Pediatric Dentistry - a Clinical Approach, 3ed.

List of Illustrations

1.  Chapter 01

a.  Figure 1.1 Until the eighteenth century, children were considered to be small adults (sort of “miniature grown‐ups”) as shown in this painting from a medieval church. Note the similarity of the facial features of the adults and the children.

2.  Chapter 02

a.  Figure 2.1 Reference ranges for fetal weight according to gestational age during pregnancy denoted by the blue lines (10th, 50th, and 90th percentiles) (8). Panel (a) shows examples of children with normal birth weights at term; a normally growing fetus ending with a birth weight which is appropriate for gestational age (AGA) and (▪) a fetus with third trimester intrauterine growth restriction (IUGR) ending with a birth weight below the genetic potential but within normal limits (AGA). Panel (b) shows examples of fetuses with intrauterine growth retardation (IUGR) ending up AGA (□) or SGA (▪).

b.  Figure 2.2 Standing height determined by a wall‐mounted stadiometer (a). Height is recorded as the mean of three measurements. Sitting height is determined by a specifically designed chair (b). Head circumference is determined using a measuring tape (c). Arm span is determined by measuring the distance from fingertips to fingertips (d).

c.  Figure 2.3 (a) Three examples for height curves and (b) height velocity curves from children with early puberty (●), normally timed puberty (□) and delayed puberty (▲). Note that final height is almost the same (a) and that peak height velocity is higher in earlier puberty (b).

d.  Figure 2.4 Normal (Gaussian) distribution of heights illustrating the 95% reference interval by percentiles or standard deviations (SDs).

e.  Figure 2.5 Normal height curve (a) based on healthy children. Lines denote mean ±1 standard deviation (SD) and ±2SD. One individual patient is depicted on the curve (●) before and after operation for a pituitary tumor (craniopharyngeoma) resulting in growth hormone deficiency. A typical deceleration is seen prior to diagnosis. Horizontal lines (red arrow) denote bone age. Following operation the child suffers from pituitary insufficiency and is substituted with L‐thyroxine, hydrocortisone growth hormone, (GH) (arrow), and testosterone (Te) (arrow). This results in a final height well within target height. T = target height range, F = father’s, and M = mother’s height expressed as SDs. (b) Normal height velocity curve based on Tanner’s longitudinal study of healthy children. The same child (●) is depicted on this curve illustrating the marked growth acceleration following GH therapy, as well as the acceleration when puberty is initiated.

f.   Figure 2.6 Two radiographs of the left hands of two healthy children. Note that the mineralization of the small bones has not yet occurred in the younger child (left).

g.  Figure 2.7 Illustrative examples showing low correlation between bone age and dental age. (a) A healthy girl, aged 10 years 9 months, with advanced dental maturity (nearly complete permanent dentition: DS4, M1) compared to the skeletal maturity (prepubertal hand–wrist radiograph). (b) A healthy girl, aged 11 years 6 months, with delayed dental maturity (early mixed dentition: DS2, M1) compared to the skeletal maturity (postpubertal hand–wrist radiograph).

h.  Figure 2.8 Illustrative growth curves of children with growth failure. (a) A child with familial short stature who has a sub‐normal predicted adult height in accordance with the short genetic height potential and retarded bone age. (b) A child with growth deceleration due to the development of a benign brain tumor, which was diagnosed and operated upon. Following the operation, growth hormone (GH) therapy was started and a normal final height was obtained. (c) A girl with Turner syndrome diagnosed in late childhood because of growth failure and a height at diagnosis below genetic height potential. Growth hormone treatment results in growth acceleration, and at age 12 years puberty induction was initiated by low‐dose estradiol treatment. (d) Prenatal and postnatal growth failure in a girl diagnosed with Silver–Russell syndrome before and after initiation of growth hormone therapy which results in marked catch‐up growth. (e) A girl with deceleration of growth from 2 to 3 years of age concomitantly with constipation. She was diagnosed with acquired hypothyroidism and substituted with L‐thyroxine which normalized growth. (f) Marked stunting of growth from 5 years of age and delayed bone age in a girl who was erroneously treated with high‐dose inhalation steroids despite the fact that she no longer had asthma. Cessation of therapy accompanied by growth hormone therapy resulted in marked catch‐up growth.

i.    Figure 2.9 Illustrative growth curves of children with tall stature and growth acceleration. (a) A boy with marked growth acceleration from early childhood who was diagnosed with Klinefelter syndrome (47,XXY). He will end up above his target height despite advanced bone age. (b) A boy with growth acceleration from early childhood who was diagnosed with double Y syndrome (47,XYY) who will end up with increased final height. (c) A boy with growth acceleration from 10 to 12 years of age who was diagnosed with gigantism and operated on for his growth hormone‐producing pituitary adenoma. (d) A boy with growth acceleration and who was obese (simple obesity) who will end up with a final height within his target range, probably because of his advanced bone age. (e) Increased growth in a girl who presented with precocious puberty (regular menstruation at the age of 9 years), and markedly advanced bone age. She will end up with a final height at the lower end of her target range. (f) A girl with familial tall stature and delayed puberty who was treated with high‐dose estrogen to accelerate epiphyseal fusion. Despite this, she reached a final height above target range.

3.  Chapter 04

a.  Figure 4.1 Cells communicate via soluble signal molecules regulating gene expression (transcription).

b.  Figure 4.2 Reciprocal interactions between the epithelial and mesenchymal tissues are mediated by conserved signaling molecules (BMP = bone morphogenetic protein; FGF = fibroblast growth factor; Shh = sonic hedgehog; Wnt). Numerous transcription factors are associated with signaling, and only those in which mutations cause dental abnormalities are indicated in the boxes (PITX2, MSX1, PAX9, RUNX2).

c.  Figure 4.3 The chronology of mineralization of primary teeth.

d.  Figure 4.4 The chronology of mineralization of permanent teeth.

e.  Figure 4.5 Distribution of children according to number of missing teeth. The horizontal axis shows the number of missing teeth per child. The vertical axis is logarithmic and shows the absolute number of children. The proportion of children is given above each column.

f.   Figure 4.6 Mesiodens in an inverted position in the midline of the maxilla.

g.  Figure 4.7 (a) Hypodontia of the permanent maxillary lateral incisors in a 15‐year‐old boy. (b) The same boy with the laterals replaced with a composite‐retained onlay bridge. The material in the Rochette bridge is stainless steel and fused porcelain.

h.  Figure 4.8 Hypodontia of permanent mandibular incisors in an 18‐year‐old boy resulting in elongation of the maxillary central incisors and a deep bite.

i.    Figure 4.9 A boy with ectodermal dysplasia. (a) Intraoral view at the age of 2 years. Conically shaped primary incisors 51 and 61. (b) Teeth 51 and 61 rebuilt with composite resin and a removable partial denture in the maxilla at the age of 3 years. (c) Radiographic examination at the age of 4 years. No teeth in the mandible. In the maxilla 16, 11, 21, 26 and 53, 51, 61, 63 are present. (d) Two fixtures installed in the mandible at the age of 6 years. (e) Removable partial denture in the maxilla and implant retained over denture in the mandible at the age of 7 years. Note small, “primary” acrylic teeth. (f) Eruption of malformed permanent maxillary central incisors at the age of 8 years. (g) Temporary crowns 11 and 21 and rebuilt maxillary and mandibular denture at 18 years of age. (h) At 20 years of age, two fixed bridges were placed in the maxilla (53 and 63 were used in the bridges as they were stable and showed no root resorption) and two more implants were placed in the mandible, enabling the construction of a bridge in the mandible as well.

j.    Figure 4.10 Double formation in (a) primary and (b) permanent teeth in the maxillary frontal region.

k.  Figure 4.11 (a) A 6‐year‐old girl with hemifacial hypertrophy on the right side. Observe the difference in size and developmental stage between the left and the right sides. (b) Orthopantomogram of the same girl taken at 4 years of age. Compare the developmental differences between the permanent first molars in the left and right sides.

l.    Figure 4.12 “Cusp‐shaped” cingulum of permanent central incisor interfering with occlusion.

m.   Figure 4.13 Some examples of invaginations. Note enamel lining inside the lumen.

n.  Figure 4.14 (a) A 4‐year‐old girl with incontinentia pigmenti. Observe the peg‐shaped primary incisors. (b) Orthopantomogram at the age of 8 years. Observe the missing premolars and molars. (c) At the age of 9 years, thin peg‐shaped permanent incisors are erupting in the mandible. (d) The same girl after rebuilding the mandibular incisors with composite resin.

o.  Figure 4.15 The treatment of dens invaginatus. The lumen is reamed out with an elongated round drill. The bottom and buccal walls of the lumen are covered with calcium hydroxide compound.

p.  Figure 4.16 Radiographic examination of a compound odontoma.

q.  Figure 4.17 Radiographic examination of a complex odontoma in a 2‐year‐old girl as a result of trauma.

4.  Chapter 05

a.  Figure 5.1 Transparent mandible at age 10 years. (a) Frontal view. Mental foramina, and segmented teeth (posterior to the incisors) from four different ages (0, 1, 7, and 10 years) are aligned automatically on the symphysis menti and the mandibular canals. Only the teeth and the mental foramen on the right side are illustrated. Lines indicate the eruption paths of the individual teeth. Tooth color code: purple = permanent third molar, blue = permanent second molar, red = permanent first molar, green = permanent premolars and the permanent canine. The mental foramen = blue. The symphysis menti = yellow. The mandibular canals = pink. (b) Lateral view. Lines indicate the eruption paths of the individual teeth. Color coding is the same as in part (a).

b.  Figure 5.2 Histologic section of a human second premolar in its initial stage of eruption. In the figure various theories behind eruption are presented. Experimental studies have shown that the following mechanisms might only play a minor role in eruption, namely: PDL and pulp tissue pressure (6 and 7), coiled vessels creating a slight tissue pressure (8 and 6), pulpal growth (4) and root elongation (3). The most important mechanisms appear to be tissue changes induced by the follicle, namely, induced coronal resorption and apical bone apposition (1 and 5). PDL traction (2) may play a role after penetration of the oral mucosa.

c.  Figure 5.3 Histologic findings associated with the palatal resorption of a primary maxillary central incisor during eruption of the permanent incisor. Note also the presence of the eruption canal (arrow).

d.  Figure 5.4 Orthopantomogram of a 16‐year‐old boy with cleidocranial dysplasia. Note the numerous supernumerary permanent teeth and the arrested eruption of many of the normal permanent teeth.

e.  Figure 5.5 Orthopantomogram of a 13‐year‐old girl with tricho‐dento‐osseous syndrome. Note the severely delayed eruption of several permanent teeth and the dense jaw bones.

f.   Figure 5.6 Orthopantomogram of a 10‐year‐old boy with pycnodysostosis. Note the delayed eruption of several permanent teeth and the osteopetrotic bones.

g.  Figure 5.7 Orthopantomogram of 10‐year‐old boy with cherubism. The large cystic lesions in the maxilla and mandible have caused premature loss of primary teeth.

h.  Figure 5.8 Natal teeth in a 2‐day‐old girl.

i.    Figure 5.9 Fibrous gingival tissue delaying eruption of primary molars.

j.    Figure 5.10 (a) Eruption cyst. (b) Gingival overgrowth caused by phenytoin medication influencing tooth eruption.

k.  Figure 5.11 Infraocclusion of primary molars. Periapical radiographs of a boy followed from 11 years 7 months to 14 years 2 months of age. Left side, extraction side. Extraction resulted in the eruption 1 year earlier of the successor compared to the nonextraction side. Normal marginal alveolar bone height at end of observational period.

l.    Figure 5.12 Impacted primary maxillary second molar (arrow) causing eruption disturbances for the permanent premolars.

m.   Figure 5.13 (a) Retention of permanent maxillary first molar caused by the primary second molar. (b) After extraction/exfoliation of the primary tooth, loss of space will often occur.

n.  Figure 5.14 Ectopic eruption of left maxillary canine which has resorbed the root of the left maxillary lateral incisor. Extraction of the primary left maxillary canine result in a changed path of eruption of the permanent canine. The resorption stopped and a normal periodontal condition was established.

o.  Figure 5.15 (a) Ectopic position of right maxillary central incisor due to a supernumerary tooth in the region causing root angulation and displacement of the central incisor. After removal of the supernumerary tooth and surgical exposure the central incisor erupted. (b) Eight years later.

p.  Figure 5.16 Maxillary second premolar erupting in the palate due to crowding.

q.  Figure 5.17 (a) Late development of impacted mandibular second premolar in a 14‐year‐old boy. (b) Two years later and after surgical exposure. (c) After another 2 years, spontaneous eruption and completed root development had occurred.

r.   Figure 5.18 Ectopically positioned maxillary third molar disturbing eruption of the second molar in a 15‐year‐old boy. Observe the curved roots of the impacted tooth close to the sinus.

s.   Figure 5.19 Premature development and eruption of a dilacerated mandibular central incisor caused by intrusive trauma against the primary incisors at the age of 1 year.

t.    Figure 5.20 Mesiodens interfering with eruption of a central incisor in a 10‐year‐old boy.

u.  Figure 5.21 Odontoma interfering with eruption of a permanent mandibular canine.

v.  Figure 5.22 (a) An 8‐year‐old girl with history of several teeth in ankylosis. Percussion test revealed slight suspicion of ankylosis of permanent left mandibular first molar. (b) Four years later severe infraocclusion and ankylosis were verified.

w.   Figure 5.23 Odontodysplasia resulting in ceased eruption both in the primary and in the permanent dentition.

x.  Figure 5.24 (a) A 12‐year‐old boy with a large dentigerous cyst emanating from nonerupted 37 and displacing germ of 38 high up in the mandible ramus. (b) Two months after fenestration of the cyst and rinsing with saline the cyst had been reduced. (c) Nine months later 37 was seen in the mouth. (d) Another two months later 37 was in occlusion and 38 could be removed with a minor surgical intervention.

5.  Chapter 06

a.  Figure 6.1 Estimated changes in prevalence of dental fear, dental anxiety, dental phobia and behavior management problems in children and adolescents

b.  Figure 6.2 The reasons for dental fear/anxiety (DF/DA) and dental behavior management problems (BMP) are multifactorial and complex. Three groups of factors have been identified: personal, external, and dental factors. The impact and relative importance of the different factors vary between children and individually over time. If DF/DA and/or BMP lead to avoidance of dental treatment, there is a risk of entering and maintaining a vicious circle which may lead to odontophobia.

c.  Figure 6.3 Exposure curve. If a patient is kept long enough in an exposure situation perceived as moderately stressful, the fear reaction will eventually decrease. This will create a feeling of ability to cope with the stimulus (red curve). If, however, the exposure is interrupted before the fear reaction decreases, the feelings of defeat and lack of coping usually increase the anxiety (blue curve).

d.  Figure 6.4 Behavior shaping based on the exposure technique. Introductory steps to the dental situation for the first dental visit for young children.

e.  Figure 6.5 A 3‐year‐old girl at her first dental visit. Behavior shaping by use of the exposure technique to introduce low speed for prophylaxis. (a) After telling the child what will happen (polishing the teeth) the low‐speed polisher is demonstrated to her. (b) The child experiences the vibrations from the low speed. (c) The low‐speed polisher is exposed closer to her, polishing a finger nail, (d) polishing tip of nose, (e) polishing the teeth while the child is still keeping a hand on the polisher to sense control. (f) The child feels safe and able to control the situation and rests her hands on her stomach.

f.   Figure 6.6 Example of exposure steps in desensitization for children who are unfamiliar with or fearful of local anesthesia. The words in parentheses are used to make the child familiar with the procedures of the steps.

6.  Chapter 07

a.  Figure 7.1 Flowchart illustrating the full procedure of anamnesis, clinical examination, and suggestions for additional tests and information.

b.  Figure 7.2 Assessment of the facial symmetry and proportions. The interpupillar line (a) defines the horizontal reference line. A perpendicular line (b) through the midpoint of the interpupillar line defines the midfacial line. The prominence of the forehead (glabella) (c) and the lower point of the chin (menton) (d) defines the total face height, which is divided into the upper face height and the lower face height, by a line plane tangent to the lower border of the nose (subnasal point) (e). The lower face height is divided into the upper lip and the lower lip by the horizontal contact line between the lips (stomion). Harmonious facial proportions are characterized by the upper face height equalizing the lower face height, and the height of the lower lip is double the height of the upper lip. Ideally, the midpoints of the nose, the lips, and the chin are on the midfacial line.

c.  Figure 7.3 Sparse eyebrows in a 12‐year‐old boy with ectodermal dysplasia.

d.  Figure 7.4 Inflamed tonsils in 13‐year‐old girl.

e.  Figure 7.5 Piercing has become a part of teenage culture. Insertion of metallic objects in the tongue increases the risk of damage to the soft oral as well as the hard dental tissues. Such objects should be removed before the clinical examination of the oral mucosa.

f.   Figure 7.6 Fistulae and abscesses due to caries in the primary dentition can vary from (a) a small sinus on the buccal mucosa, which can easily be missed during the clinical examination to (b) small abscesses, and (c) large swellings. Radiographic examination may be indicated.

g.  Figure 7.7 Asymmetric eruption of incisors should always give rise to further examination. In the present case, (a) delayed eruption of 21 was due to (b) a mesiodens.

h.  Figure 7.8 Examples of color changes in the primary dentition varying from (a) slightly yellow‐gray to (b) darker gray.

i.    Figure 7.9 Severe hypomineralization of permanent maxillary and mandibular incisors with extensive opacities on 21, 31, and 41, and discoloration of 11 complicated by posteruptive breakdown of the enamel in the distal corner of this tooth. Note the asymmetric pattern of the lesions on the mandibular central incisors.

7.  Chapter 08

a.  Figure 8.1 A tooth with a root fracture (arrows indicate direction) seen from (a) the facial aspect and (b) an approximal side. On a periapical radiograph this fracture will be shown indistinct or appear (c) as a circle in the case of a steep vertical X‐ray beam angulation and as a distinct line in the case of (d) a flat vertical beam angulation.

b.  Figure 8.2 Two different sensor sizes and five different phosphor plate sizes. The numbers indicate dimensions in millimeters.

c.  Figure 8.3 Periapical radiography of the upper front teeth. The image receptor is placed in a needle holder parallel to the occlusal plan and the X‐ray beam is orientated perpendicular to the line dividing the angle between the surface of the receptor and the long axis of the front teeth in two identical halves.

d.  Figure 8.4 A young child placed on the lap of a parent during exposure. To avoid the child moving the parent should hold the child’s hands with one hand and support the child’s head with the other. The child’s head should rest against the parent’s shoulder. The legs of very small children can be stabilized between the adult’s legs when necessary.

e.  Figure 8.5 “Tell–show–do” technique might be useful to obtain good child cooperation. Before exposure of the child the radiographic procedure can be demonstrated on a teddy bear while the child is watching from a “safe” place.

f.   Figure 8.6 Image receptor holders for bitewing radiographs. The three to the right have an extraoral beam‐aiming device.

g.  Figure 8.7 Radiographic principle for three‐dimensional object localization in the horizontal plan. A metal ball positioned on the facial side of the tooth crown and a metal paper collage positioned on the oral side—nearest the image receptor as shown in (a) will appear as superimposed objects on a radiograph (c) exposed with the X‐ray beam orientated perpendicular at the surface of the image receptor (b). On a radiograph exposed with the receptor in the same positioned as in (b) but with the X‐ray beam orientated left‐sided excentric at the surface of the receptor (d), the metal objects appear separated from each other (e). The paper collage—placed nearest to the receptor—has moved in the same direction as the X‐ray beam (to the left) whereas the metal ball—placed nearest to the X‐ray focus—has moved in the opposite direction (to the right).

h.  Figure 8.8 Horizontal, three‐dimensional object localization of an impacted 13. (a) A periapical radiograph exposed with the X‐ray beam orientated perpendicular at the region for 13. (b) A periapical radiograph exposed with the X‐ray beam orientated mesio‐excentric at the region for 13. Since 13 moves in the same direction as the X‐ray beam (mesially) in relation to the root of 12, it is placed nearest the receptor, which means palatally to the root of 12.

i.    Figure 8.9 Different panoramic segments. (a) A dental panoramic radiograph, (b) a right‐sided panoramic radiograph, (c) a lower jaw panoramic radiograph, and (d) a bilateral premolar panoramic radiograph.

j.    Figure 8.10 Stereo scanogram for depth localization of an impacted 15. The X‐ray beam orientation at 15 is “disto‐excentric” for the scanogram to the left and “mesio‐excentric” for the scanogram to the right. As 15 moves mesially in relation to the root of 14 on the scanogram to the right compared with the scanogram to the left it is located palatally to the root of 14.

k.  Figure 8.11 (a) Frontal part of a panoramic image showing impaction of 13 and 23. (b) CBCT‐scanning for detailed examination of 23. From 2D‐reconstructed images in the coronal (upper left corner), sagittal (upper right corner) and axial (lower left corner) plane transposition of the impacted 23 with 22 is seen. Palatinally to the crown of 23 a compound odontoma (blue arrow) is present. From the 3D‐model (lower right corner) the odontoma is also visible, and it seems to interfere with the eruption of 23.

l.    Figure 8.12 (a) Conventional intraoral radiograph showing an impacted, transversally located 11. (b) On a three‐dimensional image model from a CBCT examination it is clear that 11 is lacerated and placed with the crown palatally and the root facially to the neighboring teeth.

m.   Figure 8.13 A neck shield.

8.  Chapter 09

a.  Figure 9.1 Pain perception based on classical conditioning: a painful procedure based on an unconditioned stimulus (e.g., tissue damage when drilling into dentin), combined with other stimuli such as the sound and the water spray of the drill (conditioned stimuli), may result in pain perception when the conditioned stimuli are presented alone.

b.  Figure 9.2 The perception of procedural pain due to tissue damage (nociceptive pain) depends on a variety of factors, owing to the fact that the stimuli are modulated in the central part of the brain before reaching the sensory cortex. Previous pain experiences (psychological pain memory) and fear are the most important factors contributing to the affective component of pain perception.

c.  Figure 9.3 (a) Topical application of local analgesia ointment on a cotton bud at the injection spot. (b) Infiltration analgesia followed by (c) a transpapillary injection started from the buccal and (d) continuing to the palatal mucosa. Note blanching of the palatal papilla and mucosa in (c).

d.  Figure 9.4 Mandibular block analgesia in a preschool child.

e.  Figure 9.5 The position of the mandibular foramen changes during growth. However, the mandibular foramen is below the occlusive plane in children. The foramen is always situated on the line, where the ramus is narrowest, two‐thirds of the way back from the anterior concavity.

f.   Figure 9.6 Pictures of skulls. The mental foramen is located closer to the primary mandibular first molar in children and the permanent second premolar in adults.

g.  Figure 9.7 (a) The STA™ System and (b) Calaject™ are examples of computerized systems that delivers the analgesic solution with a constant and very slow speed which minimizes the pressure to the tissue and thereby the pain from the injection. (c) The AMSA injection technique.

h.  Figure 9.8 During an injection, the assistant can support the child by holding a hand and also keep the other hand on the child’s head to be sure the child does not make a sudden movement.

i.    Figure 9.9 Side‐effect of mandibular block analgesia. Bite wound in lower lip.

j.    Figure 9.10 Blanching of the cheek (sympaticus reaction) after local analgesia injection in a child.

k.  Figure 9.11 Nitrous oxide–oxygen sedation.

l.    Figure 9.12 (a) Oral administration with midazolam mixed in a juice. (b) Applicator for rectal administration of midazolam. (c) Oral sedation with needleless syringe in a 2‐year‐old child.

m.   Figure 9.13 Dental treatment under general anesthesia in a hospital setting. Notice the comprehensive equipment and the large amount of personnel.

9.  Chapter 10

a.  Figure 10.1 Contribution of initial and manifest lesions, filled and missing (due to caries) surfaces of the total caries index in Norwegian children.

b.  Figure 10.2 Mean number of decayed and filled tooth surfaces according to age in 1973, 1983, 1993, 2003, and 2013, Jönköping, Sweden. For 3‐ and 5‐year‐olds only caries in primary teeth were recorded, while only caries in permanent teeth were recorded in subjects 10 years and older. Initial, noncavitated carious lesions were included.

c.  Figure 10.3 Distribution of 15‐year‐old Danes according to DMFS (initial, noncavitated lesions not included) in 1988, 2006, and 2013.

10. Chapter 11

a.  Figure 11.1 The triad forming the base for evidence‐based practice.

b.  Figure 11.2 Basic design of the randomized controlled caries clinical trial. Study subjects should be assigned randomly to one or more experimental or intervention groups and a control or no intervention group. The outcome of the trial is measured by comparing caries increment in the group(s) from the beginning to the end of the trial (M1 to M2).

c.  Figure 11.3 A conceptual model, where disease is explained as occurring when a number of component causes (sections of the circle) act together to form a sufficient cause (closed circle). (a) High level of plaque, high sugar intake, and high susceptibility to caries will result in a caries lesion. (b) If the sugar intake is reduced, (c) if the plaque level is reduced, or (d) if the susceptibility is decreased, caries lesions will not occur.

d.  Figure 11.4 Caries balance as influenced by social, behavioral, and biological factors.

e.  Figure 11.5 Caries risk assessment with Cariogram. Ten variables are computed and the program indicates a 44% chance of avoiding new caries lesions in the near future (green sector). The blue sector indicates that high sugar amounts and frequent intakes are the main contributing factor in this case. Targeted preventive measures linked to the individual caries risk profile are suggested. The program is available in several languages at www.mah.se.

f.   Figure 11.6 Caries progression. (a) An 11‐month‐old girl exposed to frequent intakes of stewed fruits. The parents could not change the diet. (b) One year later the incisors had to be extracted. (c) A 4‐year‐old boy with developing initial caries lesions. Good parental cooperation. (d) Status after 1 year shows no progression of the caries lesions. (e) A 6‐year‐old boy with active caries. Intense prophylaxis. (f) Status 1 year later shows complete control of caries progression.

g.  Figure 11.7 The amount of fluoride toothpaste (little fingernail) for a 2‐year‐old child.

11. Chapter 12

a.  Figure 12.1 How is caries defined? Caries disease is assessed by its signs and symptoms that depend on the severity of the disease. The figure shows the time‐dependent development of a lesion from a subclinical level to increasing destruction of dental hard tissues.

b.  Figure 12.2 (a) ICDAS‐based criteria for severity grading of caries on free smooth and occlusal tooth surfaces. (b) Alternative index using a five‐graded scale for severity grading of caries on free smooth, occlusal, and approximal tooth surfaces.

c.  Figure 12.3 Active and inactive/arrested caries lesions. Upper row shows initial (noncavitated lesions) and the lower row shows cavitated lesions. (a) Active noncavitated lesions close to the gingival line on the buccal surfaces of primary upper incisors in a 2‐year‐old. There is loss of luster and the lesions are rough on probing. (b) Arrested noncavitated lesions on the buccal surfaces of primary upper incisors in a 4‐year‐old. The lesions are situated at a distance from the gingival line, and are shiny and hard on probing. (c) Active cavitated lesion in a primary lower second molar in a 5‐year‐old. The dentin is soft on probing and the cavity borders are blunt and irregular. (d) Inactive/arrested cavitated lesion in a primary lower first molar in a 7‐year‐old. The dentin is brownish‐black, hard on probing, and the cavity borders are sharp and regular.

d.  Figure 12.4 Sectioned premolar with an enamel caries lesion in the fissure before probing (left). Intense probing (right) destroys the surface zone of the lesion.

e.  Figure 12.5 A small but obvious occlusal cavity in the central fossa of a permanent first molar (arrow). The borders around the cavity are whitish and rough in texture suggesting an active caries process. There is a shadow from underlying dentin caries. The radiograph reveals a substantial radiolucency in the dentin (arrow).

f.   Figure 12.6 (a) Light brown discolored fissures in a permanent first molar of an 8‐year‐old. The enamel around the central fossa is whitish and there is softened enamel at the entrance of the fissure indicating an active lesion (arrow). (b) The radiograph reveals radiolucency in the dentin (arrow). (c) Dark brown/black discolored fissures in a permanent first molar of a 19‐year‐old with a low caries activity. The fissures are hard on probing indicating an arrested (inactive) lesion.

g.  Figure 12.7 Caries lesions on distal surfaces of two mandibular second premolars: both radiographs (a and c) showed radiolucency in outer dentin, but during cavity preparation, a clinical cavity was observed only in one of them (b).

h.  Figure 12.8 Hidden caries under a seemingly sound occlusal surface of a permanent lower second molar in a 14‐year‐old. (a) Visual–tactile examination of the surface did not reveal any clear signs of caries. (b) The bitewing radiograph shows, however, an obvious radiolucency in the dentin. The presence of soft carious dentin was confirmed at drilling.

i.    Figure 12.9 (a) to (j) A 14‐year‐old boy who was treated with bone marrow transplantation (BMT). Three months later he developed graft‐versus‐host disease, which prolonged his hospitalization to a total of 4 months. His condition and the treatment he received resulted in hyposalivation, and during the treatment period he experienced frequent supply of sugary drinks, inadequate dental hygiene, and little fluoride exposure.

j.    Figure 12.10 (a) A 3‐year‐old boy with high caries activity due to frequent intake of high sucrose‐containing meals. (b) After gross excavation of the caries lesions and application of a temporary zinc oxide–eugenol cement the child is ready for nonoperative treatment.

k.  Figure 12.11 (a–c) A 13‐year‐old girl with active caries and low motivation, treated by the use of general and local caries‐arresting interventions. (d) Five years later: adequate caries control. (e) Another 3 years later: still adequate caries control. Observe the glossy surfaces of the previously active initial caries lesions.

l.    Figure 12.12 Rubber dam for isolating the operation field before restorative therapy of primary molars.

m.   Figure 12.13 Rubber dam for isolating and drying the operation field before restorative therapy of maxillary incisors.

n.  Figure 12.14 Severe early childhood caries in a 4‐year‐old child. The caries process started in the upper incisors during the eruption of the teeth, due to sugary drinks at night. Note that first primary molars are also heavily affected. No oral hygiene habits had been introduced.

o.  Figure 12.15 Use of a thin layer of GIC for the arrest of approximal dentin caries in primary incisors of a 2‐year‐old child. A hand instrument was used to remove soft carious tissue before application of the cement.

p.  Figure 12.16 Small Class II cavity preparation for GIC in primary molars. Basically, the outline of the cavity is determined by the extent of the caries lesion, but some mechanical retention is advocated in the directions indicated by the arrows.

q.  Figure 12.17 Large Class II cavity preparation for compomer or composite materials in a primary molar. Retention of the filling is based on mechanical as well as adhesive techniques.

r.   Figure 12.18 (a) Lower right second molar with severe multi‐surface caries suitable for a stainless‐steel crown. (b) Removal of carious tissue reveals pulp exposure. (c) After pulpotomy the cavity is restored with GIC and the crown is prepared for a stainless‐steel crown. (d) The tooth is restored with a stainless‐steel crown.

s.   Figure 12.19 (a) Only just enough tooth tissue is removed to adjust the crown to the occluding and neighboring teeth. The gingival contour should be kept intact to retain the crown. (b) Extensive carious defects are initially restored with GIC and the crown is subsequently adapted to the restoration.

t.    Figure 12.20 Fissure sealing covering all parts of the fissure without overfilling and overextension.

u.  Figure 12.21 Enamel surface seen in scanning electron microscope after etching with 30% phosphoric acid for 45 seconds. As an effect of lack of cleaning before etching, black areas with organic material remain (white arrows; magnification ×300).

v.  Figure 12.22 Preventive resin/GIC restoration; R = restorative material (resin or GIC), S = sealant.

w.   Figure 12.23 Class III cavity in maxillary incisor.

x.  Figure 12.24 The relative percentage distribution of approximal (appr) and occlusal (occl) DFS (decayed and filled surfaces) at ages of 13, 19, and 27 years evaluated from radiographic examinations. For approximal surfaces decayed (D) equals a radiolucency at the enamel–dentin border or deeper and for occlusal surfaces D equals an obvious radiolucency in dentin. The same individuals (n = 250) were followed from 13 to 27 years of age.

y.  Figure 12.25 Cumulative survival curves of occlusal surfaces (first and second molars) from radiographically sound to obvious radiolucency in dentin. The slopes of the curves show that most new dentin lesions occurred between 12 and 15 years of age and particularly concerned the second molar. It should be noted that, for the first molar, the data show only those who were radiographically sound at age 12 years.

z.  Figure 12.26 Caries rates (number of new lesions/100 tooth surface‐years) of approximal surfaces from 11 to 22 years of age. Median values of all surfaces.

aa.  Figure 12.27 Survival times of approximal caries lesions from 11 to 22 years of age. The ninetieth percentiles of three progression states: from 0 to 2, from 2 to 4, and from 3 to 4.

bb. Figure 12.28 Median values of survival times (years) from caries state 3 to state 4 (progression within dentin) at different approximal surfaces.

cc.  Figure 12.29 Cumulative survival curves of approximal surfaces from radiographically sound to inner enamel caries, from inner enamel caries to caries in outer dentin, and from caries at the enamel–dentin border to caries in outer dentin from 12 to 27 years of age.

dd. Figure 12.30 Two 12‐year‐olds; one has almost fully erupted premolars and second molars while the other is still in the process of shedding primary molars.

ee.  Figure 12.31 (a) Bitewing radiographs from the same individual from 15 to 21 years of age showing slow progression of lesions on the distal surface of upper left first premolar and mesial surface of the second premolar. The enamel lesions on these surfaces have not progressed into the dentin during these 6 years. (b) A significant example of the rapid progression in newly erupted first molars (tooth 26) in an 11‐year‐old girl. At the follow up after 1 year no bitewing radiographs was taken. At the 2‐year follow‐up the tooth was extracted due to severe caries with pulp involvement.

ff. Figure 12.32 The saucer‐shaped cavity design: (a) before filling and (b) after filling with a composite resin.

gg. Figure 12.33 (a) The design of the saucer‐shaped cavity is based on adhesion of composite resins to enamel and dentin. (b) The saucer‐shaped cavity design (dotted line) saves more tooth tissue than the traditional Class II preparation.

hh. Figure 12.34 Conventional Class II amalgam preparation with minimal buccal–lingual extension.

12. Chapter 13

a.  Figure 13.1 Distribution of dental erosion by tooth and by gender. Percentages of boys and girls with dental erosion by teeth at (a) 12 years of age and (b) at 15 years of age.

b.  Figure 13.2 Severe erosion on the palatal surface of the upper incisors. The enamel close to the gingival margin is intact and a shoulder is shown.

c.  Figure 13.3 (a) Cuppings on a permanent first lower molar (tooth 36) in a young teenager. (b) Study cast from the same case.

d.  Figure 13.4 Dental erosion as a result of lemon sucking in a 6‐year‐old child. Dental erosion has caused severe endodontic problem especially in region 52 and 51.

e.  Figure 13.5 Near to pulp exposure on the palatal surfaces of anterior primary teeth. Secondary and tertiary dentin are shown.

f.   Figure 13.6 pH decrease (mean values) for three methods of drinking and nipping from a baby’s bottle using the microtouch method and Cola Light. Holding = holding the drink in the mouth for 2 min. Long sipping = sipping from a glass for 15 min. Gulping = swallowing quickly three times over 5‐min intervals. Baby bottle = nipping from a baby’s feeding bottle for 15 min.

g.  Figure 13.7 Dose‐response relationship between frequency of soft drink intake and number of teeth affected by dental erosion in 7th grade (12 year‐old) and 10th grade (15 year‐old) children.

h.  Figure 13.8 Clinical signs of erosion: cuppings on primary molars (teeth 83 and 85) and permanent molar (tooth 46).

i.    Figure 13.9 Illustrations of different severities of dental erosion graded according to the scale in Box 13.6: (f) is a study model of the patient in (e) illustrating that intraoral photographs could be combined with grading of study models as the two complement each other in assessment of dental erosion.

j.    Figure 13.10 (a) Fifteen‐year‐old girl with palatal erosion and sensitivity on maxillary anterior teeth. (b) Composite restoration took place on tooth 12, establishing a new vertical dimension sufficient for restoring 11, 21, and 22 (c). (d) As a result, posterior disocclusion is present which, however, is normalized after approximately 4 weeks due to (e) compensatory eruption and alveolar growth.

13. Chapter 14

a.  Figure 14.1 Clinically healthy primary tooth gingiva.

b.  Figure 14.2 Clinically healthy permanent tooth gingiva.

c.  Figure 14.3 Chronic gingivitis.

d.  Figure 14.4 Supragingival calculus.

e.  Figure 14.5 Bitewing radiographs showing proximal calculus on primary and permanent teeth. Arrow heads indicate subgingival calculus.

f.   Figure 14.6 Radiographs of a 14‐year‐old boy showing proximal subgingival calculus and minor bone loss at mandibular permanent first molars. Arrow indicates bone loss and arrow heads indicate subgingival calculus.

g.  Figure 14.7 Black stains can be observed in children.

h.  Figure 14.8 Gingivitis in relation to dens geminatus (tooth 41) in the incisal region of the lower jaw. (a) Frontal view of tooth 41, (b) Distofacial view of tooth 41.

i.    Figure 14.9 Poor oral hygiene and gingivitis in a patient undergoing orthodontic treatment.

j.    Figure 14.10 Chronic gingivitis associated with mouth breathing.

k.  Figure 14.11 Edematous gingival inflammatory reaction during puberty.

l.    Figure 14.12 A 14‐year‐old boy with localized aggressive periodontitis (c, d). Previously obtained and filed radiographs from the age of 8 years show loss of bone support (a, b) (arrows)

m.   Figure 14.13 A 3‐year‐old boy with a generalized form of aggressive periodontitis. The primary teeth in all quadrants are involved.

n.  Figure 14.14 (a) A 13‐year‐old girl with a localized form of aggressive periodontitis, clinically identified with a diastema between permanent maxillary incisors. (b, c and d) The radiographs show bone destruction in the same area as well as in the permanent molar regions (arrows).

o.  Figure 14.15 Severe periodontal involvement in a young child suffering from diabetes mellitus.

p.  Figure 14.16 Aggressive periodontitis in a 19‐year‐old patient with diabetes mellitus with poor metabolic control. (a) Clinical picture (b) Panoramic radiograph.

q.  Figure 14.17 Alveolar bone loss in a child with hypophosphatasia.

r.   Figure 14.18 (a, b c) Chronic periodontitis at permanent first molars of a 13‐year‐old girl. Scaling and root planning were performed. (d, e) Radiographs taken 6 months later show healing of bone defects.

s.   Figure 14.19 (a) Aggressive periodontitis at permanent molars of an 18‐year‐old adolescent. Thorough scaling and root planing were performed. (b) Radiographs taken 1 year later and (c) 3 years later show substantial healing of the bone defects.

t.    Figure 14.20 Periodontal surgery of a 14‐year‐old girl with localized marginal periodontitis in the lower left molar region. (a) A bitewing radiograph showing bone loss on tooth 36. (b) Intracrevicular incision. (c) The gingiva is retracted. (d) The exposed root surfaces are subjected to mechanical debridement. (e) The flaps are replaced and sutured.

u.  Figure 14.21 Gingival recession at permanent lower central incisor; (a) in a mixed dentition and (b) in a permanent dentition.

v.  Figure 14.22 Phenytoin‐induced gingival overgrowth.

w.   Figure 14.23 Gingival fibromatosis (a) in a newborn child and (b) at 5 years of age after surgical correction.

x.  Figure 14.24 (a) Traumatic ulcerative gingival lesion and (b) after treatment.

y.  Figure 14.25 Foreign body (a plastic ring or rubber band from children’s toys) in the oral cavity of a 6‐month‐old baby. (a) Blue plastic ring/rubber band around tooth 72; (b) Blue plastic ring around the column of tooth 72 after extraction.

14. Chapter 15

a.  Figure 15.1 Impetigo contagiosa in a 7‐year‐old girl.

b.  Figure 15.2 Forschheimer’s spots on the soft palate in a child with rubella.

c.  Figure 15.3 Koplik’s spots in the cheek mucosa in a child with measles.

d.  Figure 15.4 Vesicular lesions on the skin in a child with varicella (chickenpox).

e.  Figure 15.5 Vesicles on the mucosa of the tongue in a child with varicella.

f.   Figure 15.6 (a) Herpes simplex lesions spread over the alveolar mucosa and (b) tongue.

g.  Figure 15.7 Herpes labialis.

h.  Figure 15.8 Wart.

i.    Figure 15.9 Candidiasis lesion in cheek mucosa.

j.    Figure 15.10 Candida albicans infection of the palatal mucosa in child with a partial denture.

k.  Figure 15.11 Aphthous ulcer.

l.    Figure 15.12 Erythema multiforme: (a) oral lesions showing vesicles and bullae which rapidly burst; (b) lesions after 2–3 days; (c) crust formation (healing) 2 days later.

m.   Figure 15.13 Tongue mutilation after local anesthesia.

n.  Figure 15.14 Crohn’s disease, gingival characteristics: (a) incisal region; (b) molar region.

o.  Figure 15.15 Geographic tongue is a relatively common condition found in children.

p.  Figure 15.16 Bohn’s nodules in a newborn baby.

q.  Figure 15.17 (a) Mucous retention cyst in the lower lip. (b) Surgical removal of the cyst. (c) Healing after 1 week.

r.   Figure 15.18 Ranula located in the floor of the mouth.

s.   Figure 15.19 Pyogenic granuloma.

t.    Figure 15.20 Peripheral calcifying granuloma.

u.  Figure 15.21 Peripheral giant cell granuloma.

v.  Figure 15.22 Capillary hemangioma.

w.   Figure 15.23 Cavernous hemangioma in the palate of a newborn. Note also the capillary hemangioma in the cheek.

x.  Figure 15.24 Extraction of primary teeth: (a, b) molars in upper jaw and (c, d) lower jaw – loosen the tooth carefully with an elevator, place the forceps around the tooth and apply apical pressure and buccal–lingual movements before the tooth is lifted out. (e–g) Incisors are extracted by slight apical pressure and rotary movement.

y.  Figure 15.25 Primary first molar with pulpitis. Roots of the tooth encircle the permanent tooth bud.

z.  Figure 15.26 Primary molar cut into two halves before extraction.

aa.  Figure 15.27 (a) Radiographs of upper right canine in palatinal ectopic position with risk for resorption of the permanent incisors. (b) After a palatinal muco‐periostal flap is raised and bone is removed the canine is exposed. (c) Brackets and gold chain are etched to the lingual surface of the canine. (d) The flap is sutured and the free end of the chain is temporarily fastened to a premolar. The contralateral canine was treated at the same session. The patient is now ready for the orthodontic treatment.

bb. Figure 15.28 (a) Delayed eruption of upper central incisor. (b) Denudation of gingival mucosa to enchance eruption.

cc.  Figure 15.29 (a) Extensive dentigerous (follicular) cyst in left maxilla emerging from a supernumerary tooth and displacing tooth germs and disturbing normal eruption in a 5‐year‐old girl. (b) Radiographic examination after 5 months revealed that the cyst had been reduced considerably and was now available for surgical removal without risk of disturbing the involved teeth. (c) After 4 months and surgical removal of supernumerary teeth and residual cyst tissues. (d) Obturator inserted to facilitate rinsing of the cyst. The obturator was removed after 6 weeks.

dd. Figure 15.30 Fibrous frenulum causing bony defects in a 5‐year‐old girl.

ee.  Figure 15.31 Lingual frenuloplasty. (a) Lingual frenulum restricting the movements of the tongue. (b) Local anesthesia. (c) Curved hemostat is placed close to the tongue. (d, e) Frenulum is cut. (f) Healing after 10 days.

15. Chapter 16

a.  Figure 16.1 Histologic view of partial chronic pulpitis of a primary molar. Note the restricted area of chronic inflammation at the site of carious exposure.

b.  Figure 16.2 Radiograph showing stepwise excavation performed in two primary second molars in order to keep them in situ and without subjective symptoms at least until the permanent first molars are in occlusion.

c.  Figure 16.3 Radiograph of primary second molar after partial pulpotomy. The hard tissue barrier indicates wound healing; note absence of periradicular pathology.

d.  Figure 16.4 Pulpotomy performed in lower left second primary molar with pulp exposure and pulpitis (a). The tooth was maintained in the arch with healthy bone in the bifurcation (b), after it was restored with a stainless steel crown (c).

16. Chapter 17

a.  Figure 17.1 Stepwise excavation of a permanent molar, (a) at the time of treatment and (b) 9 months later. The formation of dentin between the temporary filling and the pulp has proceeded and the risk of pulp exposure at the time of final restoration of the tooth is minimal.

b.  Figure 17.2 Partial pulpotomy of permanent molar. (a) Radiograph taken at the time of treatment and (b) 2 years after treatment.

c.  Figure 17.3 Partial pulpotomy of a permanent incisor with complicated crown fracture. (a) At the time of treatment; (b) application of calcium hydroxide; (c) radiograph at the time of treatment; and (d) several years later.

d.  Figure 17.4 Diagrammatic representation of calcium hydroxide apexification technique. (a,b) Access pulp chamber, (c) light filing or no filing and irrigation with 0.5% sodium hypochlorite, (d) drying the canal using paper points, (e) placement of calcium hydroxide to the apical foramen (spiral filler could be used), (f) placement of cotton pledget (white) and glass ionomer filling (brown) for a minimum of 3 months until clinical or radiographic evidence of a calcific barrier is seen (g).

e.  Figure 17.5 Radiograph showing cervical root fracture of a tooth treated with calcium hydroxide apexification.

f.   Figure 17.6 Periapical radiographs showing calcium hydroxide apexification of the upper left lateral incisor over a period of 9 months. (a) 15 May 2004, (b) 21 September 2004, (c) 15 January 2005, and (d) 11 February 2005.

g.  Figure 17.7 Diagrammatic representation of MTA plug and thermal guttapercha obturation of immature teeth. (a,b) Access pulp chamber, (c) light filing or no filing of canal and irrigation with 0.5% sodium hypochlorite, (d) drying of the canal using paper points, (e) placement of 4–5 mm white MTA (light green) in the apical third of the canal, (f) incremental obturation using Obtura (orange), (g) placement of a glass ionomer based (gray) base and composite filling (brown).

h.  Figure 17.8 Radiographs showing a case treated with MTA plug and Obtura.

i.    Figure 17.9 Radiographs showing continuation of root development in a patient treated with RET using blood clot as a scaffold. (a) 23 October 2013, (b) 23 October 2014.

j.    Figure 17.10 Diagrammatic representation of RET of immature teeth. (a,b) Access pulp chamber, (c) light filing or no filing of canal and irrigation with 2.5% sodium hypochlorite, followed by 5 mL sterile saline, (d) drying of the canal using paper points. (e) A mixture of metronidazole (100 mg) and ciprofloxacin (100 mg) is mixed with distilled water and delivered into the root canal system, (f) placement of cotton pledget and a temporary glass ionomer filling until symptoms and signs of infection resolve. (g) At the second stage and after accessing the tooth again, the canal is irrigated by ccopious amounts of normal saline followed by 10 mL 17% EDTA and thoroughly dried with paper points. (h) A sterile sharp instrument (needle or a finger spreader) with a length of 2 mm beyond the working length is pushed past the confines of the root canal, into the periapical tissues to intentionally induce bleeding into the root canal. (i) The bleeding is then allowed to fill the root canal followed by placement of a cotton pledget for 5 min until a clot has formed. (j) Once the clot has formed, the access cavity is then hermetically sealed with three layers of material to prevent coronal leakage and contamination: Portland cement, followed by glass ionomer and then composite resin.

17. Chapter 18

a.  Figure 18.1 A 4‐year‐old boy with lateral luxation of three primary incisors and extensive gingival laceration.

b.  Figure 18.2 The patient has had an impact where the force has been transmitted through the upper lip to the teeth and the alveolar process. Note the lip laceration and abrasion and the displacement of the right central and lateral incisors.

c.  Figure 18.3 Percentage distribution of 1275 children with traumatic dental injuries related to age at the time of injury.

d.  Figure 18.4 Distribution of injuries of the most frequently injured permanent teeth: 97% of all injuries affected the incisors.

e.  Figure 18.5 (a) Crown fracture of mandibular lateral incisor and mandibular lip lesion. (b) A radiograph reveals the fractured tooth fragment hidden in the lip lesion.

f.   Figure 18.6 (a) Clinical condition immediately after severe intrusive luxation of the primary right central incisor. (b) The occlusal exposure shows foreshortening of the intruded tooth, indicating buccal displacement away from the permanent follicle. (c) This is evident in the lateral radiograph, since the apex of the intruded incisor is forced through the buccal bone plate.

g.  Figure 18.7 (a–c) Clinical appearance after lateral luxation of the right central incisor. (d–g) One occlusal and three periapical radiographs. Note that the occlusal exposure is optimal for showing the buccal displacement of the root. (h) The lateral radiograph illustrates where the fracture of the buccal bone plate has occurred (arrow).

h.  Figure 18.8 Percentage distribution of diagnoses for traumatized primary teeth.

i.    Figure 18.9 Distribution of 2019 traumatized permanent teeth according to diagnosis in 1275 children aged 7–18 years.

j.    Figure 18.10 Schematic drawing illustrating developmental disturbance of permanent tooth bud at the age of 2 years. The crown of the primary incisor is displaced buccally, forcing the root into the crown of the developing permanent incisor.

k.  Figure 18.11 Procedure for examination of a young child’s mouth (see text).

l.    Figure 18.12 (a) Fractured roots of both central incisors with dislocation of the coronal fragments. (b) Normal resorption of the apical fragments after removal of the coronal fragments.

m.   Figure 18.13 Severe soft tissue damage with extensive hemorrhage. Both central incisors and the right lateral incisor are extruded and extremely mobile.

n.  Figure 18.14 (a) Severe palatal luxation of the right central incisor. No treatment other than observation was performed. (b) Two months later, the tooth is back in normal position due to tongue pressure.

o.  Figure 18.15 Clinical condition immediately after buccal displacement of the left central incisor in an 8‐month‐old girl.

p.  Figure 18.16 (a) Clinical examination after trauma of an 18‐month‐old child. The parents assumed that the right central incisor was lost. (b) The radiograph reveals severe intrusive luxation. Additional radiographs should be taken to disclose the exact direction of the intrusion (see Figure 18.6).

q.  Figure 18.17 (a) Condition immediately after intrusive luxation of both central incisors. (b) Re‐eruption is evident 6 months later.

r.   Figure 18.18 Uncomplicated crown fracture involving either mesial corners or entire incisal edge. The gingival bleeding indicates that intrusive luxation has also occurred in the right central incisor.

s.   Figure 18.19 (a) Both subluxation and uncomplicated crown fracture have occurred in the left central incisor. (b) The tooth is stabilized with a splint, and a temporary crown restoration is applied.

t.    Figure 18.20 (a) Enamel–dentin fracture of the left central incisor in an 8‐year‐old boy. (b) The fractured crown fragment. (c) Condition immediately after reattachment of the fragment.

u.  Figure 18.21 (a) A 12‐year‐old girl with enamel–dentin fracture of the left central incisor. (b) Condition shortly after the composite crown build‐up.

v.  Figure 18.22 Right central incisor with a small pulpal exposure, but with loosening and marked tenderness to percussion. Partial pulpotomy was decided to be the treatment of choice.

w.   Figure 18.23 Crown–root fracture of the left lateral incisor. (a) Buccally, the fracture line is located close to the gingival margin. (b) The radiograph only demonstrates the position of the buccal part of the fracture, whereas the palatal part cannot be seen.

x.  Figure 18.24 (a) Root fracture in the right central incisor with severe dislocation of the coronal fragment. (b) Optimal repositioning performed within 1 hour. (c) Condition 1 year later, with normal findings in the fracture area and partial pulp canal obliteration.

y.  Figure 18.25 (a) Subluxation of both central incisors with mobility in both the horizontal and vertical directions. (b) The teeth are stabilized with an orthodontic twisted wire, resin material, and the acid‐etch technique (see Box 18.7).

z.  Figure 18.26 (a) Extrusive luxation of the right central incisor. The tooth appears elongated and is also very mobile. (b) The radiograph shows increased periodontal width apically. (c) A radiograph taken after repositioning illustrates optimal position of the tooth in its socket.

aa.  Figure 18.27 Palatal luxation of the crown. The apex is forced through the buccal bone. Repositioning requires disengagement of the tooth from its bony lock. Apply firm digital pressure in an incisal direction, and move the tooth back through the fenestration into the socket. Thereafter, axial pressure will bring the tooth back to its original position.

bb. Figure 18.28 Resin splint (Protemp®) applied after surgical repositioning of severely intruded left central incisor.

cc.  Figure 18.29 Complete intrusion of the left central incisor in a 9‐year‐old boy. (a) The incisal edge is barely visible 5 days after the accident. It was decided to await re‐eruption. (b) Partial re‐eruption is evident a month later. (c) Complete re‐eruption 10 months after trauma. (Delayed eruption of the right incisor is due to a supernumerary tooth.)

dd. Figure 18.30 (a) A 10‐year‐old girl with avulsion of the left central incisor after a skiing accident. The tooth was found in the snow 4 hours later. (b, c) The avulsed tooth is replaced in the socket with gentle finger pressure and a splint is applied.

ee.  Figure 18.31 Successful replantation of the left central incisor in a 7‐year‐old boy. The avulsed tooth was immediately pushed back in place by the boy’s father. (a, b) Six days and 1 year after replantation, respectively. (c) Four years after the accident with completed root formation and almost total pulp canal obliteration. Note also obliteration in the right central incisor after a subluxation injury.

ff. Figure 18.32 Frequency of dental and other sports injuries per 10,000 people from 1981 to 1983 in Norway.

gg. Figure 18.33 www.dentaltraumaguide.org.

18. Chapter 19

a.  Figure 19.1 Later wound healing events; macrophages (m) form the healing front, followed by endothelial cells (e) and fibroblasts (f).

b.  Figure 19.2 Nature of trauma in the case of separation injury.

c.  Figure 19.3 Nature of trauma in the case of crushing injury.

d.  Figure 19.4 Severe malformation of permanent lateral incisor following intrusive luxation of predecessor at the age of 2 years. (a) Condition 1 year after trauma. (b,c) Further development of deformed incisor and uncomplicated eruption, respectively.

e.  Figure 19.5 (a) Radiograph taken 1 week after slight intrusive luxation of right central incisor. (b) Three months after the trauma there is marked periapical inflammation (arrows).

f.   Figure 19.6 Subluxation of both central incisors leading to pulp canal obliteration. (a) At time of injury. (b) Two years later, there is almost total obliteration of the pulps.

g.  Figure 19.7 Disturbance of development of permanent tooth bud due to intrusion of primary incisor. Due to laceration of the follicle, disturbances in enamel formation will develop.

h.  Figure 19.8 Enamel defects in three mandibular incisors (arrows) resulting from avulsion of corresponding predecessors at the age of 2 years.

i.    Figure 19.9 External enamel hypoplasia of right central incisor caused by intrusion of predecessor at the age of 18 months. The hypoplastic area is covered with composite.

j.    Figure 19.10 A simplified model of the different stages of amelogenesis. The secretory stage where the ameloblasts are secreting the enamel matrix and the early and late maturation fases where the enamel crystals are growing and the mineral content reaches 96% prior to tooth eruption. The reduced enamel epithelium is fusing with the oral epithelium when the tooth is erupting.

k.  Figure 19.11 (a) Intrusive luxation of immature right central incisor. (b) Spontaneous re‐eruption, closure of apical foramen, and pulp canal obliteration have occurred.

l.    Figure 19.12 Partial pulp canal obliteration in left central incisor. (a) At time of injury. (b) Condition 15 years later. Pulp chamber completely obliterated and root canal slightly reduced in size (arrow).

m.   Figure 19.13 Obliteration after successful replantation of right central incisor. The tooth was replanted within a few minutes. (a) Normal findings 3 weeks later. (b) A radiograph taken 6 months later shows apical closure. (c) Seven years after replantation, there is total pulp canal obliteration and no sign of root resorption.

n.  Figure 19.14 (a) Left central incisor in 10‐year‐old boy discolored within 1 week after subluxation injury. (b) Three months later. Discoloration has disappeared and the tooth responds normally to electrometric pulp testing.

o.  Figure 19.15 Pulp necrosis of right central incisor following intrusion. (a) Re‐eruption took place 3 months after injury. (b) No further root development. Hard tissue formation (arrow) is found together with continued vitality. (c) Pulp necrosis is diagnosed from a periapical radiolucency (arrow), which developed 1 year after injury.

p.  Figure 19.16 Spontaneous root fracture of nonvital immature central incisor. (a, b) During long‐term treatment with calcium hydroxide. (c) The fracture was observed 1 year after completed endodontic treatment.

q.  Figure 19.17 External repair related resorption along the root surface and the apex of an extruded central incisor. (a‐c) Clinical and radiographic appearance at the time of injury. (d‐f) Repair related resorption is diagnosed after one year (arrows).

r.   Figure 19.18 External infection‐related root resorption along root surface of an intruded lateral incisor. (a) Six weeks after injury. (b) During endodontic treatment, the pulp cavity was temporarily filled with calcium hydroxide. Persistent defects are seen on the root surface (arrows), but no further progression has taken place.

s.   Figure 19.19 External infection‐related root resorption following intrusive luxation of a right central incisor. (a) An area of resorption (arrow) was seen 8 weeks after injury. The pulp canal was temporarily filled with calcium hydroxide. (b) Two years later, there is a persistent defect (arrow), but no further progression of resorption.

t.    Figure 19.20 Progression of replacement resorption after avulsion and subsequent replantation of left lateral incisor. (a–c) Radiographs taken 6 months, 2 and 4 years after injury. (d) Condition at time of removal of lateral incisor 7 years after replantation.

u.  Figure 19.21 Infraposition of a left central incisor due to replacement resorption (ankylosis).

v.  Figure 19.22 Radiographs and diagrams illustrating various modalities of healing after root fractures. (a) Healing with calcified tissue. (b) Interposition of connective tissue. (c) Interposition of bone and connective tissue. (d) Interposition of granulation tissue.

w.   Figure 19.23 Root fractures of both central incisors. (a) Retained pulpal vitality and calcified tissue repair in the right incisor, whereas radiolucency corresponding to fracture line (arrow) indicates necrosis in the left incisor. (b) Two years after completed root filling of left incisor PDL union between segments is evident.

x.  Figure 19.24 Successful replantation of a left central incisor (arrows). The tooth was stored in the mouth of the child’s mother for 45 min. (a–c) Radiographs taken before, 12 days and 6 months after replantation, respectively. (d) One year after injury, with continued root development and narrowing of pulp canal.

19. Chapter 20

a.  Figure 20.1 Perikymata shown as horizontal lines on buccal surfaces of central incisors. White, opaque patches and lines represent enamel disturbances (mild dental fluorosis). Seven‐year‐old child.

b.  Figure 20.2 Schematic representation of hemi‐sectioned tooth with incremental lines in enamel. SEM images show perikymata on the enamel surface (a) and striae of Retzius (arrows) and cross‐striations of enamel prisms (arrowheads) in an acid‐etched longitudinal section (b). Prism cross‐striations indicate a daily rhythm while striae of Retzius indicate a longer (about 7–10 days) rhythm in enamel formation. Perikymata are the surface representations of the striae of Retzius and run horizontally around the tooth. Prism‐free enamel (PFE) is shown close to enamel surface. P = prism.

c.  Figure 20.3 Schematic overview showing a systematic approach to the collection of data and classification of findings related to developmental disturbances of the dental hard tissues.

d.  Figure 20.4 Classification and examples of types of enamel defects due to disturbances in the tooth formation. The natural appearance of the incisor 21 (a) is manipulated to illustrate (b) demarcated opacity (white), (c) diffuse opacities (white) with no well‐defined margins, (d) discolored enamel which has some translucency, (e) single hypoplasia (single deep pit), (f) multiple hypoplastic defects, and (g) posteruptive breakdown due to hypomineralized enamel. Note that very often in cases with enamel defects, several teeth in the dentition will be affected.

e.  Figure 20.5 Hypoplasia and opacity of permanent maxillary left central incisor due to intrusion trauma of primary incisor at the age of 30 months (the child is now 10 years old).

f.   Figure 20.6 Dental mutilation resulting in (a) hypoplasia with exposure of dentin of the right lower permanent canine and (b) absence of the left lower permanent canine due to removal of the tooth germ (germectomy). (c) Panoramic radiograph shows absence of the permanent left canine. (d) Radiograph of the right lower permanent canine shows apparently normal development of the root despite the malformed tooth crown due to the damage previously performed towards the tooth germ. (e) Intraoral radiograph of a malformed and hypoplastic permanent mandibular canine in a 14‐year‐old Ethiopian girl as a result of dental mutilation. An odontoma on the root surface and periapical destruction are present.

g.  Figure 20.7 Erupting defective 24 in a 6‐year‐old girl who had 64 extracted 6 months earlier. The extracted tooth had a longstanding, chronic periapical periodontitis.

h.  Figure 20.8 Arrested root development in a 13‐year‐old girl who was treated by irradiation (50.4 Gy/28 fractions) at age 6 because of rhabdomyosarcoma in the pharynx.

i.    Figure 20.9 Neonatal lines of dentin (left) and enamel (right) demarcate the respective hard tissues formed/mineralized before and after birth.

j.    Figure 20.10 Hypoplasia of enamel of a preterm child.

k.  Figure 20.11 A 7‐year old child with pigmentation in both primary and permanent teeth due to bilirubine deposits in teeth caused by biliary atresia in early life.

l.    Figure 20.12 (a) A 14‐year‐old girl with cystic fibrosis who was treated with repeated courses of tetracyclines for recurrent chest infection. (b) Histologic sections of a tooth showing the bands of tetracycline staining.

m.   Figure 20.13 Mild fluorosis in a 15‐year‐old girl.

n.  Figure 20.14 Dental fluorosis with posteruptive breakdown of the enamel and tooth wear in a 12‐year‐old boy with natural high (≈5 ppm) fluoride concentration in the drinking water.

o.  Figure 20.15 (a) Mild dental fluorosis in a 14‐year‐old girl. (b) The surface is rubbed using a wooden pin with 18% hydrochloric acid in pumice. (c) The surfaces are covered by 2% sodium fluoride gel. (d) Treatment result.

p.  Figure 20.16 Porcelain veneers in a 13‐year‐old girl with moderate dental fluorosis.

q.  Figure 20.17 Molar–incisor hypomineralization in an 8‐year‐old boy showing different manifestations in similar teeth: (a) 16 with a defective restoration; (b) 26 with seriously disintegrated enamel and caries; the tooth is very sensitive and toothbrushing is impossible; (c) 46 healthy; (d) 36 disintegrated enamel, but no frank cavitation; (e) demarcated white opacities in the upper front teeth.

r.   Figure 20.18 X‐ray micro‐computed tomography image of a MIH tooth. The more opaque areas represent hypomineralized enamel.

s.   Figure 20.19 (a) A severely hypomineralized lower first molar is erupting. Normal morphology. (b) Heavy disintegration 6 months later.

t.    Figure 20.20 Scanning electron microscopy. The cut surface has been etched with 30% phosphoric acid for 30 s. (a) Normally mineralized enamel. (b) Hypomineralized enamel. (c) The border between normal and hypomineralized enamel.

u.  Figure 20.21 (a) An 8‐year‐old girl with an MIH‐affected molar to be restored. Porous, soft enamel was removed by a bur until hard, sound enamel appeared. (b) After acid etch of the cavity walls, dentin–enamel bonding agent was applied and the tooth was restored with composite.

v.  Figure 20.22 (a) A 13‐year‐old boy with MIH. (b) Enamel disintegration in 11 was restored with a porcelain veneer.

w.   Figure 20.23 (a) Hypomineralized permanent first molars with opacities, posteruptive breakdown of enamel and insufficient conservative treatment, i.e., posteruptive enamel breakdown along the margins of composite fillings. (b) Treatment with cast‐gold copings after minimal preparation due to the scarce thickness required to be able to make a cast‐gold coping. (c) A cast‐gold coping on the cast. (d) The cast‐gold coping can be made with surface roughening by use of sugar crystal impression method with the purpose of improving the retention.

x.  Figure 20.24 Clinical manifestation of amelogenesis imperfecta. (a) Hypomaturation type (generalized white opacities with brownish discolorations on upper central incisors). (b) Hypomaturation type (generalized yellowish opacities). (c) Hypomaturation type, mixed dentition. Chipping of enamel. (d) Hypocalcified type. (e) Hypoplastic type (rough, pitted). (f) Hypoplastic type (rough, vertical grooves). (g) Hypoplastic type (rough, thin enamel) (h) Combination of hypomaturation and hypoplastic type (g) and (h)

y.  Figure 20.25 Hypocalcified amelogenesis imperfecta (AI) in the primary dentition of a 3‐year‐old girl.

z.  Figure 20.26 (a1) A 9‐year‐old girl with AI (hypoplastic type). (a2) Same girl at the age of 14 years. Maxillary incisors restored with ceramic veneers. (b1) Dentition of a 12‐year‐old boy with AI (hypocalcified type) before orthodontic treatment and placement of crowns. (b2) Same boy at the age of 20 years with single metalloceramic crowns in the mandible and single conventional gold crowns with composite facades in the maxillary teeth

aa.  Figure 20.27 A boy with teeth affected by hypocalcified AI: (a) 3.5 years, problems with sensitivity and chipping of enamel; (b) 3.5 years, the molars are restored by stainless‐steel crowns; (c, d) 9 years, time for dressing the permanent molars with steel crowns due to chipping and attrition of enamel.

bb. Figure 20.28 Treatment of hypoplastic, rough pitted AI. (a) Prior to treatment, (b) pits are cleaned by the bur, (c) etching, and (d) the teeth are dressed with flowable composite.

cc.  Figure 20.29 A 5‐year‐old child with DI showing extreme tooth wear in the primary molars. No operative treatment has been offered so far, although the child would have benefited from stainless‐steel crowns in the molar regions to keep the occlusion. Permanent lower central incisors are in eruption.

dd. Figure 20.30 Panoramic radiograph of a 10‐year‐old boy with DI inherited as a single trait (type II). Note the obliterated pulp chambers and the cervical constrictions of the crowns.

ee.  Figure 20.31 Osteogenesis imperfecta. (a) Blue sclerae in a 4‐year‐old boy. (b) Characteristic dentin defect (DI type I) in the same boy.

ff. Figure 20.32 A boy with DI type II. (a) Mandibular teeth at the age of 3 years 5 months. The primary left second molar was infected due to attrition and had to be extracted. Stainless‐steel crowns have been made to prevent further attrition. (b) The permanent molars have been fitted with stainless‐steel crowns and the incisors with laboratory‐made composite crowns (c) Same patient at the age of 10 years 4 months

gg. Figure 20.33 Dentin dysplasia type II. (a) A 3‐year‐old boy with DD type II. (b) Panoramic radiograph showing pulpal obliteration in the primary molars. (c) Radiograph of the mother showing characteristic thistle‐tube‐shaped pulp chambers and narrowed root canals.

hh. Figure 20.34 Vitamin D deficiency rickets (nutritional rickets). (a–c) Chronological and symmetrical hypoplasia in permanent incisors and first molars in a breastfed 8‐year‐old boy who was not given a vitamin D supplement in the first year of life. (d) Defects can often be seen on a panoramic radiograph. (e) An 11‐year‐old boy with severe hypoplasia on upper permanent incisors due to vitamin D deficiency rickets. Often cusp tips of permanent canines are affected.

ii.  Figure 20.35 Familial hypophosphatemia. (a) A 6‐year‐old boy with several infected primary teeth. (b) Radiograph of mandibular primary teeth in a 4‐year‐old boy. Note the enlarged pulp chambers. (c) Microradiograph of a primary molar. Note the enlarged pulp chamber and pulp horns extending to dentino–enamel junction. Defective circumpulpal dentin, mantle dentin seemingly normal. (d) Panoramic radiograph showing periapical radiolucency in the lower incisor region and two lower incisors that have already been endodontically treated in a 14‐year‐old boy. Note also the enlarged pulp chambers and the extended pulp horns in the permanent dentition. (e) Clinical picture of the lower jaw of the same 14‐year‐old boy.

jj.  Figure 20.36 A 7‐year‐old boy with damage of permanent maxillary teeth after localized, high‐dose radiation (56 Gy) at 3.5 years of age due to a tumor in the right maxilla. Very short roots in permanent teeth are seen in the affected area.

kk. Figure 20.37 Hypophosphatasia. (a) A 3‐year‐old boy with a benign form of hypophosphatasia. Mandibular right central incisor is poorly attached and mobile. (b) Radiograph of incisor teeth showing severe alveolar bone loss in the lower incisor region. (c) Histologic section showing thin cementum on the root surface.

ll.  Figure 20.38 Regional odontodysplasia. (a) Malformed teeth in the lower right quadrant in a 3‐year‐old boy. An abscessed incisor is seen. (b) Dental treatment under general anesthesia consisted of extraction of all teeth in the lower right quadrant except a more robust lower right second primary molar which would contribute in maintenance of the functional height of the primary dentition and in continuation of some alveolar growth in the region. (c) First primary molar after tooth extraction showing enamel hypoplasia of the tooth crown. (d) The complete tooth is fragile, and the amount of tooth substance is scarce. The root complex has an open apex, and the pulp chamber is abnormally large. (e) A denture was inserted when the boy was 4 years old. As seen on the picture where the child is 6 years old, the denture may need adjustment when primary teeth are gradually lost due to shedding. (f) Panoramic radiograph shows that the successors are also affected. The denture was in place when the radiograph was taken as the retentive elements are visible on the photograph.

mm.             Figure 20.39 Regional odontodysplasia. (a) Abscessed incisors in the maxillary left quadrant. (b) Panoramic radiograph shows involvement of all the teeth in the quadrant. (c) The child was treated by extraction of the affected teeth except the permanent first molar, which was thought to maintain some alveolar growth in the region. The maxillary partial denture was placed after extractions at the age of 3 years.

20. Chapter 21

a.  Figure 21.1 Changes in body proportions during development and growth.

b.  Figure 21.2 Changes in proportions of the head.

c.  Figure 21.3 Facial growth in a normal girl from 2 months to 5 years 2 months of age. Superimposition was made on the nasion–sella line registered at sella. Note the magnitude of mandibular growth from a marked retruded position.

d.  Figure 21.4 With a mesial step in the terminal plane of the primary dentition, the permanent molars may erupt directly into normal occlusion (left). If the primary dental arches end in the same vertical plane, the permanent molars will erupt into a cusp‐to‐cusp relation (right).

e.  Figure 21.5 The permanent maxillary incisors erupt at a more labial inclination than their primary predecessors. Consequently, the dental arch becomes wider and longer.

f.   Figure 21.6 The primary canines and molars occupy more space than is necessary for the corresponding group of permanent teeth. The difference is called the “leeway space” and is greater in the mandible (2.5 mm) than in the maxilla (1.5 mm).

g.  Figure 21.7 Posterior cross bite (patient’s left side), midline deviation and mandibular lateral shift, and frontal open bite in a dummy sucker.

h.  Figure 21.8 Results of finger sucking. Asymmetrical left side open bite and overjet.

i.    Figure 21.9 Bilateral scissors bite in combination with forced distal occlusion.

j.    Figure 21.10 Skeletal class III malocclusion without compensation. Note mesial relations between canines.

k.  Figure 21.11 Dentoalveolar anterior cross bite.

l.    Figure 21.12 Unilateral scissors bite in the primary dentition.

m.   Figure 21.13 Forced posterior cross bite. The jaws are symmetrical, but the maxillary jaw is narrow. In the retruded position, the molars occlude cusp‐to‐cusp (a). Full occlusion needs forcing of the bite to the left (b).

n.  Figure 21.14 “Classical” unilateral posterior cross bite. Narrow maxilla with the mandibular midline forced to the cross bite side. Note lack of space in the maxilla.

o.  Figure 21.15 (a) Incompetent lip closure, (b) maxillary overjet, incisor proclination, distal occlusion, and (c) deep bite is a common combination.

p.  Figure 21.16 Dentoalveolar frontal open bite.

q.  Figure 21.17 (a) Unilateral cross bite in the early mixed dentition. (b) Note the narrow maxilla in retruded position which needs active transversal expansion.

r.   Figure 21.18 Radiograph showing two mesiodens as the cause of large median diastema.

s.   Figure 21.19 Boy at 18 years of age with persisting 85 and agenesis of 45. The tooth is in good condition and may continue functioning for many years.

t.    Figure 21.20 Early extraction (a, b) of the primary canine may spontaneously change the path of eruption (c) of palatal ectopic maxillary canines.

u.  Figure 21.21 Ankylosis of primary molars resulting in infraposition of 75 (secondary retention) and tipping of 36.

v.  Figure 21.22 Persisting 65 due to a slight ectopic position of 25. The buccal roots are resorbed, while the palatal root is still intact.

w.   Figure 21.23 (a, b) Ectopic eruption of 26.

x.  Figure 21.24 Ectopic eruption of 13,23 has almost completely destroyed the roots of 12,22 and also resorbed the roots of 11,21. Extraction of 12,22 was needed.

y.  Figure 21.25 Same case as in Figure 21.24 after extraction of 12,22 and orthodontic treatment and grinding of canine cusps.

z.  Figure 21.26 Removable appliance for frontal expansion of the maxillary front.

21. Chapter 22

a.  Figure 22.1 Diagrams showing prevalence of one or more (a) subjective symptoms and (b) clinical signs of TMD presented in different epidemiologic studies of children and adolescents. The single dots represent the prevalence figure found in different studies. Note the wide variations within the same age groups, ranging from single percent to more than 70%.

b.  Figure 22.2 Measurement of maximal jaw opening capacity.

c.  Figure 22.3 Bilateral palpation of the lateral aspects of the TMJs.

d.  Figure 22.4 Palpation of the anterior part of the superficial portion of the right masseter muscle.

e.  Figure 22.5 Schematic illustration of the apparent paradoxical peripheral delineation of the condylar heads of normal and pathologic joints in the child and the adult. A normal delineation of the condylar head of a child (1) has characteristics in common with that of a pathologic adult TMJ (4) and the pathologic condylar head of a child (2) with that of a normal adult (3).

f.   Figure 22.6 Examples of therapeutic jaw exercises. (a) Active jaw opening against a slight resistance. (b) Active lateral excursion to the right against a slight resistance.

g.  Figure 22.7 Soft interocclusal appliance placed in the mandible.

h.  Figure 22.8 (a) A 12‐year‐old girl in whom the canines in the maxilla are not completely erupted. (b) She is provided with a hard acrylic appliance (Shore‐plate), where the acrylic is removed in the region of the canines to allow further eruption. (c) A 7‐year‐old boy with a mixed dentition and a deep bite. Severe bruxism and frequent headaches. (d) He is provided with a hard acrylic bite‐plate to prevent the teeth from further wear, to unload the jaw muscles, and eventually to decrease the deep bite.

22. Chapter 23

a.  Figure 23.1 A 3‐year‐old boy with cerebral palsy and showing severe gingival overgrowth.

b.  Figure 23.2 (a) A 10‐year‐old girl on phenytoin medication exhibiting severe gingival overgrowth. (b) At 13 years of age, exhibiting a normal gingival 1 year after gingivectomy and discontinuation of phenytoin medication.

c.  Figure 23.3 (a) A 15‐year‐old boy with aplastic anemia prescribed cyclosporine medication. (b) At 18 years of age, deteriorating gingival health coincidental with a hematological crisis.

d.  Figure 23.4 A 14‐year‐old girl with restricted and asymmetric growth of the mandible due to unilateral TMJ arthritis in her right side.

e.  Figure 23.5 A 9‐year‐old boy with a congenital HIV infection exhibiting periodontal disease.

f.   Figure 23.6 A 3‐year‐old boy with a malabsorption syndrome with daily vomiting and regurgitation. Note erosive change on anterior teeth.

g.  Figure 23.7 A 16‐year‐old boy with severe obesity exhibiting high caries activity and extensive gingivitis.

h.  Figure 23.8 Discoloration and enamel hypomineralization in a 14‐year‐old boy with cystic fibrosis.

i.    Figure 23.9 A 12‐year‐old boy with immunoglobulin A and G deficiency exhibiting ulceration of the marginal gingiva.

j.    Figure 23.10 Panoramic radiograph showing severe periodontal breakdown in a 6‐year‐old boy with cyclic neutropenia.

k.  Figure 23.11 (a) Blistering of hand and fingers in a 10‐year old boy with dystrophic epidermolysis bullosa. (b) Oral blistering and scarring in a 1‐month‐old boy with dystrophic epidermolysis bullosa.

l.    Figure 23.12 Severe oral ulceration in a 5‐year‐old boy during induction chemotherapy for acute lymphoblastic leukemia.

m.   Figure 23.13 (a) Panoramic radiograph showing premature apical closure of permanent first molars in an 8‐year‐old boy treated with 10 Gy total body irradiation at 5 years of age. (b) At 17 years of age, all permanent teeth exhibit short V‐shaped roots.

23. Chapter 24

a.  Figure 24.1 The ICF theoretical, biopsychosocial model defines functioning and disabilities in relation to outcomes between the health conditions of a person and the context in which they operate. This context is defined at three levels of functioning, at the level of a body part, at the level of the whole individual, and the functioning that occurs at the level of society.

b.  Figure 24.2 Examples of photographs that can be used as pedagogic tools in patients with neuropsychiatric disorders. Based on individual needs: pictures showing the entrance, the dental chair, the operatory light, a toothbrush, a mirror and an open mouth (symbolizing “open your mouth”) were chosen in this case. The photos can be put in sequence in a photo album.

c.  Figure 24.3 Large, fissured tongue of a boy with Down syndrome.

d.  Figure 24.4 Drooling in a child with cerebral palsy.

e.  Figure 24.5 A vacuum‐moulded splint in place to prevent further self‐mutilation in a child with cerebral palsy (note calculus as a consequence of nil‐by‐mouth PEG feeding).

f.   Figure 24.6 (a) A prop, with and without an occlusal “guard”, and (b) in use.

g.  Figure 24.7 A finger brush that can be used for gentle cleaning of the child’s teeth and/or for oral motor stimulation.

h.  Figure 24.8 A Superbrush® on the left and two Collis Curve® brushes on the right.

i.    Figure 24.9 A prop to facilitate brushing.

j.    Figure 24.10 A “touchette” or sponge stick for cleaning mouths.

k.  Figure 24.11 Body cushions to give support to a child during treatment.

l.    Figure 24.12 (a) An oral screen; (b) a patient training with an oral screen by straining lip muscles and pulling the screen out with a light, balanced force.

m.   Figure 24.13 Palatal plates used for oral motor training in children.

24. Chapter 25

a.  Figure 25.1 Infant with Robin sequence and cleft palate showing marked hypoplasia of the mandible.

b.  Figure 25.2 A child with fetal alcohol syndrome. Note the small palpebral fissures, short nose, flat philtrum, and thin upper lip.

c.  Figure 25.3 A 2‐year‐old girl with Münke syndrome and unicoronal synostosis. Note the marked craniofacial asymmetry.

d.  Figure 25.4 A 5‐year‐old girl with Apert syndrome. Note hypertelorism, short nose, trapezoidal shape of mouth, and midface hypoplasia.

e.  Figure 25.5 Symmetrical syndactyly of (a) hands and (b) feet in a 5‐year‐old girl with Apert syndrome. Early hand surgery was performed to release fingers 2 and 5.

f.   Figure 25.6 Skull X‐ray of a 5‐year‐old girl with Apert syndrome. Note craniosynostosis, hyperbrachycephaly, midface hypoplasia, and constriction of the nasopharyngeal airway.

g.  Figure 25.7 A 2‐year‐old boy with Crouzon syndrome. Note hypertelorism, ocular proptosis, and midface hypoplasia.

h.  Figure 25.8 A 3D CT‐scanning of an infant with Crouzon syndrome with acanthosis nigricans. (a) Frontal view showing facial soft‐tissue morphology with hypertelorism, ocular proptosis, and midfacial hypoplasia. (b) Frontal view showing a wide calvarial midline defect. (c) Lateral view showing synostosis of the coronal and the lambdoid sutures and hyperbrachycephaly.

i.    Figure 25.9 A 5‐year‐old girl with Treacher Collins syndrome. Note the downslanting palpebral fissures, colobomas of the lower eyelids, mandibular hypoplasia, and microtia.

25. Chapter 26

a.  Figure 26.1 Gripping a child’s cheeks during forced feeding will leave an impression of the thumb on one cheek and impressions of the four other fingers on the other cheek.

b.  Figure 26.2 Slap marks on the cheek. The fingers of the hand will leave impressions. Petechial bruising at a finger width spacing. Marks form between the fingers on the slapped area.

c.  Figure 26.3 Helpful illustrations to distinguish (a) accidental injuries from (b) non‐accidental injuries.

d.  Figure 26.4 Flowchart of how to manage a suspicion of child maltreatment

26. Chapter 27

a.  Figure 27.1 The level of autonomy varies throughout life depending on the individual’s capacity, while integrity remains complete during the whole lifespan. The graph depicts how autonomy varies depending on the situation.

b.  Figure 27.2 Scheme for an ethical analysis. The ethical principles respect for autonomy, beneficence–maleficence, and justice should be discussed from different perspectives: that of the child, parents, dental team, and society. The analysis is made following the boxes from A to L starting with the perspective of the child and respect for autonomy in box A. Here the dentist assesses the pros and cons of carrying out a treatment or not and sums up the results in A. Thereafter beneficence–maleficence is assessed. After the perspective of the child, the dentist moves on to the perspective of the parents. Finally, all pros and cons are weighed together thereby giving a guide for decision‐making and treatment.