia (small teeth)
i s an expression of hypodontia.
Associated with syndromes: Albright's
osteodystrophy; hypothyroidism; Down syndrome;
ectodermal dysplasia; Goltz syndrome;
Hallermann-Streiff syndrome; orofaciodigital
syndrome; cleft lip and palate.
Management Joint orthodontic, prosthodontic, oral surgery and
paediatric dentistry treatment planning. For
orthodontic management see p. 21.
Fig. 130 Supplemental upper primary incisor.
Odontomes
Definition Non-neoplastic, developmental anomalies or
malformations derived from dental formative
tissues.
Complex odontome is an irregular mass of
recognisable enamel, dentine and pulp (Fig. 134).
Compound odontome is a collection of
numerous discrete tooth-like structures with
enamel dentine and pulp arranged as in a normal
tooth.
Dilated odontome ( dens in dente; dens
i nvaginatus) is an invagination of enamel and
dentine to form a pouch of enamel (Fig. 135).
Clinical features Compound and complex odontomes obstruct
normal tooth eruption. Dilated odontomes are
prone to caries and pulpal infection.
Management Surgical removal of compound and complex
odontomes. Dilated odontomes may be root-
treated as long as the pouch of enamel is coronal,
and can be removed competely. Otherwise usually
extraction is required.
Fig. 133 Talon cusp.
Erosion
Incidence • 52% of 5-year-olds have palatal erosion on upper
primary incisors.
• 27% of 15-year-olds have palatal wear on upper
permanent incisors.
Aetiology Dietary.
• Citrus fruits
• Fruit juices
• Carbonated drinks
• Vinegar and pickles
• Yoghurt
• Vitamin C tablets.
Gastric regurgitation.
• Gastro-oesophageal reflux
• Oesophageal strictures
• Chronic respiratory disease
• Overfeeding
• Mental disability
• Feeding problems.
Management • Dietary modification.
• Composite/metal veneers or onlays.
Fig. 137 Early erosion of primary molars.
Fig. 146 Enamel dentine fracture; immature Fig. 147 Enamel dentine fracture. Continued
apex, left central incisor. development and maturity of tooth in Fig.
146.
Permanent tooth trauma I: reattachment of
crown fragments
Definition Reattachment to the tooth (immediately or
delayed) of enamel dentine or minor enamel
dentine pulp fractures.
Clinical Procedure is possible since the development of
features and dentine bonding agents. If there is a minor pulp
management exposure then appropriate pulp treatment can be
carried out, storing the fractured tooth fragment in
normal saline - replenished weekly - until the pulp
treatment is finished. The fragment is reattached
using dentine bonding agent and composite resin
as a luting cement (Figs 148, 149, 150).
Fig. 152 Pulpotomy: early treatment (different Fig. 153 Pulpotomy: full root growth with
case to Fig. 151). vital radicular pulp (same case as Fig. 152).
Permanent tooth trauma I: induced apical
closure
Definition Removal of non-vital pulp in a tooth with an
i mmature (open) apex and placement into the roof
canal of non-setting calcium hydroxide cement to
i nduce apical closure.
Investigations Periapical radiography to ascertain apical maturity
and to calculate the working length of the canal.
Subsequent radiographs should assess the extent
of apical closure.
Clinical features To induce apical closure which will allow adequate
obturation of the canal with gutta percha.
Management Remove pulp under local anaesthetic and rubber
dam. File canal. Working length is 1 mm short of
radiographic apex (Fig. 154). Dry canal. Spin non-
setting calcium hydroxide into the canal to the
working length (Fig. 155). Review and change the
non-setting calcium hydroxide 3-6 monthly.
Average time to apical closure is 1 year. Obturate
with gutta percha when apical closure has
occurred (Figs 156, 157).
Complications Non-closure. Obturation will be difficult by either
the orthograde or the retrograde route.
Fig. 154 Working length calculation. Fig. 155 Non-setting calcium hydroxide in
root canal.
Fig. 169 Tooth fragment in upper lip. Fig. 170 Tooth fragment in lower lip
l ocalised by radiography.
Permanent tooth trauma III: resorption
I nternal resorption
Definition Resorption of the walls of the root canal giving the
pulp space a ballooned appearance. External root
surfaces are intact (Figs 171, 174).
Aetiology I nduction of multipotent pulpal cells into
osteoclastic cells by necrotic pulp tissue.
Differential Other types of resorption.
diagnosis
Investigations Clinical and radiographic assessment of pulpal and
periodontal status.
Management Pulpal extirpation followed by mechanical and
chemical debridement of the root canal. Non-
setting calcium hydroxide. Obturation with gutta
percha when there is no progressive resorption.
External resorption
Definition Resorption of the external root surfaces to give an
ill-defined 'punched-out' surface. Internal root
canal surfaces are intact (Figs 172, 174).
Aetiology I nduction of multipotent periodontal ligament cells
i nto osteoclastic cells by damage initially, and
subsequently by pulpal necrotic products via
dentinal tubules.
Differential Other types of resorption.
diagnosis
Investigations Clinical and radiographic assessment of pulpal and
periodontal status.
Management Same as internal resorption.
Replacement resorption
Definition Loss of periodontal ligament and periodontal
l i gament space with direct union of cementum and
bone (Figs 173, 174).
Aetiology Extensive damage to PDL and cementum during
l uxation and avulsion injuries.
Differential Other types of resorption.
diagnosis
Investigations Clinical and radiographic assessment of pulpal and
periodontal status.
Management Placement of non-setting calcium hydroxide into
the root canal. If resorption is progressive, then
plan for prosthetic replacement.
Fig. 171 Internal resorption. Fig. 172 External inflammatory resorption.
Childhood cancer
Incidence 1 in 600 children under the age of 15 in the UK.
Bleeding disorders
Definition Any disorder that upsets the normal: local
reactions of the blood vessels; platelet activities;
i nteraction of specific coagulation factors that
circulate in the blood (Fig. 180).
Classifications Coagulation defects
• Inherited: factor deficiency, e.g. VIII haemophilia
A.
• Acquired: liver disease; vitamin deficiency;
anticoagulant drugs.
Thrombocytopenic purpura
• Primary: lack of platelets, e.g. idiopathic
thrombocytopenic purpura (ITP).
• Secondary: systemic disease, e.g. leukaemia;
drug induced; radiation.
Non-thrombocytopenic purpura
• Vascular wall alteration: scurvy; infections;
allergy.
• Disorders of platelet function: inherited von
Willebrand's disease; drugs; allergy;
autoimmune.
Management Close liaison with medical colleagues essential.
Aggressive prevention.
Fig. 178 Finger clubbing.
Fig. 179 Cyanosis of oral mucosa. Fig. 180 Deep haematoma in haemophilia
A factor VIII deficiency.
Fig. 181 Primary herpetic gingivostomatitis.
Hand-foot-and-mouth disease
Aetiology and Coxsackie A virus infection (commonly A-16).
pathology
Diagnosis • Small, painful vesicles surrounded by
i nflammatory haloes, especially on the dorsum
and lateral aspect of the fingers and toes.
• Rash is not always present.
• May also affect more proximal limbs (Fig. 185) or
buttocks.
• Oral lesions are shallow, painful, small and
surrounded by inflammatory haloes.
Management Supportive.
Fig. 184 Herpes zoster of the cervical
region.
Chronic gingivitis
Aetiology and I nflammatory infiltrate in response to the
pathology accumulation of dental plaque next to the gingival
margin. Early flora in plaque are Gram-positive
cocci after 4-7 days, followed by filamentous and
fusiform Gram-negative organisms after 2 weeks.
Diagnosis Swelling and erythema of gingival margins.
Bleeding on brushing or eating. Halitosis (Figs.
189, 190).
Management Toothbrush instruction. Initial use of chlorhexidine
0.2% mouthwash.
I f left untreated it will progress to periodontitis.
Fig. 188 Acute necrotising ulcerative gingivitis in the primary
dentition.
Localised recession
Aetiology and Narrow zone of keratined gingiva (e.g. when teeth
pathology erupt labially to their predecessors). Aggravating
factors such as gingivitis or mechanical irritation
from excessive and incorrect toothbrushing may
exacerbate recession.
Diagnosis Characteristic appearance (Fig. 195).
Management Conservative. Record the maximum distance from
the gingival margin to cementum - enamel
junction. Correct abnormal toothbrushing. Monitor
i nto adolescence as attachment will creep
coronally spontaneously.
Surgical.
Guided tissue regeneration or other
muco-gingival surgery.
Fig. 194 Gingivitis artefacta: gingival recession in the upper and lower canine
regions.
Fig. 201 Giant cell granuloma on the labial aspect of the upper
alveolus.
Traumatic lesions I
Fibroepithelial polyp
Aetiology and Chronic trauma, usually from biting, resulting in
pathology fibrous hyperplasia (Fig. 202).
Diagnosis Differentiate from other soft tissue lesions by
histological examination of the excised lesion.
Management Excisional biopsy and histological confirmation.
Mucocele
Aetiology and Most are caused by saliva extravasation into the
pathology tissues from damage to minor salivary gland ducts.
They are commonly seen in the lower labial and
ventral lingual mucosa (Fig. 203).
Diagnosis History of trauma and characteristic appearance.
Management Surgical removal may be required if there is
regular trauma. Recurrence may occur.
Ranula
Aetiology and A mucocele that occurs from the sublingual gland.
pathology Blue transparent appearance (Fig. 204).
Diagnosis Characteristic appearance and location.
Management Excision of the sublingual gland.
Fig. 202 Fibroepithelial polyp.
Fia.203 Mucocele.
Denture stomatitis
Aetiology and Poor appliance hygiene, trauma from an ill-fitting
pathology appliance and Candida albicans.
Diagnosis Diffuse erythema associated with the appliance
base, often asymptomatic (Fig. 212).
Management • Correct oral and appliance hygiene and adjust
ill-fitting appliances.
• Soak the appliance overnight in hypochlorite
solution.
• Use of antifungals such as amphotericin,
miconazole and nystatin.
Infective papilloma
Aetiology and Human papilloma virus (HPV).
pathology
Diagnosis Papillomatous cauliflower-like appearance (Fig.
213). Common on palate, gingiva and oral mucosa.
Management Spontaneous regression or excision.
Fig. 211 Pericoronitis.
Paediatric Dentistry
Scully C, Welbury RR 1994 A colour atlas of oral
disease in children and adolescents. Wolfe
Publications, London
Welbury RR ed. 1997 Paediatric dentistry. Oxford
University Press, Oxford
Andreasen JO, Andreasen FM 1994 Textbook and
colour atlas of traumatic injuries of the teeth, 3rd
edn. Munksgaard, Copenhagen
Erosion, 107-108 resorption, 33-34
Eruption cysts, 83-84 retained primary, 29-30
Erythromycin, 125 root-filled, 110
Extrusion, 123 supplemental, 101
talon cusp, 103-104
Facebow with locking device, 61-62 Index of orthodontic treatment need (IOTN),
Facial asymmetry, 75-76 7-10
Fibroepithelial polyp, 153-154 I ntrusion, 123-124
Fibromatosis, hereditary gingival, 149-150 I ron supplements, 89
Finger clubbing, 136
First permanent molars Labial segment
enamel hypoplasia, 25-26, 27-28 fixed appliance alignment, 74
eruption times, 83 problems, 27-34
Fissure sealant, 87 Langenbeck procedure, 81
Fixed appliances, 63-66 Le Fort osteotomies, 77, 81
anchorage reinforcement, 61-62 Leukaemias, 133
li ngual crossbite, 53 Leukoplakia, 134
malocclusion, 41-42, 45-46, 49-50 Lichen planus, 157-158
Flat anterior biteplane (FABP), 59-60 Lingual appliance, 65
Fluoride, 87 Lingual arch
Fluorosis, 91, 95-96 anchorage control, 63
Frankel II appliance, 67-68 crowding, 38
Frankel III appliance, 50 space maintenance, 15
Functional appliances, 67-70 Lips
cleft see Cleft lip and palate
Gardner's syndrome, 101 orofacial granulomatosis, 157-158
Gastric regurgitation, 107 tooth fragment, 129-130
Genioplasty, 77 Lips, incompetent
Geographic tongue, 157-158 anterior open bite, 55
Giant cell granuloma (giant cell epulis), 151-152 gingivitis, 39
Gingival overgrowth, 149-150 malocclusion, 39-40, 47
Gingival recession, 147-148 Lisp, 55
Gingivitis, 143-144 Liver disease, 91-92
artefacts, 147-148 Local anaesthesia, 155-156
Gingivostomatitis, primary herpetic, 137-138 Long labial bow, 58, 59
Goltz syndrome, 101 Lower anterior face height, increased, 75-76
Graft-versus-host disease, 134 Luxation, 123-124
Granulomas, 151-152 Lymphomas, 133
Growth modification, 41
anterior open bite, 55 Malocclusion, 5-10
functional appliances, 69-70 adults, 71-74
malocclusion, 45, 49-50 class I, 35-38
class II division, 1, 39-42
Haematoma, sublingual, 126 class II division, 2, 43-46
Haemophilia, 135-136 class III, 47-50
Hallermann-Streiff syndrome, 101 classification, 5-10
Hand-foot-and-mouth disease, 139-140 functional appliances, 69-70
Harvold appliance, 67 Index of orthodontic treatment need (IOTN), 7
Headgear, 61-62 Mandible
Herbst appliance, 67 prognathism, 47-48, 77
Herpes labialis, 137-138 retrognathism, 79
Herpes simplex virus, 137 surgical procedures, 77
Herpes zoster, 139-140 Maxilla
Holdaway line, 13 retrognathism, 47-48, 71, 77
Human papilloma virus, 159-160 surgical procedures, 77
Hyperdontia, 101-102 Melkersson-Rosenthal syndrome, 157
Hyperplasia, localised gingival, 149-150 Mesial drift tendency, 61
Hypodontia, 21-22, 101-102 Mesiodens, 19-20
Hypothyroidism, 101 i nverted, 101-102
Hyrax screw, 54 Miconazole, 159
Microdontia, 101
I mpacted 66,23 Midface retrusion, 81
I ncisors Millard technique, 81
cleft lip and palate, 81 Minocycline, 89
crossbite, 29-30 Mixed dentition, 1, 15-34
crowding, 1, 2, 3, 4 cleft lip and palate, 81
drifting, 73-74 early loss of primary teeth, 15-16
enamel hypoplasia, 112 hypodontia, 21-22
eruption times, 83 labial segment problems, 27-34
hypodontia, 21-22, 101-102 spacing, 1
luxation, 110 supernumerary teeth, 19-20
periapical infection, 162 MOCDO, 7
proclination, 57 Molars
eruption, 83 serial extraction, 17
normal relationship, 3, 4 space maintenance, 15
Mucocele, 153-154 spacing, 1, 2
Mucosal disease, 151-162 trauma, 109-112
Proclination, 47
Nasal retrusion, 77 Pulp polyp, 88
Natal teeth, 83 Pulp tissue, necrotic, 91-92
Neonatal teeth, 83-84 Pulpotomy, 117-118
Nephroblastomas, 133 Purpura, 135
Neuroblastomas, 133 Pyogenic granuloma, 151-152
Neutropenias, 145-146
Neutrophil defects, 145-146 Quadhelix appliance, 53-54
Nifedipine, 149
Nursing caries, 85-86 Ranula, 153-154
Nystatin, 159 Rapid maxillary expansion, 53-54
Recurrent aphthous stomatitis, 141-142
Occlusion Reduced bony support, 71-72
cleft lip and palate, 79-80 Removable appliances, 57-60
edge-to-edge, 1 Resorption, 91, 131-132
functional relations, 3 Retention
i nterdigitation, 61 adults, 71
malocclusion see Malocclusion cleft lip and palate, 81
maturational changes, 3 commonly used means, 59
normal development, 1, 2 malocclusion, 45
static relations (Andrews' six keys), 3 post-surgical, 77
Ocular herpes, 137-138 Retroclination, 43-46, 47
Odontomes, 103-104 Ricketts' E-line, 13
Oral hygiene, poor Rifabutin, 89
caries, 87-88 Roberts retractor, 57-58
tooth discoloration, 89-90 Root fractures, 121-122
Orofacial granulomatosis, 157-158 Root surface area (RSA), 61
Orofaciodigital syndrome, 101 Roth prescription, 65
Orthodontic camouflage see Camouflage
Orthognathic surgery, 41, 45 Sagittal split osteotomy, 77
Osteotomies, 77-78 Screw section, 53
Overbite Screws, 57, 60
adults, 73-74 Sectional appliance, 65
flat anterior biteplane, 59-60 Segmental procedures, 77
functional appliances, 69-70 Skeletal relationships, 13
malocclusion, 39-40, 43-46, 47, 49, 69-70 Soft tissue
Overjet cephalometric analysis, 13
early correction, 29 i njuries, 129-130
malocclusion, 39-42, 47, 49 Southend clasp, 59-60
retention, 41-42 Space maintenance, 15, 38
Splinting, 127-128
Palatal arches, 63-64 Springs, 57
Palatal finger springs, 58 Sub-apical osteotomy, 77
Papilloma, infective, 159-160 Subluxation, 123
Peer assessment rating (PART, 9, 10 Supernumerary teeth, 19-20, 79, 101-102
Periapical infection, 161-162 Supplemental teeth, 101-102
Pericoronitis, 159-160 Surgical orthodontic treatment, 75-78
Periodontal disease, 71
Periodontal ligament injuries, 123-124 Talon cusp, 103-104
Periodontitis, 145-146 Temporomandibular joint
Permanent dentition ankylosis, 75
cleft lip and palate, 81 dysfunction syndrome, 51
developing, anatomy, 112 Tetracycline staining, 91-92
eruption, 83 Thrombocytopenic purpura, 135
primary tooth trauma, 111-112 Thumb-sucking
trauma, 113-132 anterior occlusion, 29-30
Phenytoin, 149 anterior open bite, 55
Porphyria, 91 buccal crossbite, 51
Posterior bite platform, 59-60 posterior crossbite, 23
Post-surgical orthodontics, 77 Tip-edge appliance, 65-66
Pre-surgical orthodontics, 77 Tongue thrust, endogenous, 55
Primary dentition, 1 Tooth discoloration, 89-92
balancing, 15 Tooth eruption, 83-84
cleft lip and palate, 81 Tooth loss, adults, 71-72
early loss, 15-16 Tooth movements
eruption, 83 active components, 57
extraction, 15 adults, 71
infra-occluded molars, 23-24 Tooth position, 13
retained teeth, 23-24, 51 Tooth surface loss, 107-108