Pit and Fissure Sealants: Scientifc and Clinical Rationale










418 Part 4 The Transitional Years: Six to Twelve Years
19. Marshall TA, Eichenberger-Gilmore JM, Larson MA, et al. Comparison
of the intakes of sugars by young children with and without caries
experience. J Am Dent Assoc. 2007;138:39–46.
20. Sheiham A, James WPT. Diet and dental caries: the pivotal role of
free sugars reemphasized. J Dent Res. 2015;94(10):1341–1347.
21. Holbrook WP, Arnadottir IB, Takazoe I, et al. Longitudinal study
of caries, cariogenic bacteria and diet in children just before and after
starting school. Eur J Oral Sci. 1995;103(1):42–45.
22. Ismail AI, Burt BA, Eklund SA. e cariogenicity of soft drinks in
the United States. J Am Dent Assoc. 1984;109:241–245.
23. Bibby BG. Fruits and vegetables and dental caries. Clin Prev Dent.
1983;5:3–11.
24. Kashket S, van Houte J, Lopez LR, et al. Lack of correlation between
food retention on the human dentition and consumer perception of
food stickiness. J Dent Res. 1991;70:1314–1319.
25. Luke GA, Hough H, Beeley JA, et al. Human salivary sugar clearance
after sugar rinses and intake of foodstus. Caries Res. 1999;33:123–129.
26. Rugg-Gunn AJ. Nutrition and Dental Health. Oxford: Oxford Medical
Publications; 1993.
27. Nizel AE, Harris RS. e eects of phosphate on experimental dental
caries: a literature review. J Dent Res. 1964;43:1123–1136.
28. Lilienthal B. Phosphates and dental caries. In: Myers H, ed. Monographs
in Oral Science. Basel, Switzerland: Karger; 1976.
29. Featherstone JDB, Mundor SA. Identication of the Cariogenic
Elements of Foods. Final report for period September 1981–May 1984.
Alexandria, VA: National Technical Information Service; 1984.
30. Mundor SA, Glowinsky D, Grin C. Fluoridated sucrose eect
on rat caries. J Dent Res. 1986;65(special issue):282(abstract 1017).
31. Caldwell RC. Physical properties of foods and their caries-producing
potential. J Dent Res. 1970;49:1293–1298.
32. Stookey GK. Developing the perfect snack food. In: Alfano MC, ed.
Changing Perspectives in Nutrition and Caries Research. New York:
Medcom; 1979.
33. Moynihan PJ, Kelley SAM. Eect on caries of restricting sugars
intake: systematic review to inform WHO guidelines. J Dent Res.
2014;93(1):8–18.
34. Meyer BD, Lee JY. e conuence of sugar, dental caries, and health
policy. J Dent Res. 2015;94(10):1338–1340.
35. Edelstein BL, Ng MW. Chronic disease management of strategies
of early childhood caries: support from the medical and dental lit-
erature. Pediatr Dent. 2015;37(3):281–287.
36. Ng MW, Fida Z. Early childhood caries prevention and management.
In: Berg JH, Slayton RL, eds. Early Childhood Oral Health. Hoboken,
NJ: John Wiley & Sons; 2016.
References
1. Kuczmarski RJ, Ogden CL, Guo SS, et al. CDC Growth Charts for
the United States: Methods and Development. Washington, DC: National
Center for Health Statistics; 2000.
2. Broadbent BH Sr, Broadbent BH Jr, Golden WH. Bolton Standards
of Developmental Growth. St Louis: Mosby; 1975.
3. Kapust AJ, Sinclair PM, Turley PK. Cephalometric eects of face
mask/expansion therapy in Class III children: a comparison of three
age groups. Am J Orthod Dentofacial Orthop. 1998;113(2):204–212.
4. Smith BH, Garn SM. Polymorphisms in eruption sequence of
permanent teeth in American children. Am J Phys Anthropol.
1987;74:289–303.
5. Broadbent BH. e face of the normal child. Angle Orthod.
1937;7:183–208.
6. Piaget J. e stages of the intellectual development of the child. In:
Marlowe BA, Canestrari AS, eds. Educational Psychology in Context:
Readings for Future Teachers. ousand Oaks, CA: Sage; 2006:98–106.
7. Eccles JS. e development of children ages 6 to 14. Future Child.
1999;9(2):30–44.
8. Stendler CB, Young N. Impact of rst grade entrance upon the
socialization of the child: changes after eight months of school. Child
Dev. 1951;22:113–122.
9. Dye BA, Lopez G, Mitnik MS, et al. Trends in dental caries in
children and adolescents according to poverty status in the United
States from 1999 through 2004 and 2011 through 2014. J Am Dent
Assoc. 2017;148:550–565.
10. Moynihan P, Petersen PE. Diet, nutrition and the prevention of
dental caries. Public Health Nutr. 2004;7(1A):201–226.
11. Newbrun E. Sucrose, the arch criminal of dental caries. J Dent Child.
1969;36:239–248.
12. Koulourides T, Bodden S, Keller S, et al. Cariogenicity of nine sugars
tested with and intraoral device in man. Caries Res. 1976;10:427–441.
13. Stephan RM. Eect of dierent types of human foods in dental
health of experimental animals. J Dent Res. 1966;45:1551–1561.
14. Gustafsson B, Quensel CE, Lanke L, et al. e Vipeholm dental
caries study: the eect of dierent carbohydrate intake on 436 individu-
als observed for ve years. Acta Odontol Scand. 1954;11:232–264.
15. Sullivan HR, Goldsworthy NE. Review and correlation of the data
presented in papers 1-6 (Hopewood House study). Aust Dent J.
1958;3:395–398.
16. Sullivan HR, Harris R. Hopewood House study 2. Observations on
oral conditions. Aust Dent J. 1958;3:311–317.
17. Walker ARP, Cleaton-Jones PE. Sugar intake and dental caries: where
do we stand? ASDC J Dent Child. 1989;56:30–35.
18. Burt BA, Pai S. Sugar consumption and caries risk: a systematic
review. J Dent Educ. 2001;65:1017–1023.

CHAPTER 30 The Dynamics of Change 418.e1
Case Study: Chronic Disease Management of
Caries
Man Wai Ng and Rosalyn M. Sulyanto
Ethan, an anxious 6-year-old, presents for recare with his mom. Eight
months ago, after bitewing radiographs identied interproximal caries on his
mandibular primary molars, Ethan required sedation for restorative
treatment. His mom was advised to help brush with uoride toothpaste twice
daily, oss, and limit sugary snacks and beverages.
Ethan cooperates for an examination, prophylaxis, uoride varnish (FV),
and bitewing radiographs. The clinical examination found partially erupted
permanent rst molars with heavy plaque and demineralization of the pits
and ssures. Radiographic assessment found intact restorations and new
incipient interproximal caries on the maxillary primary molars. Caries risk
assessment (CRA) found the following pertinent factors: Ethan (1) brushes in
the morning only without help, (2) does not oss, (3) drinks juice four times
daily and little water, and (4) eats fruit snacks at lunch.
Dental caries is a chronic disease that is signicantly inuenced by
social and behavioral factors. Because it is largely preventable and can be
controlled, there must be a better outcome for children like Ethan than a
potential lifetime of caries burden.
Chronic disease management (CDM) of dental caries is a science-based
approach that is tested in clinical practice to prevent and manage caries and
is separate and distinct from prevention and restorative treatment. Effective
CDM requires customized patient self-management of etiologic factors. An
important role of the dental team is to effectively engage the patient and
family to make the necessary lifestyle changes.
A CDM clinical protocol (Fig. E30.1 and Tables E30.1 and E30.2)
includes seven components: (1) CRA (2) effective communication,
Caries lesion
charting by
tooth surface
and activity
Remineralization
modalities
Self-management
goals
Recare intervals
based on
caries risk
Treatment based
on patient’s
clinical needs and
caregiver’s or
patient’s desires
Caries risk
assessment
Effective
communication
Figure E30.1 Chronic disease management of caries clinical proto-
col. (From DentaQuest Institute. Early Childhood Caries [ECC] Manage-
ment Efforts [website]; 2017. https://www.dentaquestinstitute.org/learn/
quality-improvement-initiatives/early-childhood-caries-ecc-manage-
ment-efforts. Accessed September 13, 2017.)
Caries risk assessment Performed in full or abbreviated format during each visit
Effective communication With permission, explain the caries process to parent; and use structured communication strategies such as:
• Fixing the cavities does not x the problem
• Without a change in diet and home care, new cavities and broken llings will result
• Change is hard and will not happen overnight
Visual aids such as ip charts and handouts may be used to guide conversations
Self-management goal
setting
Engage and coach parent to select one or two goals to work on until the next visit
Goals may include more frequent tooth brushing, topical uoride use, and specic diet modication strategies
Caries charting Use a charting system, such as ICDAS or ADA Caries, to:
• Documentcariesbytooth,surface,andactivity
• Monitordiseaseimprovementorprogression
Fluorides and other
remineralization strategies
Topical uorides, including over-the-counter toothpaste, prescription uoride toothpaste, and stannous uoride, as well
as xylitol and/or calcium phosphate products, can be offered
In-ofce silver diamine uoride treatment or uoride varnish applications can be offered
Restorative treatment Treatment options are presented based on each patient’s needs and parent’s desires, including:
• Conventionaltreatment(includinguseofpharmacologicmanagement)
• Interimtherapeuticrestorationsforcariescontrolandsealants
Risk-based recare intervals Patients are recommended to return for recare frequency based on their caries risk and desires:
• 1–3months(ifhighrisk)
• 3–6months(ifmediumrisk)
• 6–12months(iflowrisk)
At the recare/disease management visit, perform:
• Cariesriskassessment
• Self-managementgoalssetting/reassessed
• Examandcharting
• X-raysifindicated
• Silverdiamineuorideoruoridevarnish
Recare should be coordinated with restorative treatment whenever possible
ADA, American Dental Association; ICDAS, International Caries Detection and Assessment System.
Chronic Disease Management of Caries Clinical Protocol
TABLE
E30.1
Continued

418.e2 Part 4 The Transitional Years: Six to Twelve Years
(3) self-management goal (SMG) setting, (4) caries charting, (5) uorides and
other remineralizing strategies, (6) restorative treatment as needed and
desired by patient/family, and (7) risk-based recare periodicity.
Regularly assessing caries risk and providing support and coaching to
control risk factors are the cornerstones of CDM. Caries etiology is explained,
followed by coaching on SMG setting. Fig. E30.2 shows an example of an
SMG handout.
When asked about what is most important to her, Ethan’s mom states
that she does not wish him to have more cavities and to get upset when
having his teeth xed. She is advised that with positive changes in Ethan’s
diet and oral hygiene practices, the small new cavities can be brought under
control and restorative treatment may be deferred. These SMG strategies are
discussed: (1) limit juice and increase water intake, (2) replace with sugar
substitute, (3) help with brushing and use a prescription 5000 ppm uoride
toothpaste, (4) chew sugar-free gum and eat sugar-free snacks, not fruit
snacks. Ethan’s mother chooses 2 and 3. She also agrees to return for a
1-month recare visit to review CRA and SMGs, apply FV, and place sealants
on Ethan’s permanent molars.
CDM of caries strategies help patients to make changes that lead to
better outcomes and can fulll expectations of accountability (providing
payment incentives/disincentives for better performance such as through
value-based reimbursement) and transparency (publicly reporting
performance scores), which are now commonplace in medicine and will
become more familiar landscape to dentistry in the near future.
Questions
1. Why is the caries risk assessment tool inadequate as the only
component in chronic disease management counseling?
Answer: Effective management of dental caries requires the patient and
family to make necessary lifestyle changes. Regularly assessing caries
risk is necessary but insufcient to improving the dental health of
patients. The dental care team has an important role to develop an
individualized care plan and provide meaningful coaching to patients and
families to mitigate specic responsible risk factors while enhancing
protective factors.
2. Should the dentist discuss chronic disease management strategies with
a new patient without caries? Why?
Answer: An important goal of an infant oral health visit or a new dental
visit for a patient without caries is to prevent caries development. Timely
assessment of causative risk factors (e.g., dietary factors, plaque
accumulation, and inadequate uoride exposure) and optimization of
protective factors can be expected to reduce the incidence of caries. The
dental care team should provide education, counseling, and a prevention
plan to address the risk factors that are specic to each patient and
family.
3. Why is a 6-month recall periodicity inappropriate for every patient?
Answer: Because lifestyle changes are hard to make and sustain, high
caries risk patients would benet from receiving more frequent
assessment of risk factors, self-management support and coaching, and
uoride varnish treatments. Whenever possible, these activities should be
coordinated with restorative and other preventive treatment.
Existing Risk
Category New Clinical Findings
Fluoride Varnish
Interval
a
Sample Self-
Management Goals
Restorative
Treatment
DM Return
Interval Other
Low No disease indicators
b
of
caries; or
Completely remineralized
(arrested) carious
lesions
6–12months Twice daily brushing
with F toothpaste
c
6–12months
Medium No disease indicators
b
but
has risk factors
d
; and/or
inadequate protective
factors
e
Disease indicators present
with some
remineralization
3–6months Twice or more daily
brushing with F
toothpaste
c
or
5000 ppm F toothpaste
Dietary changes
Sealants
ITR
Conventional
restorative
3–6months Xylitolorsorbitolgum
or candies or
wipes
Calcium phosphate
paste
High Active caries (disease
indicators present)
No remineralization
occurring
Heavy plaque
1–3months Twice or more daily
brushing with F
toothpaste
c
or
5000 ppm F toothpaste
Dietary changes
ITR
Sealants
Conventional
restorative
Sedation/GA
1–3months Xylitolorsorbitolgum
or candies
Calcium phosphate
paste
a
May use silver diamine uoride instead of uoride varnish.
b
Examples of disease indicators include demineralization, cavitated lesions, existing restorations, enamel defects, deep pits, and ssures.
c
Brush with a smear of 1000 ppm F toothpaste.
d
Examples of risk factors include patient/maternal/family history of decay, plaque on teeth, frequent snacks of sugars/cooked starch/sugared beverages.
e
Examples of protective factors include uoride exposure (topical and/or systemic) or xylitol use.
DM, Disease management; F, uoride; GA, general anesthesia; ITR, interim therapeutic restoration.
Risk-Based Chronic Disease Management Protocol
TABLE
E30.2

CHAPTER 30 The Dynamics of Change 418.e3
Figure E30.2 Example of a self-management goals handout. (Modied courtesy Boston Children’s Hospital.)
Tue Wed Th
on
4
Planner
5
GOALS FOR HEALTHY TEETH (6 years and older)
The pictures checked are the areas you should focus on between today and your next visit.
Your child has been assessed to have the following risk for caries (cavities):
Medium LowHigh
Next fluoride visit
in months
Healthy snacks such
as fruit, carrot sticks,
yogurt, low-fat
cheeses, pretzels,
whole grain crackers
No soda/energy drinks Less or no candy and
junk food
No juice
Juice only with meals
Chew sugar-free gum
(e.g., Trident, Extra, xylitol)
Rinse mouth with
water after eating
Drink fluoridated water,
tap water
Daily flossing wtih floss
string or pick
Brush morning and
before bed with fluoride
toothpaste. Do not
rinse mouth after brushing.
Fluoride varnish was applied
in clinic today.
Wait until tomorrow to brush/floss.
Avoid hard, crunchy, and
sticky foods.
IMPORTANT:
The last thing that touches your
child’s teeth before bedtime is the
toothbrush with fluoride toothpaste.
On a scale of 1–5, how likely do you think you or your child will meet these goals?
Clinician’s Comments:
34512
Not sure Very likelyNot likely
Brush with 5000-ppm
prescription-strength
fluoride toothpaste.
Wait 30 minutes before eating,
drinking, or rinsing after.
Patient’s Name: Date of Visit:

419
31
Examination, Diagnosis, and
Treatment Planning
SCOTT B. SCHWARTZ AND JOHN R. CHRISTENSEN
CHAPTER OUTLINE
The History
The Examination
Behavioral Assessment
General Appraisal
Head and Neck Examination
Facial Examination
Intraoral Examination
Supplemental Orthodontic Diagnostic Techniques
Photographs
Diagnostic Casts
Analysis of Cephalometric Head Films
Radiographic Evaluation
Treatment Planning for Nonorthodontic Problems
3. Development of skills in personal oral hygiene. e child emerging
from the middle school years should have acquired the skills
and knowledge to conduct eective personal oral hygiene.
4. Participation in health care decisions. Historically, dentists
are taught to see the school-aged child as a passive recipi-
ent of care; however, the current health care landscape has
become a dynamic decision-making environment. e dentist
should be prepared to manage issues and challenges related
to parental consent versus patient assent as young children
transition into their teenage years. Usually during this period,
children begin to develop an image of themselves, aspects
of which will relate to their facial and dental esthetics.
Although this image may be inuenced by their parents, it
is often unique to the child’s perspective. e development
of this self-image may inuence the compliance of the child
and affect the desire to take responsibility for his or her
own health.
The History
Elements of history taking and recording are discussed in Chapter
19. An important aspect of history taking in this group should be
the involvement of the child. While the parent remains the historian
of choice, the role of the child can evolve from being the listener
into the active participant. By adolescence, the child can provide
accurate, valuable information. Adolescents should be encouraged
to become participants in relaying an accurate medical history,
particularly through a well-developed physician-patient relationship.
A health history form should address issues like those applicable
to the younger child, but with dierent expectations. e dierences
in patient history for children in this age group in general include
the following:
1. Medical intervention has usually occurred. Most children have a
physician and may have experienced an emergency visit or some
invasive procedure. School enrollment has required a physical
examination and other treatment for most children.
2. e health history is more involved. By this time, most childhood-
onset disorders have manifested themselves, but some may not
have been noted. erefore, it is important to continue to
conduct a thorough systems review. Because more children are
surviving early childhood cancer, additional attention should
be given to determine the types of treatments encountered.
Full body or smaller eld radiation therapy, chemotherapy, and
the use of bisphosphonates all carry risks related to tooth
E
xamination of the child in the transitional years presents a
diagnostic dilemma of managing oral health at a dynamic
stage of development. Although the preschoolers dentition
is relatively stable, the child in the transitional years progresses
from a full complement of primary teeth through a mixed dentition
to a full permanent dentition excluding the third molars. Maintain-
ing the ease and success of this transition constitutes the main
challenge for the dentist treating this age group. A large part of
this chapter is devoted to orthodontic considerations, but the other
elements of signicance in dental management of this age group
should not be ignored. ey are as follows:
1. Preventive considerations related to dental sealants, nutrition, and
uoride intake. e eruption of permanent teeth requires that
a decision be made about sealant application. Entry into the
more heterogeneous, less controlled environment of school places
the child at risk for increased carbohydrate exposure. e child’s
access to uoride in school, diet, and other sources makes regular
reevaluation of uoride exposure a necessity. Preventive strategies
must be reviewed as caries risk factors change during this dynamic
period.
2. Prevention and management of trauma. e school-aged child
may be active in sports. For a period in the school years, the
permanent maxillary incisors are at greater risk for traumatic
injury, especially if they protrude.

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418 Part 4 The Transitional Years: Six to Twelve Years19. Marshall TA, Eichenberger-Gilmore JM, Larson MA, et al. Comparison of the intakes of sugars by young children with and without caries experience. J Am Dent Assoc. 2007;138:39–46.20. Sheiham A, James WPT. Diet and dental caries: the pivotal role of free sugars reemphasized. J Dent Res. 2015;94(10):1341–1347.21. Holbrook WP, Arnadottir IB, Takazoe I, et al. Longitudinal study of caries, cariogenic bacteria and diet in children just before and after starting school. Eur J Oral Sci. 1995;103(1):42–45.22. Ismail AI, Burt BA, Eklund SA. e cariogenicity of soft drinks in the United States. J Am Dent Assoc. 1984;109:241–245.23. Bibby BG. Fruits and vegetables and dental caries. Clin Prev Dent. 1983;5:3–11.24. Kashket S, van Houte J, Lopez LR, et al. Lack of correlation between food retention on the human dentition and consumer perception of food stickiness. J Dent Res. 1991;70:1314–1319.25. Luke GA, Hough H, Beeley JA, et al. Human salivary sugar clearance after sugar rinses and intake of foodstus. Caries Res. 1999;33:123–129.26. Rugg-Gunn AJ. Nutrition and Dental Health. Oxford: Oxford Medical Publications; 1993.27. Nizel AE, Harris RS. e eects of phosphate on experimental dental caries: a literature review. J Dent Res. 1964;43:1123–1136.28. Lilienthal B. Phosphates and dental caries. In: Myers H, ed. Monographs in Oral Science. Basel, Switzerland: Karger; 1976.29. Featherstone JDB, Mundor SA. Identication of the Cariogenic Elements of Foods. Final report for period September 1981–May 1984. Alexandria, VA: National Technical Information Service; 1984.30. Mundor SA, Glowinsky D, Grin C. Fluoridated sucrose eect on rat caries. J Dent Res. 1986;65(special issue):282(abstract 1017).31. Caldwell RC. Physical properties of foods and their caries-producing potential. J Dent Res. 1970;49:1293–1298.32. Stookey GK. Developing the perfect snack food. In: Alfano MC, ed. Changing Perspectives in Nutrition and Caries Research. New York: Medcom; 1979.33. Moynihan PJ, Kelley SAM. Eect on caries of restricting sugars intake: systematic review to inform WHO guidelines. J Dent Res. 2014;93(1):8–18.34. Meyer BD, Lee JY. e conuence of sugar, dental caries, and health policy. J Dent Res. 2015;94(10):1338–1340.35. Edelstein BL, Ng MW. Chronic disease management of strategies of early childhood caries: support from the medical and dental lit-erature. Pediatr Dent. 2015;37(3):281–287.36. Ng MW, Fida Z. Early childhood caries prevention and management. In: Berg JH, Slayton RL, eds. Early Childhood Oral Health. Hoboken, NJ: John Wiley & Sons; 2016.References1. Kuczmarski RJ, Ogden CL, Guo SS, et al. CDC Growth Charts for the United States: Methods and Development. Washington, DC: National Center for Health Statistics; 2000.2. Broadbent BH Sr, Broadbent BH Jr, Golden WH. Bolton Standards of Developmental Growth. St Louis: Mosby; 1975.3. Kapust AJ, Sinclair PM, Turley PK. Cephalometric eects of face mask/expansion therapy in Class III children: a comparison of three age groups. Am J Orthod Dentofacial Orthop. 1998;113(2):204–212.4. Smith BH, Garn SM. Polymorphisms in eruption sequence of permanent teeth in American children. Am J Phys Anthropol. 1987;74:289–303.5. Broadbent BH. e face of the normal child. Angle Orthod. 1937;7:183–208.6. Piaget J. e stages of the intellectual development of the child. In: Marlowe BA, Canestrari AS, eds. Educational Psychology in Context: Readings for Future Teachers. ousand Oaks, CA: Sage; 2006:98–106.7. Eccles JS. e development of children ages 6 to 14. Future Child. 1999;9(2):30–44.8. Stendler CB, Young N. Impact of rst grade entrance upon the socialization of the child: changes after eight months of school. Child Dev. 1951;22:113–122.9. Dye BA, Lopez G, Mitnik MS, et al. Trends in dental caries in children and adolescents according to poverty status in the United States from 1999 through 2004 and 2011 through 2014. J Am Dent Assoc. 2017;148:550–565.10. Moynihan P, Petersen PE. Diet, nutrition and the prevention of dental caries. Public Health Nutr. 2004;7(1A):201–226.11. Newbrun E. Sucrose, the arch criminal of dental caries. J Dent Child. 1969;36:239–248.12. Koulourides T, Bodden S, Keller S, et al. Cariogenicity of nine sugars tested with and intraoral device in man. Caries Res. 1976;10:427–441.13. Stephan RM. Eect of dierent types of human foods in dental health of experimental animals. J Dent Res. 1966;45:1551–1561.14. Gustafsson B, Quensel CE, Lanke L, et al. e Vipeholm dental caries study: the eect of dierent carbohydrate intake on 436 individu-als observed for ve years. Acta Odontol Scand. 1954;11:232–264.15. Sullivan HR, Goldsworthy NE. Review and correlation of the data presented in papers 1-6 (Hopewood House study). Aust Dent J. 1958;3:395–398.16. Sullivan HR, Harris R. Hopewood House study 2. Observations on oral conditions. Aust Dent J. 1958;3:311–317.17. Walker ARP, Cleaton-Jones PE. Sugar intake and dental caries: where do we stand? ASDC J Dent Child. 1989;56:30–35.18. Burt BA, Pai S. Sugar consumption and caries risk: a systematic review. J Dent Educ. 2001;65:1017–1023. CHAPTER 30 The Dynamics of Change 418.e1 Case Study: Chronic Disease Management of CariesMan Wai Ng and Rosalyn M. SulyantoEthan, an anxious 6-year-old, presents for recare with his mom. Eight months ago, after bitewing radiographs identied interproximal caries on his mandibular primary molars, Ethan required sedation for restorative treatment. His mom was advised to help brush with uoride toothpaste twice daily, oss, and limit sugary snacks and beverages.Ethan cooperates for an examination, prophylaxis, uoride varnish (FV), and bitewing radiographs. The clinical examination found partially erupted permanent rst molars with heavy plaque and demineralization of the pits and ssures. Radiographic assessment found intact restorations and new incipient interproximal caries on the maxillary primary molars. Caries risk assessment (CRA) found the following pertinent factors: Ethan (1) brushes in the morning only without help, (2) does not oss, (3) drinks juice four times daily and little water, and (4) eats fruit snacks at lunch.Dental caries is a chronic disease that is signicantly inuenced by social and behavioral factors. Because it is largely preventable and can be controlled, there must be a better outcome for children like Ethan than a potential lifetime of caries burden.Chronic disease management (CDM) of dental caries is a science-based approach that is tested in clinical practice to prevent and manage caries and is separate and distinct from prevention and restorative treatment. Effective CDM requires customized patient self-management of etiologic factors. An important role of the dental team is to effectively engage the patient and family to make the necessary lifestyle changes.A CDM clinical protocol (Fig. E30.1 and Tables E30.1 and E30.2) includes seven components: (1) CRA (2) effective communication, Caries lesioncharting bytooth surfaceand activityRemineralizationmodalitiesSelf-managementgoalsRecare intervalsbased oncaries riskTreatment basedon patient’sclinical needs andcaregiver’s orpatient’s desiresCaries riskassessmentEffectivecommunication• Figure E30.1 Chronic disease management of caries clinical proto-col. (From DentaQuest Institute. Early Childhood Caries [ECC] Manage-ment Efforts [website]; 2017. https://www.dentaquestinstitute.org/learn/quality-improvement-initiatives/early-childhood-caries-ecc-manage-ment-efforts. Accessed September 13, 2017.)Caries risk assessment Performed in full or abbreviated format during each visitEffective communication With permission, explain the caries process to parent; and use structured communication strategies such as:• Fixing the cavities does not x the problem• Without a change in diet and home care, new cavities and broken llings will result• Change is hard and will not happen overnightVisual aids such as ip charts and handouts may be used to guide conversationsSelf-management goal settingEngage and coach parent to select one or two goals to work on until the next visitGoals may include more frequent tooth brushing, topical uoride use, and specic diet modication strategiesCaries charting Use a charting system, such as ICDAS or ADA Caries, to:• Documentcariesbytooth,surface,andactivity• MonitordiseaseimprovementorprogressionFluorides and other remineralization strategiesTopical uorides, including over-the-counter toothpaste, prescription uoride toothpaste, and stannous uoride, as well as xylitol and/or calcium phosphate products, can be offeredIn-ofce silver diamine uoride treatment or uoride varnish applications can be offeredRestorative treatment Treatment options are presented based on each patient’s needs and parent’s desires, including:• Conventionaltreatment(includinguseofpharmacologicmanagement)• InterimtherapeuticrestorationsforcariescontrolandsealantsRisk-based recare intervals Patients are recommended to return for recare frequency based on their caries risk and desires:• 1–3months(ifhighrisk)• 3–6months(ifmediumrisk)• 6–12months(iflowrisk)At the recare/disease management visit, perform:• Cariesriskassessment• Self-managementgoalssetting/reassessed• Examandcharting• X-raysifindicated• SilverdiamineuorideoruoridevarnishRecare should be coordinated with restorative treatment whenever possibleADA, American Dental Association; ICDAS, International Caries Detection and Assessment System.Chronic Disease Management of Caries Clinical ProtocolTABLE E30.1 Continued 418.e2 Part 4 The Transitional Years: Six to Twelve Years(3) self-management goal (SMG) setting, (4) caries charting, (5) uorides and other remineralizing strategies, (6) restorative treatment as needed and desired by patient/family, and (7) risk-based recare periodicity.Regularly assessing caries risk and providing support and coaching to control risk factors are the cornerstones of CDM. Caries etiology is explained, followed by coaching on SMG setting. Fig. E30.2 shows an example of an SMG handout.When asked about what is most important to her, Ethan’s mom states that she does not wish him to have more cavities and to get upset when having his teeth xed. She is advised that with positive changes in Ethan’s diet and oral hygiene practices, the small new cavities can be brought under control and restorative treatment may be deferred. These SMG strategies are discussed: (1) limit juice and increase water intake, (2) replace with sugar substitute, (3) help with brushing and use a prescription 5000 ppm uoride toothpaste, (4) chew sugar-free gum and eat sugar-free snacks, not fruit snacks. Ethan’s mother chooses 2 and 3. She also agrees to return for a 1-month recare visit to review CRA and SMGs, apply FV, and place sealants on Ethan’s permanent molars.CDM of caries strategies help patients to make changes that lead to better outcomes and can fulll expectations of accountability (providing payment incentives/disincentives for better performance such as through value-based reimbursement) and transparency (publicly reporting performance scores), which are now commonplace in medicine and will become more familiar landscape to dentistry in the near future.Questions1. Why is the caries risk assessment tool inadequate as the only component in chronic disease management counseling?Answer: Effective management of dental caries requires the patient and family to make necessary lifestyle changes. Regularly assessing caries risk is necessary but insufcient to improving the dental health of patients. The dental care team has an important role to develop an individualized care plan and provide meaningful coaching to patients and families to mitigate specic responsible risk factors while enhancing protective factors.2. Should the dentist discuss chronic disease management strategies with a new patient without caries? Why?Answer: An important goal of an infant oral health visit or a new dental visit for a patient without caries is to prevent caries development. Timely assessment of causative risk factors (e.g., dietary factors, plaque accumulation, and inadequate uoride exposure) and optimization of protective factors can be expected to reduce the incidence of caries. The dental care team should provide education, counseling, and a prevention plan to address the risk factors that are specic to each patient and family.3. Why is a 6-month recall periodicity inappropriate for every patient?Answer: Because lifestyle changes are hard to make and sustain, high caries risk patients would benet from receiving more frequent assessment of risk factors, self-management support and coaching, and uoride varnish treatments. Whenever possible, these activities should be coordinated with restorative and other preventive treatment.Existing Risk Category New Clinical FindingsFluoride Varnish IntervalaSample Self-Management GoalsRestorative TreatmentDM Return Interval OtherLow No disease indicatorsb of caries; orCompletely remineralized (arrested) carious lesions6–12months Twice daily brushing with F toothpastec6–12monthsMedium No disease indicatorsb but has risk factorsd; and/or inadequate protective factorseDisease indicators present with some remineralization3–6months Twice or more daily brushing with F toothpastec or5000 ppm F toothpasteDietary changesSealantsITRConventional restorative3–6months Xylitolorsorbitolgumor candies or wipesCalcium phosphate pasteHigh Active caries (disease indicators present)No remineralization occurringHeavy plaque1–3months Twice or more daily brushing with F toothpastec or5000 ppm F toothpasteDietary changesITRSealantsConventional restorativeSedation/GA1–3months Xylitolorsorbitolgumor candiesCalcium phosphate pasteaMay use silver diamine uoride instead of uoride varnish.bExamples of disease indicators include demineralization, cavitated lesions, existing restorations, enamel defects, deep pits, and ssures.cBrush with a smear of 1000 ppm F toothpaste.dExamples of risk factors include patient/maternal/family history of decay, plaque on teeth, frequent snacks of sugars/cooked starch/sugared beverages.eExamples of protective factors include uoride exposure (topical and/or systemic) or xylitol use.DM, Disease management; F, uoride; GA, general anesthesia; ITR, interim therapeutic restoration.Risk-Based Chronic Disease Management ProtocolTABLE E30.2 CHAPTER 30 The Dynamics of Change 418.e3 • Figure E30.2 Example of a self-management goals handout. (Modied courtesy Boston Children’s Hospital.)Tue Wed Thon4Planner5GOALS FOR HEALTHY TEETH (6 years and older)The pictures checked are the areas you should focus on between today and your next visit.Your child has been assessed to have the following risk for caries (cavities):Medium LowHighNext fluoride visitin monthsHealthy snacks suchas fruit, carrot sticks,yogurt, low-fatcheeses, pretzels,whole grain crackersNo soda/energy drinks Less or no candy andjunk foodNo juiceJuice only with mealsChew sugar-free gum(e.g., Trident, Extra, xylitol)Rinse mouth withwater after eatingDrink fluoridated water,tap waterDaily flossing wtih flossstring or pickBrush morning and before bed with fluoridetoothpaste. Do notrinse mouth after brushing.Fluoride varnish was appliedin clinic today.Wait until tomorrow to brush/floss.Avoid hard, crunchy, andsticky foods.IMPORTANT:The last thing that touches yourchild’s teeth before bedtime is thetoothbrush with fluoride toothpaste.On a scale of 1–5, how likely do you think you or your child will meet these goals?Clinician’s Comments:34512Not sure Very likelyNot likelyBrush with 5000-ppmprescription-strengthfluoride toothpaste.Wait 30 minutes before eating,drinking, or rinsing after. Patient’s Name: Date of Visit: 41931 Examination, Diagnosis, and Treatment PlanningSCOTT B. SCHWARTZ AND JOHN R. CHRISTENSENCHAPTER OUTLINEThe HistoryThe ExaminationBehavioral AssessmentGeneral AppraisalHead and Neck ExaminationFacial ExaminationIntraoral ExaminationSupplemental Orthodontic Diagnostic TechniquesPhotographsDiagnostic CastsAnalysis of Cephalometric Head FilmsRadiographic EvaluationTreatment Planning for Nonorthodontic Problems3. Development of skills in personal oral hygiene. e child emerging from the middle school years should have acquired the skills and knowledge to conduct eective personal oral hygiene.4. Participation in health care decisions. Historically, dentists are taught to see the school-aged child as a passive recipi-ent of care; however, the current health care landscape has become a dynamic decision-making environment. e dentist should be prepared to manage issues and challenges related to parental consent versus patient assent as young children transition into their teenage years. Usually during this period, children begin to develop an image of themselves, aspects of which will relate to their facial and dental esthetics. Although this image may be inuenced by their parents, it is often unique to the child’s perspective. e development of this self-image may inuence the compliance of the child and affect the desire to take responsibility for his or her own health.The HistoryElements of history taking and recording are discussed in Chapter 19. An important aspect of history taking in this group should be the involvement of the child. While the parent remains the historian of choice, the role of the child can evolve from being the listener into the active participant. By adolescence, the child can provide accurate, valuable information. Adolescents should be encouraged to become participants in relaying an accurate medical history, particularly through a well-developed physician-patient relationship. A health history form should address issues like those applicable to the younger child, but with dierent expectations. e dierences in patient history for children in this age group in general include the following:1. Medical intervention has usually occurred. Most children have a physician and may have experienced an emergency visit or some invasive procedure. School enrollment has required a physical examination and other treatment for most children.2. e health history is more involved. By this time, most childhood-onset disorders have manifested themselves, but some may not have been noted. erefore, it is important to continue to conduct a thorough systems review. Because more children are surviving early childhood cancer, additional attention should be given to determine the types of treatments encountered. Full body or smaller eld radiation therapy, chemotherapy, and the use of bisphosphonates all carry risks related to tooth Examination of the child in the transitional years presents a diagnostic dilemma of managing oral health at a dynamic stage of development. Although the preschooler’s dentition is relatively stable, the child in the transitional years progresses from a full complement of primary teeth through a mixed dentition to a full permanent dentition excluding the third molars. Maintain-ing the ease and success of this transition constitutes the main challenge for the dentist treating this age group. A large part of this chapter is devoted to orthodontic considerations, but the other elements of signicance in dental management of this age group should not be ignored. ey are as follows:1. Preventive considerations related to dental sealants, nutrition, and uoride intake. e eruption of permanent teeth requires that a decision be made about sealant application. Entry into the more heterogeneous, less controlled environment of school places the child at risk for increased carbohydrate exposure. e child’s access to uoride in school, diet, and other sources makes regular reevaluation of uoride exposure a necessity. Preventive strategies must be reviewed as caries risk factors change during this dynamic period.2. Prevention and management of trauma. e school-aged child may be active in sports. For a period in the school years, the permanent maxillary incisors are at greater risk for traumatic injury, especially if they protrude. 420 Part 4 The Transitional Years: Six to Twelve Yearsseveral standpoints. First, the school-aged child should have developed gross motor skills and any variations from normal should be obvious. For example, the toddler may be active but still clumsy. e school-aged child, even at the early end of this age group, can play with skill. Speech development should also well exceed that of the preschooler as should the child’s emotional and intellectual status. is adaptation is really a manifestation of development of the brain and is one reason why schooling begins at this age.One advantage available to the dentist who treats children in this age group is the host of health professionals with whom he or she can work if problems are noted. School placement often has identied problem areas and the appropriate therapy usually has been initiated. ese professionals can assist in clarifying ndings made during the dental visit. Table 31.1 lists some characteristics of the school-aged child that are important in the diagnostic process.Determination of Developmental StatusPatients in early adolescence are clearly growing, but in the later stages growth slows dramatically and at some point, nearly ceases. e same is roughly true for facial growth. When patients are clearly growing, growth modication can be attempted. Many development, eruption, and bone quality when considering surgical interventions and tooth movement.3. e dental history is evolving. Children usually have undergone a dental visit as part of school enrollment. In the transitional years, the patient increases independence at school and in social venues. Diet history, caries risk, and the preventive regimen at home change signicantly.4. e history should capture those children early on the curve of health experiences. As children transition into this age group, sensitive topics may become relevant to the dentist. Some instances in which the involvement of an adolescent historian may have profound benets for both health care provider and patient are (1) onset and frequency of sexual activity related to presence of various oral pathologies and pregnancy; (2) use of alcohol, tobacco, and other substances that can increase risk of disease; and (3) psychiatric issues such as anorexia nervosa and bulimia. Adolescents who are pregnant are more visible in the current social climate. Given the sensitive nature of the informa-tion that may be disclosed by the patient at this age, the dentist should try to provide appropriate space from parent or guardian to ensure the condentiality of responses.The ExaminationAs in younger children, the dental examination includes a behavioral assessment; general appraisal; and head and neck, facial, intraoral, and radiographic examinations.Behavioral AssessmentAnother advantage for the dentist is the child’s emergence into a period when few children experience behavioral problems that cannot be resolved with simple, nonpharmacologic behavior guid-ance techniques. Even early in this period, many children can be reasoned with to accept dental treatment. e child who resists attempts at careful and compassionate explanations of care may require special attention and further evaluation from a medical provider. e rising awareness and prevalence of attention disorders and other conditions such as autism spectrum disorder pose new challenges for the dental provider. A thorough review of the patient’s history should identify current pharmacologic and other therapeutic approaches to behavioral and psychological diagnoses. It is impera-tive that the dentist is familiar with the diagnostic criteria for such conditions and is prepared to implement a more nuanced approach to care. e next step is to “chair-test” the child, using the dentist’s proven techniques of managing children. e technique used may be tell-show-do, positive reinforcement, voice control, or some other method that has worked consistently in the past. Remember that consent must be obtained from the parent if the behavior management technique used is not one that a reasonable parent would expect.1 New environments, particularly the dental clinic, can exacerbate anxiety and behavior issues for any child, especially those with a previously identied behavioral diagnosis. If behavioral intervention fails, the dentist should consider further evaluation or referral. Some causes of extreme behavior problems in this age group include substance abuse, physical or sexual abuse, family problems, or a learning disability.General Appraisale school-aged population provides a wide range of physical and emotional proles, yet the general appraisal should be easier from Intellectual Development Physical DevelopmentDemonstrates school readiness early in this periodShould be able to read and write in this periodBecomes capable of logical thoughtRenement of motor skills occurs as central nervous system developsSpine straightens to improve postureSinuses enlargeLymphoid system reaches high point of developmentPsychological DevelopmentAcquires a sense of accomplishment for tasksLearns responsibility for actionsDevelops a sense of right and wrongLooks outside the home for standards or valuesPhysiologic Development6-Year-Old 9-Year-Old 12-Year-OldHeightBoys = 121 cm Boys = 140 cm Boys = 154 cmGirls = 119 cm Girls = 137 cm Girls = 157 cm(Growth rate is approximately 6 cm/year in this period.)Weight (75th Percentile)Boys = 24 kg Boys = 33 kg Boys = 44 kgGirls = 23 kg Girls = 32 kg Girls = 45 kg(Growth rate is approximately 3–3.5 kg/year in this period.)Pulse (Average for Age)100 beats/min 90 beats/min 85–90 beats/minRespiration (50th Percentile)23 breaths/min 20 breaths/min 18 breaths/minBlood Pressure (Average for Age)105/60 mm Hg 110/65 mm Hg 115.65 mm HgSelected Developmental Characteristics of the 6- to 12-Year-Old ChildTABLE 31.1 CHAPTER 31 Examination, Diagnosis, and Treatment Planning 421 the only index of facial growth. ere are several problems with this method of determining developmental status by the dentists. First, it requires an additional radiograph. Second, the ability to reliably read hand-wrist radiographs requires consistent practice that is rarely gained in routine patient care.Another radiographic method that does not require additional radiation exposure is the use of cervical vertebral maturation from diagnostic cephalometric radiographs (Fig. 31.3). is method uses the maturation stages of the second through fourth cervical vertebrae (Fig. 31.4) to evaluate mandibular growth potential. It is claimed that the peak mandibular growth occurs between stages 2 and 3 in the ve-stage method.3 Timing treatment for growth modication during this period of growth, according to some, could enhance the treatment eects.4 ere is some disagreement regarding the reliability of this method but is has been shown to be highly reliable for making the determination whether a patient’s mandibular growth rate is still increasing or has passed its peak (i.e., stage 1 or 2 vs. stage 3, 4, or 5). e stage of mandibular growth is the clinically relevant determination for the patient being considered for growth modication.5Secondary sexual characteristics provide some information about the amount of growth the patient has yet to experience. In females, breast stage development and menarche are markers that can be used to assess developmental status. Breast development determina-tion as an objective clinical evaluation is obviously not practical in the dental oce and is of little clinical use. Menarche, however, can be determined from the health history questionnaire or from an interview at the initial patient examination. Unfortunately, the pubertal growth spurt precedes menarche by more than 1 year.6 erefore, menarche is basically used to decide whether growth modication is still feasible.In males, there is no single indicator such as menarche by which to judge developmental status. e amount and texture of facial hair and the patient’s general physical appearance are two highly variable indicators of male developmental status and maturity. Facial hair usually appears near or following peak statural growth.For a person with an obvious skeletal problem, more than one cephalometric head lm of the patient may be available. ese head lms can be superimposed to provide information about the amount and direction of growth that has occurred over time (see later discussion on cephalometric analyses and Fig. 31.53). Although past growth tendencies do not guarantee that the patient will continue to grow or will grow according to the same pattern, comparing head lms provides a great deal of information about the patient’s growth history. However, it is unlikely for the average patient to have a series of head lms available for pretreatment review. It is sometimes benecial to obtain a cephalometric head lm on a parent if the patient closely resembles the parent. While not denitive, the lm can provide a “blueprint” to predict the patient’s growth.e patient’s developmental status can also be judged from the developmental stage of the dentition. Panoramic or periapical radiographs can be used to determine the stage of development of individual permanent teeth. e results can be compared with standards relating dental development to chronological age.7 However, studies indicate that the relationship between dental age and skeletal maturation is weak and clinically useless.8In summary, several biological markers are available by which the clinician can assess the developmental status of the patient. Unfortunately, no one marker by itself provides denitive informa-tion about the patient’s growth potential. e most logical approach is to gather all available information and then make a judgment clinicians believe that growth modication is easiest when the child is undergoing accelerated growth during the adolescent growth spurt.is judgment on treatment timing would be much easier if a biological marker could be identied that provided denitive information about the developmental status of the patient. Growth modication could be started if the marker indicated that sucient growth remained to alter skeletal relationships. To be clinically useful, this biological marker would have to be reliable, easily identied, recognized in both sexes, and closely correlated with the growth of the facial bones. Unfortunately, a single biological marker of this description is not available. Several clinical markers have been identied. However, studies have indicated that the relationship between the markers and facial growth, although statistically signicant, is not so precise that growth can be predicted accurately. Because of the limited predictive value of the markers, one marker alone is seldom used; instead, several are combined with multiple evaluations.Height and weight measurements are often used to determine the patient’s growth status. Measurements are plotted on standard-ized growth charts to indicate the relative size of the patient. An average-sized child is located near the 50th percentile, and a large child is somewhere near the 90th percentile. A single measurement does not provide the clinician with all pertinent growth information, but it does give some idea about where the patient is developmentally compared with other children at this age.A series of measurements, which may be available from the patient’s physician or school nurse, provides much more information. e dentist should record height and weight measurements at each periodic visit. e measurements can be plotted in one of two ways. e rst way is to plot the measurements on a cumulative growth chart (Fig. 31.1). is provides information about the patient’s total amount of growth up to the last measurement. e normal growth curve is sigmoidal and the pubertal growth spurt corresponds to the steepest portion of the slope. Because growth charts are based on mean growth rates, the individual patient may show an accelerated or delayed growth spurt if his or her growth rate is not coincident with the mean growth rate. More importantly, some concern should be expressed if the patient is not following the percentiles (e.g., dropping from the 50th to the 40th to the 30th percentile over time). is suggests there may be a physical or psychological problem requiring medical attention.Height and weight measurements can also be plotted as yearly growth increments rather than as total growth achieved up to that point (Fig. 31.2). By plotting measurements this way, changes in the growth rate can be easily identied. A sharp rise in height usually signals the start of the pubertal growth spurt and growth modication treatment should be initiated immediately if it is required.Height and weight measurements also can be compared with the height and weight of the patient’s natural parents and siblings. Although the interaction between environment and heredity is not clearly understood, there is some familial inuence on ultimate size, and it may be possible to glean useful information from the comparison.Hand-wrist radiographs have been used by some investigators to judge the skeletal age and development of the patient. e size and maturational stage of certain hand and wrist bones are compared with published standards of normal bone development and skeletal age.2 Unfortunately, the correlation between the appearance of reliable bone markers (skeletal growth status) and mean maximal mandibular growth velocity is not perfect and should not serve as 422 Part 4 The Transitional Years: Six to Twelve Years• Figure 31.1 A standardized growth chart is used to indicate the relative size of the patient. A single measurement does not provide the clinician with all pertinent growth information, but it does give some idea of the developmental level of the patient compared with other children at a particular time. A series of measurements plotted on a standardized growth chart provides much more information than a single measurement. The measurements may be plotted in two ways. In the cumulative growth chart method, illustrated here, asterisks plot the measurements. This chart shows the patient’s total growth up to the last measurement. This female patient has been measured yearly, starting at age 6 years, and is roughly following the 75th percentile line. (Modied from Hamill PVV, Drizd TA, Johnson CL, et al. Physical growth: National Center for Health Statistics percentiles. Am J Clin Nutr. 1979;32:607–629. Data from the National Center for Health Statistics, Hyattsville, MD; Courtesy Ross Laboratories.) CHAPTER 31 Examination, Diagnosis, and Treatment Planning 423 regarding the patient’s growth potential and suitability for growth modication.Head and Neck Examinatione head and neck examination should be completed in a manner similar to that outlined in Chapter 19.Facial ExaminationFacial examination of the 6- to 12-year-old child is a systematic examination of the face in three planes of space. It is essentially the same as the facial examination described in Chapter 19, and the reader should review that information if necessary. is section comments on ndings that are particularly important for the 6- to 12-year-old.In examination of the prole, one notes the anteroposterior and vertical dimensions of the face and the position of the lips and incisors relative to the face. e ideal soft tissue prole is slightly convex (Fig. 31.5), practically speaking a bit straighter with more mandibular contribution than that of the preschool-aged group. Most clinicians nd that detection of anteroposterior skeletal problems is somewhat easier in this age group, possibly because of reduced soft tissue thickness. A mild mandibular deciency in a 4-year-old child may have been dicult to diagnose initially, but it is more apparent at age 8 years and even more obvious at age 12 years. In most cases, skeletal relationships can be conrmed by the dental relationships (molar and overjet). at means that if the facial form (convex, straight, or concave) matches the dental relationships (respectively, class I molar and moderate overjet, class II molar and 5- to 6-mm overjet, or class III molar and zero or negative overjet), there is usually not much doubt about the skeletal relationships. If a skeletal problem exists, the source of the 87654321InchesYearsAge 6123456 789101112• Figure 31.2 Growth information also can be plotted as yearly growth increments rather than as total growth achieved to a certain point. The growth data for the female patient described in Fig. 31.1 are plotted here incrementally, beginning at age 6 years. By plotting measurements this way, changes in the growth rate can be easily identied. A sharp rise usually signals the start of the pubertal growth spurt. • Figure 31.3 Another method used to gauge growth status is evaluation of the shape of cervical vertebrae 2, 3, and 4. These images are available on routine cephalometric radiographs and require no additional radiation. It appears they can be reliably read and are interpreted according to the stages described in Fig. 31.4. CVMS I CVMS II CVMS III CVMS IV CVMS V• Figure 31.4 The ve stages of cervical vertebrae maturation are described in this diagram. These stages are equated with physical matura-tion, somatic growth, and mandibular growth. According to the reported data, peak mandibular growth is experienced before stage III. A concavity develops on the lower border of the third vertebra during stage II and a similar one develops on the lower border of the fourth vertebra during stage III. Vertebrae 3 and 4 undergo gradual transformation from horizon-tally rectangular shape to square to vertically rectangular shape during the maturation process. CVMS, Cervical vertebrae maturation stage. (Redrawn from Baccetti T, Franchi L, McNamara JA Jr. An improved version of the cervical vertebral maturation [CVM] method for the assessment of man-dibular growth. Angle Orthod. 2002;72:316–323.)• Figure 31.5 The ideal soft tissue prole for the bridge of the nose, the base of the upper lip, and the chin is slightly convex to straight in the anteroposterior dimension in the 6- to 12-year-old child. This child dem-onstrates that type prole and well-balanced vertical proportions with the lower face slightly larger than the middle facial third. 424 Part 4 The Transitional Years: Six to Twelve Yearsage group with incompetent lips (lips that do not approximate or have more than a couple of millimeters of separation at rest). e maximum display of incisors at rest and maximum lip incompetence occur around 11 years in females and 12 years in males.10 Most children become more lip competent as they mature. Ideally a child shows about 2 mm of tooth below the relaxed lip line. At full smile, they show nearly the full tooth with the upper lip retracting to a couple of millimeters below the cervical area of the tooth. Gingival exposure of not more than 2 mm is considered esthetically acceptable for this age group. Of course, there can be much variation while still maintaining good esthetics, but these are generally accepted guidelines.Intraoral Examinatione procedures used for oral examination are like those used in the preschool group and include charting of teeth and dental caries. Less emphasis on managing the child’s behavior during the examination process is needed because these children are more cooperative. e areas of evaluation that require more emphasis are the periodontal, preventive, and orthodontic aspects.Periodontal EvaluationA thorough examination of this age group involves both periodontal probing and use of a gingival index (GI) if inammation is a problem. If orthodontic treatment is a consideration, it may be delayed or the treatment plan altered if the periodontal tissues are not healthy. Orthodontic treatment initiated during periods of active gingival or periodontal disease may further compromise periodontal health because xed appliances are dicult to keep clean, and existing inammatory conditions are exacerbated, resulting in further loss of supporting structures. e periodontal examination should address the following aspects:1. Selective probing of anterior teeth and permanent rst molars. A periodontal probe is necessary to evaluate the health of the tissues properly (Fig. 31.7). e probe measures the depth of the sulcus and the amount of free marginal and attached gingiva. Bleeding upon probing is also an indication of active gingival disease. Sulcular depths of greater than 3 mm and attached gingiva of less than 1 mm indicate possible periodontal problems, and further evaluation is warranted. e likelihood of bone loss and apical migration of the attachment is low, but some children in this age group experience aggressive periodontitis. Erupting teeth usually have a deep sulcus until the crown is fully erupted. Gingival inammation in early puberty may also confound pocket-depth measurements.2. Evaluation of tissue attachments, especially those of the lower anterior teeth. Facial clefts and recession due to malpositioned teeth and inammation, if identied early, can be successfully managed with tissue grafting, tooth movement, or a combination of both (Fig. 31.8). e amount of attached gingiva also should be considered in the context of the type of tooth movement being planned. Facial movement of a lower incisor with minimal attached gingiva may cause further loss of attachment, and an evaluation by a periodontist is indicated. Often simply proceeding cautiously will be acceptable, but in other instances a gingival grafting procedure may be considered. Lingual movement of the same incisor does not involve the risk of attachment loss and may even contribute to an increase in health or the amount of attached tissue. Last, the position of the frena and their height of attachment on the alveolar ridge should be determined via gentle manipulation of the lips and cheeks. Occasionally discrepancy is identied by comparing the position of the maxilla and mandible with a vertical reference line through soft tissue nasion (see Chapter 19, Figs. 19.1 and 19.2). is helps to direct treatment, if indicated, to the skeletal component at fault.Again, in this age group, vertical prole assessment continues to concentrate on the proportionality of the middle and lower facial thirds. At this point, growth has increased the vertical linear facial dimensions, and the proportionality of the well-balanced face remains basically the same, but the lower facial third is slightly larger than the middle facial third. Research has indicated that vertical dysplasia usually is conned to the lower facial third in this age group.9 erefore the middle third can be compared with the lower facial third (see Fig. 31.5).Incisor and lip position should be examined carefully in this age group. e child is entering the mixed dentition period, and the position of the erupted permanent incisors generally is reected in the position of the lips. e upper lip gives a good indication of the underlying position of the maxillary incisor. e position of the lower lip also depends on the position of the maxillary incisor because the lower lip normally covers 1 to 2 mm of the maxillary incisal edge at rest. erefore lip posture is a strong indicator of maxillary dental protrusion. Lip and incisor position should always be considered in the context of the nose and chin. A large nose and chin are more able to accommodate protrusive incisors and lips than are a small nose and chin. As a rule, for white children, the lips should be positioned on or slightly behind a line connecting the tip of the nose with the chin (Fig. 31.6). Most Asian and African American children have more incisor and lip protrusion than white children. When the incisors are fully erupted, it is possible to begin to consider their vertical position relative to the lips. is gives an indication of some critical esthetic relationships. Lips tend to grow vertically throughout the early adolescent years. It is not uncommon to see children early in this • Figure 31.6 In this age group, the lips are positioned on or slightly behind a line connecting the tip of the nose with the soft tissue chin. Lip position must be considered in the context of the nose and chin. A large nose and chin are better able to accommodate protrusive lips than are a small nose and chin. CHAPTER 31 Examination, Diagnosis, and Treatment Planning 425 process and extend into the palantine papilla. Generally a frenum is indicated for removal when there is an aberrant attachment causing a midline diastema or when the frenum is attached so closely to the attached gingival tissue that there is inadequate gingival tissue covering the tooth or there is gingival recession.3. Identication of problem areas, such as mandibular and maxillary anterior teeth. Calculus accumulation, inammation secondary to anterior crowding, poor cleaning, and eruptive gingivitis are examples of localized problems that require specialized attention.Numerous gingival indices exist to assess inammation.12 e GI13 can be adapted for pediatric use. e GI uses the following scoring system: 0 = normal gingiva; 1 = mild inammation: slight change in color, slight edema, no bleeding on probing; 2 = moderate inammation: redness, edema, and glazing, or bleeding on probing; 3 = severe inammation: marked redness and edema, tendency toward spontaneous bleeding, ulceration.In the private practice setting, it may be easier to modify an existing index, using key teeth to provide baseline readings and progress. ese readings can be recorded on the examination form adjacent to the data for the teeth being examined. Routine per-formance of full-mouth probing is not warranted.Oral Hygiene Evaluatione assessment of clinical needs and patient skills in oral hygiene is a part of the examination process. e history should reveal a pattern of personal care and the clinical examination should docu-ment the eectiveness of care and address problem areas in the oral cavity. A patient’s brushing skills and dexterity in ossing can be judged at chairside and are generally directly correlated with classically dicult-to-clean areas such as plaque accumulation on teeth opposite to the side on which the brush is held, buccally placed canine teeth, and lingual surfaces. is information should be used to formulate an individual hygiene strategy. If orthodontic treatment is being considered, oral hygiene instructions should be given before orthodontic treatment is started and should be consistently reinforced during the treatment. In some cases it is prudent to delay orthodontic treatment until oral hygiene can be maintained at an acceptable level.Occlusal Evaluatione occlusal evaluation is organized around a systematic approach to alignment and the anteroposterior, transverse, and vertical planes of space.14Alignmente intraoral occlusal examination in the mixed dentition begins with an assessment of arch form and alignment characteristics. An ideal arch should be symmetric in the anteroposterior and transverse dimensions. Minor asymmetry may exist but is usually conned to the anterior region if there is inadequate space for eruption of the permanent incisors. Signicant asymmetry is rare and is usually indicative of skeletal asymmetry or some type of oral habit or crossbite that has displaced the teeth and alveolus. e arch form is described as U or V shaped. Alignment problems are usually the result of a true arch length deciency or a transitional arch length deciency due to the size of the erupting permanent teeth. ese are most common in the anterior portions of the arch but can occur anywhere. e type of alignment problem should be noted during the examination. e teeth can be tipped, bodily positioned, or rotated in their aberrant location. ese types of frenal attachments near the crest of the ridge must be repositioned before or after orthodontic treatment because they pull on attached marginal tissue and compromise gingival health or prevent space closure. ere are four types of frenal attachments (Box 31.1).11 e rst is mucosal. is is when the frenal bers attach up to the mucogingival junction. When bers insert within the attached gingival tissue, the frenal attachment is termed gingival. A papillary attachment is dened as bers extending into the interdental papilla. Lastly, the papilla penetrat-ing attachment occurs when the frenal bers cross the alveolar • Figure 31.7 During examination of each arch, a periodontal probe is used to evaluate gingival health. Special attention should be paid to increased pocket depth, lack of attached gingiva, and bleeding upon probing. Orthodontic treatment that is initiated during periods of active gingival or periodontal disease may further compromise periodontal health. • Figure 31.8 This labial gingival cleft is just beginning, probably caused by poor oral hygiene and the heavy occlusion on the prominent lower incisor. It should be evaluated before orthodontic treatment. Mucosal—when the frenal bers are attached up to the mucogingival junction.Gingival—when the bers are inserted within the attached gingiva.Papillary—when the bers are extending into the interdental papilla.Papilla penetrating—when the frenal bers cross the alveolar process and extend up to the palatine papilla.Types of Frenal Attachments• BOX 31.1 426 Part 4 The Transitional Years: Six to Twelve Yearstooth loss when there is a mutation.17 It is apparent that future genetic study may identify more genes that aect tooth development. e practical implication of a missing anterior tooth is to look elsewhere in the mouth for more eruption or tooth development issues (additional missing teeth, impaction, or transpositions).Another cause of missing or malformed teeth is radiation therapy or chemotherapy. is can aect the formation and eruption of the teeth developing at the time or those in the eld of the thera-peutic beam. Generally patients treated with radiation before age 5 years will have more anomalies of dental development, but patients receiving chemotherapy and older patients who still have developing teeth are also likely aected (Fig. 31.11).18Supernumerary teeth are teeth added to the normal complement of teeth. ese teeth are found in about 2% of the population and are most often found in the maxillary midline region.19 Midline supernumerary teeth are also called mesiodens (Fig. 31.12). Supernumerary teeth are also found distal to the maxillary molars and in the mandibular premolar regions.Although not a tooth in the strictest sense, the odontoma is discussed in this section on tooth number. e odontoma is a benign mixed tumor of enamel and dentin that is diagnosed radiographically. Two types of odontomas are identied. Odontomas that resemble teeth are called compound odontomas; those that are irregularly shaped are labeled complex odontomas. Both types may interfere with normal tooth eruption and are usually treated by surgical removal before eruption problems arise but late enough to avoid surgical trauma to adjacent developing teeth (Fig. 31.13).Tooth StructureDisturbances in the morphodierentiation and histodierentiation stages of tooth development result in alterations of tooth size and shape. Each arch should be examined for generalized large (mac-rodontia) or small (microdontia) teeth and for localized tooth size discrepancies. Generalized large or small teeth usually can be aligned so that there is a compatible occlusal relationship if the teeth in both arches are equally aected. However, localized tooth size problems make it dicult to establish good dental relationships. Again, the most distal tooth in the dental class is the one most often aected. Undersized maxillary lateral incisors and mandibular second premolars are the most common isolated problems in tooth size (see Fig. 31.10A). ese also appear to be genetically linked positioning errors have denite implications for the type of treatment that can be recommended.Tooth NumberAfter the form and symmetry of each arch have been characterized, it is imperative to count the number of permanent and primary teeth. A clinical examination and appropriate radiographs allow the practitioner to determine which teeth are present, developing, or missing. Disturbances in the initiation and proliferation stage of tooth development may lead to an abnormal number of teeth. Teeth that do not form are referred to as congenitally missing (Fig. 31.9). e most common missing teeth in the permanent dentition, apart from the maxillary and mandibular third molars, are the mandibular second premolar, maxillary lateral incisor, and maxillary second premolar in that order.15 In general, the most distal tooth in a class of teeth is most liable to be congenitally missing. Some have looked at whether there is a genetic component to missing and impacted teeth. It is reported that patients with palatally impacted canines exhibit a higher incidence of missing permanent teeth than the general population and that several generations in the family will exhibit the same palatal impaction (Fig. 31.10).16 Recent evidence suggests there are specic genes that cause specic • Figure 31.9 This patient is congenitally missing both permanent maxil-lary lateral incisors, and the permanent maxillary canines have spontane-ously substituted in their places. The most common missing teeth in the permanent dentition, besides the third molars, are the maxillary lateral incisor and the mandibular second premolar. BA• Figure 31.10 (A) The occurrence of multiple anomalies of tooth position, number, and shape linked by genetics is demonstrated in this patient who has an erupted peg-shaped permanent maxillary right lateral incisor and a retained primary maxillary right canine. (B) The occlusal radiograph shows the peg lateral, the missing permanent maxillary left lateral incisor, and the ectopically erupting permanent maxillary right canine. CHAPTER 31 Examination, Diagnosis, and Treatment Planning 427 reduced in size by selective equilibration to eliminate occlusal interference (Fig. 31.16). Both conditions usually require tooth movement before denitive restorative care to obtain an esthetically pleasing and functional result. Root structure abnormalities such as signicant dilaceration may make orthodontic movement of teeth dicult (Fig. 31.17). Often the portion of the root apical to the irregularity is resorbed or remodeled during tooth movement. If a tooth with root abnormalities is scheduled for extraction, it may be prudent to refer the patient to a specialist because the abnormality will certainly complicate the extraction. Finally, fused or geminated teeth can pose diculties due to their size. e clini-cian should consult with other dental specialists because the treatment will often involve a combination of endodontics, surgery, orthodontics, and restorative care.20,21Clearly, in this age group four upper and lower incisors should be evident early on. When they are not, concern and follow-up are warranted. e clinician should recognize that it is highly anomalies, so evaluating patients with peg laterals should include evaluation for palatally displaced canines, additional missing teeth, and transpositions. Sometimes complex orthodontic and restorative treatment is necessary to achieve a harmonious occlusal relationship and satisfy esthetic requirements when local tooth size problems exist. is type of treatment usually amounts to distributing space between the teeth so that when the teeth are restored to normal size and contour, they t in a good occlusal relationship with good anterior esthetics (Fig. 31.14). Other times, treatment may mean reducing the mesiodistal dimension of oversized crowns through interproximal reduction (Fig. 31.15).Teeth with abnormal crown and root morphologic characteristics may create occlusal problems. Careful clinical and radiographic examination is necessary to diagnose these problems. If the abnormality involves the crown (maxillary peg lateral or talon cusp), either the crown should be recontoured by addition of restorative material to increase its size or the talon cusp should be L• Figure 31.11 This patient was diagnosed with a primitive neuroectodermal tumor and was treated with radiation and chemotherapy from the ages of 2 to 4 years. The teeth developing during that time period are stunted, missing, or have arrested root development. Of interest, the third molars are develop-ing normally because their development started after the end of the therapy. • Figure 31.12 A midline supernumerary tooth, or mesiodens, is situated between the unerupted maxillary central incisors. Arrows indicate the position of the mesiodens, which can cause disturbances in eruption and adjacent tooth formation. • Figure 31.13 An odontoma is impeding the eruption of the maxillary right lateral incisor and canine. The odontoma should be surgically removed before eruption problems arise but late enough to avoid surgical trauma to the adjacent developing teeth. (Courtesy Dr. Phillip R. Parker.) 428 Part 4 The Transitional Years: Six to Twelve Yearswhich can reveal other related anomalies when missing anterior teeth (lateral incisors or canines) or peg-shaped lateral incisors are encountered. en, depending on the ndings, a small eld of view CBCT may be indicated. ese views can be supplemented with a traditional cephalometric digital image if required for limited or comprehensive orthodontic care. is exposes the patient to less radiation than would be delivered if a full eld CBCT was initially obtained. e details of these examinations are noted later in the chapter.unusual for a child 9 years of age not to have all the upper and lower incisors (Fig. 31.18). If not present, the clinician should investigate why they are not and develop an appropriate treatment plan to address it. Likewise, maxillary permanent canines should be positively palpated or their existence conrmed radiographically by age 10 years. It appears that cone beam computed tomography (CBCT) images are superior to two-dimensional (2D) images for determining the status of canines and the adjacent teeth.22 A sensible method, then, is to obtain a panoramic radiograph, B CA• Figure 31.14 (A) In this case, a maxillary tooth size deciency contributed to the diastema. If the space was closed with orthodontics, the resulting occlusion would not be correct. In addition, the tapered crown form of the central incisor would result in less than ideal esthetics. (B) Composite resin was added to the mesial surface of both central incisors before orthodontic treatment to correct the tooth size deciency and give the teeth normal contour. (C) The orthodontic result shows excellent occlusion and esthetics. BA• Figure 31.15 (A) The permanent maxillary right central incisor is substantially larger than the contra-lateral left central incisor. (B) The permanent maxillary left lateral incisor shown here in a lingual position is at least 2 mm larger than normal and the contralateral tooth. Isolated teeth such as these often require mesiodistal interproximal reduction to t harmoniously in a nal occlusion. CHAPTER 31 Examination, Diagnosis, and Treatment Planning 429 position problems. Several studies have shown a genetic link between missing teeth, tooth anomalies, and altered eruption paths.16,23–25 ere seems to be clustering of these problems. If one of these conditions is identied, the clinician should examine the patient for these other related problems as mentioned earlier.Ectopic eruption describes a path of eruption that causes root resorption of a portion or all of the adjacent primary tooth. Ectopic eruption is most often associated with the permanent maxillary rst molar, mandibular lateral incisor, and maxillary canine.26–28 In ectopic eruption of the permanent rst molar, a portion of the erupting rst molar resorbs the distal root of the primary second molar and is inhibited from erupting by the distal portion of the primary molar (Fig. 31.19). In many cases, the permanent molar spontaneously “jumps” or moves distally and erupts into the correct position. In other cases, the permanent molar lodges under the primary molar crown and no longer erupts. Usually, no pain or discomfort is associated with ectopic eruption unless communication develops between the oral cavity and the pulpal tissue of the primary molar, causing an abscess. Permanent molar ectopic eruption is often detected during clinical examination and conrmed with routine bitewing radiographs.e prevalence of permanent rst molar ectopic eruption is reported to be 3% to 4%.29 Several possible causes of ectopic molar eruption have been proposed: (1) the maxillary teeth are larger than normal, (2) the maxilla is smaller than normal, (3) the maxilla is positioned further posteriorly than normal in relation to the cranial base, or (4) the angulation of the erupting maxillary per-manent rst molar is abnormal.30,31 Although ectopic molar eruption may occur in the mandibular arch, it is more common in the maxilla.Ectopic eruption of the permanent lateral incisor is most common in the mandibular arch. e erupting incisor resorbs all or a portion of the primary canine root because the path of eruption is abnormal, there is transitional crowding from the primary to the permanent dentition, or there is a true arch length deciency. e diagnosis is generally signaled by premature primary canine exfoliation, often accompanied by a midline shift to the side of the ectopic eruption or impeded eruption of the lateral incisor, or it is discovered on an occlusal radiograph (Fig. 31.20).e third common type of ectopic eruption occurs with maxillary permanent canine eruption and associated resorption of the per-manent lateral incisor (Fig. 31.21). Studies have shown that if canines erupt from a more medial position in the dental arch and with a slightly more mesial horizontal path of eruption (an average of 10 degrees), there is a greater risk of lateral incisor resorption. Tooth Positione position of erupted and unerupted permanent teeth in this age group should be noted and compared with the normal sequence and time of eruption. Minor asymmetry in dental eruption is normal, and there is little cause for concern if less than 6 months’ dierence in eruption exists between contralateral sides of the mouth. Five tooth positioning problems are associated with the mixed dentition: ectopic eruption, transposition, impaction, and primary failure of eruption, and the midline diastema. Interestingly, there appears to be a genetic component to some of these tooth • Figure 31.16 This patient has a talon cusp on the maxillary right lateral incisor. The enamel protuberance may have a pulp horn in it and cannot just simply be reduced by abrasion with a bur. These anomalies can cause interference in the occlusion and prohibit normal overbite and overjet. Usually, periodic gradual reduction with a bur will allow the pulp horn to recede, preserve tooth vitality, and improve the morphology toward a normal occlusion. • Figure 31.17 Root structure abnormalities, such as this dilacerated maxillary left lateral incisor, make orthodontic movement of teeth very dif-cult. A dilaceration of this magnitude makes the root more susceptible to apical resorption and complicates the nal positioning of the crown and root. • Figure 31.18 All permanent incisors should have erupted by 9 years of age. This patient has a retained primary maxillary central incisor and obvious eruption problems. This clinical sign should not be overlooked and has an impact on the developing dentition and the child’s self-esteem. 430 Part 4 The Transitional Years: Six to Twelve YearsBA• Figure 31.19 In ectopic eruption, the permanent rst molar resorbs a portion of the distal root of the primary second molar. (A) In this case, the permanent rst molar has lodged under the primary second molar crown. In other cases, the permanent molar spontaneously “jumps” or moves distally and erupts into the normal position. (B) The distal resorption of the primary molar root is evident on this radiograph. BA• Figure 31.20 When a primary canine is lost because of ectopic eruption of a permanent lateral incisor, the midline often shifts to the side of the lost primary canine. (A) It is apparent from this view that the mandibular midline has shifted to the patient’s right. (B) The permanent right lateral incisor is now blocked to the lingual as a consequence of the mandibular midline shift. • Figure 31.21 The maxillary right canine has erupted into the lateral incisor space and resorbed a portion of the root. This type of resorption is more common than believed, but often not to this extent. CHAPTER 31 Examination, Diagnosis, and Treatment Planning 431 Tooth impaction, as noted earlier, is diagnosed during the clinical examination or from appropriate radiographs. Over-retained primary teeth, supernumerary teeth, severe crowding, or a failure in the eruption mechanism can cause impaction of the anterior teeth (Fig. 31.24A). Often the permanent tooth erupts if the over-retained primary tooth or supernumerary tooth is removed. If the tooth is impacted as a result of crowding, it is necessary to provide space either orthodontically or by extraction to allow eruption. Generally the last tooth to erupt in an arch or quadrant is impacted because the space is reduced or no longer available. is eruption mechanism or the aberrant eruption direction usually is the cause of impaction of the maxillary canine. e maxillary canine is most often the last tooth to erupt into the arch. It also erupts or travels the longest distance to take its place in the arch. ese two factors combine to make the maxillary canine the most common impacted tooth in the maxillary arch and indeed the mouth (see Fig. 31.24B). Posterior tooth impaction is normally the result of inadequate arch length. Inadequate arch length is caused by a tooth–jaw size discrepancy or space loss as a result of premature primary tooth loss. If the arch length problem is generalized, either permanent teeth should be removed or the arch should be expanded to allow eruption of all the permanent teeth. Limited, localized crowding due to space loss can be treated by orthodontically regaining the lost space.At times the permanent rst molar fails to erupt or erupts partially. e dilemma for the clinician is to diagnose the problem. ere seem to be three diagnoses for an unerupted permanent molar. e rst is primary failure of eruption. Primary failure of eruption is an unusual eruption problem that aects the posterior teeth (Fig. 31.25). It is diagnosed when a tooth fails to erupt despite the presence of adequate space and the absence of overlying hard tissue that prevents eruption. Furthermore, all teeth distal to the aected tooth also fail to erupt. e cause of primary failure of eruption is unknown but appears to have a genetic component.35–37 e second cause of an unerupted permanent molar is mechanical failure of eruption. Two characteristics distinguish mechanical failure of eruption from primary failure of eruption. e rst is that some type of mechanical obstruction can explain the lack of eruption. e path of eruption is not clear like primary failure eruption. Obstruction can be from lack of space, a developmental problem with the tooth, or placement of the tongue. Removal of the obstruction will generally allow tooth movement. e other characteristic distinguishing primary from mechanical failure of eruption is that teeth distal to the aected tooth will erupt. is is dicult to determine early in treatment. Ankylosis of the tooth is the third diagnosis for an unerupted tooth. A tooth with ankylosis will not erupt even if there is space and the teeth distal are not aected.38A small, maxillary midline diastema in the early mixed dentition is normal (Fig. 31.26). Typically it is caused by the position of the unerupted lateral incisors or canines (Fig. 31.27A). e unerupted teeth are positioned superior and distal to the roots of the central incisors, and they direct the central incisor roots toward the midline and the crowns toward the distal (see Fig. 31.27B). As the lateral incisors or canines erupt, the incisors upright themselves slowly and the midline space begins to close. Treatment to close a diastema is usually delayed until the permanent canines are fully erupted unless the space available for eruption of the lateral incisors or canines is severely limited or the esthetics are a compelling concern. If the diastema is larger than 2 mm, the cause may be a mesiodens (see Fig. 31.12), a localized tooth size problem, or abnormal incisor positioning. A mesiodens is usually discovered on radiographic examination, and its removal normally allows the diastema to close. A size mismatch between the upper and lower teeth may result It is recommended to remove the primary canine to promote more ideal canine eruption if the canine cusp on images is positioned medially to the midline of the lateral incisor.26,32 Some investigations suggest additional treatment to improve canine position, such as primary canine removal in conjunction with maxillary expansion.33A related phenomenon is lingual eruption of the permanent incisors, predominantly the mandibular incisors (Fig. 31.22). e prevalence of lingually erupting mandibular incisors is about 10%.34 e cause of ectopic and lingually erupting incisors is not well established. One explanation suggests that ectopic and lingual eruption of the incisors results from an abnormal pattern of resorption. Alternatively, it has been suggested that lingual eruption is a variation of the normal eruption pattern because the lower incisor tooth buds form lingual to the primary incisors and may not migrate facially.Transposition occurs when there is “a positional interchange of two adjacent teeth, especially their roots or the development or eruption of a tooth in a position occupied normally by a nonadjacent tooth.”25 Usually transpositions are observed later in the transitional dentition years. e early-stage transposition is uncommon but is the type of transposition observed in the early mixed-dentition years (Fig. 31.23). is usually is a transposition of the mandibular lateral incisor and canine.24 e lateral incisor will show distal tipping, resorption of the primary canine (and sometimes the primary rst molar), and rotation as it migrates. Other transpositions that are observed later in the transitional years are likely to be the mature mandibular lateral and canine, and the more prevalent transpositions of the maxillary canine and rst premolar and maxillary canine and lateral incisor.25• Figure 31.22 Ectopic eruption of the permanent lateral incisors is most common in the mandibular arch. In this example, the mandibular lateral incisors erupted lingual to their ideal position and the primary laterals are still present. In some cases, the lateral incisors erupt into a more normal position but cause premature exfoliation of the primary canine. • Figure 31.23 Early-stage transposition of the mandibular lateral inci-sors and the canines. Note that the permanent mandibular right lateral incisor has resorbed the primary canine and the primary rst molar is about to be lost. If intercepted early, true transposition will not occur. 432 Part 4 The Transitional Years: Six to Twelve YearsAB• Figure 31.24 In the transitional years, tooth impaction in the anterior region is usually caused by over-retained primary teeth, supernumerary teeth, or severe crowding. In a few cases, a failure in the eruption mechanism is responsible for the delayed eruption. (A) In this case, the maxillary right central incisor is completely inverted and is directed toward the nasal cavity. (B) The ultimate sequela of a lack of space is illustrated by this impacted maxillary right canine even though the orientation of the tooth is correct. Note that the maxillary left canine will successfully erupt. • Figure 31.25 Primary failure of eruption usually presents as a posterior segment of open bite. It appears to cause eruption problems with all teeth posterior to the most anterior affected tooth in that quadrant. In this case, given the occlusal plane, it appears that the lower teeth are involved. Treatment can be challenging and the open bite must be closed surgically or prosthetically after growth has ceased. • Figure 31.26 A small maxillary midline diastema is normal in the mixed dentition. The diastema tends to close with the eruption of the permanent maxillary lateral incisors and canines. CHAPTER 31 Examination, Diagnosis, and Treatment Planning 433 Incisor position is not always ideal, however, and estimates of dental arch discrepancies must be adjusted if both upper and lower anterior teeth are either protrusive or retrusive.Transverse RelationshipDental midline and posterior crossbite evaluation is conducted in the same manner described in Chapter 19. Usually dental midline deviations are either the result of simply moderate to severe crowding or ectopic eruption and tooth loss with a shift of the midline as teeth realign in the newly available space (see Fig. 31.20). Functional deviations of the mandible are identied by noting discrepancies between centric relation and centric occlusion. Posterior crossbites are determined to be either unilateral or bilateral. In the early mixed-dentition years, treatments for both skeletal and dental crossbites are essentially the same. As the child becomes older, it becomes more critical to identify whether a crossbite is due to skeletal or dental causes because the midpalatal suture becomes more interdigitated over time. e management of posterior crossbite in the complete permanent dentition varies according to whether the crossbite is skeletal or dental in origin and the estimate of whether the midpalatal suture is open, bridged, or closed.Vertical Dimensione vertical dental examination is concerned with overbite and open-bite measurements and ankylosis. Normal overbite in this age group is approximately 2 mm. If there is a deviation from normal, the clinician should try to determine if the deviation is due to a dental or a skeletal problem. If the facial examination in a diastema. In this situation, the maxillary incisor crowns are small or excessively tapered, although the mandibular teeth may be too large in relation to the maxillary teeth. If large spaces are present, a combination of tooth movement and anterior restora-tions is required to correct the size discrepancy. Abnormal incisor positioning and protrusion also may result in a midline diastema. e abnormal positioning may be due to past or present nger habits or to abnormal eruption. e best treatment is to rst eliminate the habit and then to retract the incisors orthodontically and consolidate space.Anteroposterior DimensionPermanent molar and canine relationships should be noted and compared with the anteroposterior skeletal relationships that were determined during the extraoral examination. Permanent molar and canine relationships are illustrated in Fig. 31.28. Dental relationships generally reect the underlying skeletal relationships, including asymmetry, although it is feasible to have dierent dental and skeletal relationships if teeth are missing or have drifted. For example, a person with a class I skeletal relationship may have a class II molar relationship if there has been posterior space loss and the permanent maxillary rst molar drifted forward into the space (Fig. 31.29).If the permanent teeth are properly aligned in the alveolar bone at a normal angulation, overjet is a direct measurement of the relationship between the dental arches. Normal overjet is approximately 2 mm; therefore the discrepancy between the arches can be calculated by subtracting 2 mm from the measured overjet. AB• Figure 31.27 (A) The “ugly duckling” stage is evident when the crowns of the lateral incisors tip distally and open diastema between the anterior teeth. (B) The permanent canines are pushing against the roots of the permanent lateral incisors. Some of the anterior space will close with the eruption of the canines. 434 Part 4 The Transitional Years: Six to Twelve Yearsof adjacent teeth, and vertical bone loss. Most of these problems, with the exception of space loss, resolve when the permanent tooth erupts. Ankylosed teeth and associated problems are discussed in Chapter 19, and the reader is referred to that chapter for a more detailed discussion. One aspect of ankylosed primary teeth that must be addressed dierently is when the primary tooth is ankylosed and the permanent tooth is missing. If the vertical occlusal step becomes exaggerated, and by denition the vertical bone level relative revealed a vertical skeletal problem, it is sometimes reected in the dental relationships. Treatment of the malocclusion varies with the source of the problem.Ankylosis of the primary teeth can present several problems because of the magnitude of vertical dentoalveolar growth. Dental eruption and vertical growth of the alveolus may amount to as much as 10 mm from age 6 to 12 years. us ankylosis of a primary tooth at an early age may result in large marginal ridge discrepancies, tipping CBA• Figure 31.28 (A) In the permanent dentition, permanent molar and canine relationships are determined and compared with the anteroposterior skeletal relationships. To determine molar relationships, the posi-tion of the mesiobuccal cusp of the permanent maxillary rst molar is related to the position of the facial groove of the permanent mandibular rst molar. If the mesiobuccal cusp occludes in the facial groove, the molar relationship is called class I. The canine relationship is determined by the relationship of the maxillary canine to the embrasure between the mandibular canine and the rst premolar (or primary rst molar). If the maxillary canine occludes in the embrasure, the canine relationship is also called class I. (B) If the mesiobuccal cusp of the permanent maxillary rst molar occludes mesial to the mandibular facial groove, the molar relationship is called class II. The canine relationship is called class II if the maxillary canine occludes mesial to the mandibular canine–rst premolar embrasure. (C) If the mesiobuccal cusp of the permanent maxillary rst molar occludes distal to the mandibular facial groove, the molar relation-ship is called class III. The canine relationship is class III if the maxillary canine occludes distal to the mandibular canine–rst premolar embrasure. CHAPTER 31 Examination, Diagnosis, and Treatment Planning 435 software programs available to the clinician to store and manipulate the images. A minimum of three extraoral images of the face are obtained: a frontal face with lips relaxed, a frontal face with posed smile, and a lateral face with lips relaxed. Five intraoral images consisting of a frontal, right and left lateral, and maxillary and mandibular occlusal views are obtained. ese images are stored in a montage for study and to present during case reviews (Fig. 31.31). Some like to supplement these images with a three-quarter view with lip relaxed, a three-quarter view with posed smile, and a lateral view with a posed smile (Fig. 31.32).Diagnostic CastsOrthodontic treatment in the mixed dentition is more complex than treatment in the primary dentition. e clinician must consider the dierence in size between the primary and permanent denti-tions, the amount of space available for the permanent teeth, and the dental and skeletal status of the patient. is formidable job requires supplemental information to make accurate orthodontic diagnoses and to develop coherent treatment plans. Diagnostic study casts are an essential part of a thorough evaluation if to adjacent teeth is exaggerated, intervention is indicated. is is the case because there is no permanent tooth to erupt and bring alveolar bone with it. If the primary tooth is allowed to remain, its eventual extraction will leave a bony defect adjacent to the remaining permanent teeth (Fig. 31.30). Timely removal of the primary tooth and further treatment will have to be considered. A second option for treatment is to decoronate the primary molar rather than remove it in cases where there is no permanent successor. ere still is loss of vertical height of the alveolus but decoronation seems to maintain the alveolar width. Loss of bone due to extraction of a primary tooth without a successor is more rapid and severe in the anterior than in the posterior areas of the mouth.Supplemental Orthodontic Diagnostic TechniquesPhotographsAmong the most basic diagnostic records routinely obtained are facial and intraoral photographs. ere are several commercial BA• Figure 31.29 Space loss can cause dental relationships to not reect skeletal relationships. (A) This patient had maxillary posterior space loss with mesial drift so that the molars are class II and not reective of the skeletal class I relationships. (B) The space loss caused the permanent canines to erupt to the facial. • Figure 31.30 The ankylosed primary mandibular second molar demonstrates the alteration of bone level that can occur when ankylosed primary teeth without successors are maintained too long. Timely removal of the ankylosed tooth and treatment planning for orthodontic movement of the adjacent teeth or prosthetic replacement are critical.

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