TL;DR

Key Facts

What Is Growth and Development in Orthodontics?

Growth refers to a measurable increase in size — the addition of new tissue. Development is the broader process by which an organism matures toward a fully functional adult form, encompassing not only size increases but also differentiation, tissue remodelling, and changes in proportion. In the context of orthodontics, growth and development describes the sequential changes in the craniofacial skeleton, dentition, and soft tissues from embryonic life through early adulthood.

This knowledge underpins orthodontic practice at every level. The timing of treatment, the choice of appliance, the prognosis of growth modification, the risk of post-treatment relapse, and the decision of whether a patient needs orthodontics alone or combined orthodontic-surgical treatment all hinge on an accurate understanding of the patient’s developmental stage and remaining growth potential.

The craniofacial region does not grow as a single unit — different structures have distinct growth patterns, timings, and mechanisms. The skull vault follows a neural growth curve, reaching near-adult size by age 7. The midface and mandible follow a somatic growth curve, with significant increments continuing into mid-adolescence. The nose, lips, and chin continue to change even after skeletal growth has ceased. Recognising these independent timelines is essential for planning treatment that will still look correct when the patient reaches adulthood.

Why It Matters (Clinical + Exam Context)

Growth and development is among the most heavily weighted topics in orthodontic specialty examinations and appears regularly in general dentistry licensing exams (INBDE, NBDE). Clinically, it is foundational to every decision about when to treat, what to use, and what to expect.

Clinical Relevance

• Timing of interceptive treatment: Many malocclusions — Class III with maxillary deficiency, posterior crossbite, anterior open bite from habits — can be partially or fully corrected with growth modification if treated at the right developmental stage. The same appliance used two years too late may produce no skeletal effect at all.
• Functional appliance efficacy: Twin blocks, Herbst appliances, and other functional appliances work primarily by redirecting and enhancing condylar growth. Their effectiveness is greatest during the pubertal growth spurt — knowing when a patient is approaching, in, or past that window is critical to appliance selection and timing.
• Orthognathic surgery timing: Surgery to correct skeletal discrepancies is deferred until growth is complete — typically age 17–18 in females and 18–21 in males — to prevent relapse from continued post-surgical growth. Assessing growth completion is the critical gatekeeping step before surgical referral.
• Relapse prevention: Late mandibular growth — which continues beyond maxillary growth and into early adulthood, particularly in males — is a major driver of late lower incisor crowding and Class III relapse. Knowing this drives decisions about long-term retention.
• Eruption timing and space management: Understanding the normal sequence and timing of tooth eruption allows early identification of eruption problems — delayed eruption, ectopic eruption, impacted canines — and timely intervention.

Craniofacial Growth

The craniofacial skeleton develops from two cell populations: cranial neural crest cells (which give rise to most of the facial skeleton and dental structures) and paraxial mesoderm (which contributes to the cranial vault). Growth occurs by three distinct mechanisms, each predominating in different regions.

Mechanisms of Bone Growth

• Endochondral ossification: Bone forms by replacing a cartilage model. In the craniofacial region, this occurs at the synchondroses of the cranial base (sphenoethmoidal, spheno-occipital) and at the condylar cartilage of the mandible. The spheno-occipital synchondrosis is the most important — it remains active until approximately age 15–17 and drives anterior growth of the middle cranial fossa, influencing the position of both maxilla and mandible.
• Intramembranous (periosteal) ossification: Bone forms directly within a connective tissue membrane, without a cartilage precursor. This is the dominant mechanism for most facial bones — the maxilla, zygoma, orbital rims, nasal bones, and the body and ramus of the mandible all grow primarily by periosteal apposition and resorption. Bone is deposited on surfaces under tension and resorbed from surfaces under compression, a process called surface remodelling.
• Sutural growth: Bone is deposited at the edges of adjacent bones where they meet at fibrous sutural joints. In the midface, the major sutures (frontomaxillary, zygomaticomaxillary, zygomaticotemporal, and pterygopalatine) allow downward and forward displacement of the maxilla as the cranial base expands. Sutural growth is a passive, reactive process — it responds to the displacement forces generated by growth at remote sites rather than being an independent growth engine.

The Cranial Base

The cranial base connects the neurocranium (brain case) to the face and plays a critical role in determining the anteroposterior relationship of the jaws. The cranial base angle (saddle angle, or NSAr — the angle between the anterior and posterior cranial base measured at sella turcica) influences whether the face tends toward a Class II or Class III skeletal pattern. A larger-than-average saddle angle positions the glenoid fossa — and therefore the mandible — further back relative to the maxilla, predisposing to a Class II relationship. A smaller saddle angle does the opposite.

The spheno-occipital synchondrosis is the primary growth site of the cranial base, producing growth that drives the entire midface forward and downward. It is active from birth until approximately age 15–17, at which point it fuses and cranial base growth effectively ceases. This timing is important: it means mid-facial growth continues well into the teen years, driven partly by this posterior cranial base expansion.

Maxillary Growth

The maxilla grows downward and forward relative to the cranial base. This movement is achieved by two simultaneous processes working in concert:

• Passive displacement: The maxilla is carried downward and forward as the posterior cranial base expands and the nasomaxillary sutures deposit new bone reactively.
• Active surface remodelling: The anterior surface of the maxilla undergoes resorption (moving the bony surface backward), while bone is deposited on the posterior surface of the tuberosity, lengthening the arch. The palatal vault is lowered by resorption on its nasal surface and deposition on its oral surface.

The net direction of maxillary growth is downward and forward, but the remodelling pattern means the anterior surface does not actually move forward — the entire maxilla is carried forward while its anterior surface simultaneously resorbs. This is a classic example of the apparent paradox of bone growth: a surface can resorb yet still end up in a more forward position due to displacement of the whole bone.

Maxillary growth is largely complete by age 14–15 in females and 15–17 in males. The mid-palatal suture closes progressively during adolescence, which is why rapid maxillary expansion (RME) is most effective before approximately age 14–16 and becomes progressively more difficult — eventually requiring surgical assistance — after that window.

Mandibular Growth

The mandible grows primarily at the condylar cartilage, a secondary cartilage (unlike the primary cartilages of the synchondroses, it is not a remnant of the embryonic cartilaginous skeleton but forms de novo). Condylar growth displaces the mandible downward and forward, while extensive surface remodelling reshapes the ramus and body.

The direction of condylar growth is predominantly superiorly and posteriorly (upward and backward), but because this occurs within the glenoid fossa, the net effect on the chin is displacement downward and forward. The ramus grows upward and backward by posterior apposition and anterior resorption, maintaining the ramus height as the body of the mandible lengthens anteriorly.

Critically, mandibular growth continues later and for longer than maxillary growth — particularly in males. In some individuals, mandibular growth continues into the early-to-mid 20s. This is clinically significant for two reasons: it explains why Class III surgical corrections ideally wait until late adolescence or early adulthood, and it explains the phenomenon of late lower incisor crowding seen in post-orthodontic patients who were inadequately retained.

Growth Timing and Prediction

Knowing that a patient will grow is less useful than knowing when and how much. Growth prediction allows the orthodontist to time treatment to coincide with periods of rapid growth (for growth modification) or to confirm growth completion (before surgery or when relapse risk is high).

The Pubertal Growth Spurt

Craniofacial growth does not proceed at a constant rate — it follows a characteristic pattern of rapid growth in infancy, slower growth in childhood, a second acceleration during puberty (the pubertal growth spurt), and deceleration to completion in late adolescence or early adulthood.

The pubertal growth spurt is the critical window for orthodontic growth modification because it represents the period of greatest mandibular growth velocity. Functional appliances and orthopaedic forces are most effective when applied just before or at the peak of the pubertal spurt, when condylar growth is maximal and most responsive to mechanical stimulation. The timing of the spurt varies considerably between individuals and between sexes:

• Females: Peak height velocity (PHV) occurs at approximately 10–12 years; craniofacial growth spurt closely parallels this.
• Males: PHV occurs approximately 2 years later than females — typically 12–14 years — and the magnitude of the growth increment is greater.

Chronological age is a poor predictor of pubertal timing due to the wide individual variation. A 12-year-old boy may be prepubertal, mid-pubertal, or post-pubertal — hence the need for biological maturation indicators rather than relying on age alone.

Skeletal Maturation Indicators

Several methods are used to assess biological maturity and predict growth potential:

• Cervical Vertebral Maturation (CVM): Currently the preferred method in orthodontic practice because it uses the lateral cephalogram already taken for orthodontic records — no additional radiation. The shapes of the second, third, and fourth cervical vertebrae change in a predictable sequence from concave inferior borders to increasingly rectangular, cuboidal shapes. Six stages (CS1–CS6) have been described by Baccetti, Franchi, and McNamara (2002). The pubertal growth spurt occurs between CS3 and CS4; the peak of mandibular growth occurs at or just after CS3. This method is now the standard clinical tool for growth assessment.
• Hand-wrist radiography: Historically the gold standard. The maturation of specific carpal bones (pisiform, sesamoid of the thumb), epiphyseal fusion at the middle phalanges, and other markers correlate closely with the pubertal growth spurt and growth completion. The appearance of the sesamoid bone at the metacarpophalangeal joint of the thumb (MP3 sesamoid) signals the onset of the pubertal spurt. Less commonly used today because it requires additional radiation not otherwise justified by dental treatment.
• Dental maturation: Tooth development stages (Demirjian stages) correlate with skeletal maturation but less precisely than CVM or hand-wrist. Useful as a supplementary indicator, particularly in younger children.
• Secondary sexual characteristics and menarche: Menarche in females typically occurs after PHV — i.e., after the peak of the growth spurt has passed. A patient who has just experienced menarche has already passed the optimal window for growth modification. This is a useful clinical screen: a pre-menarchal female has more remaining growth than a post-menarchal one of the same age.
• Chronological age: A crude indicator only. Useful as a first estimate in the absence of other data, but individual variation is too great for clinical decisions to be based on age alone.

Dentition Development

The human dentition passes through three recognisable stages — primary, mixed, and permanent — each with distinct orthodontic characteristics and clinical implications.

Primary (Deciduous) Dentition

The primary dentition consists of 20 teeth — 5 per quadrant: central incisor, lateral incisor, canine, first molar, second molar. The primary dentition is complete by approximately age 2.5–3 years and remains the sole dentition until the first permanent teeth begin to erupt at around age 6.

Key orthodontic features of the primary dentition include:

• Spacing: Generalised spacing between primary teeth — particularly the primate spaces (between the maxillary lateral incisor and canine, and between the mandibular canine and first molar) — is normal and desirable. Spacing accommodates the larger permanent successors. A tightly packed primary dentition with no spacing (closed primary dentition) is a risk factor for crowding in the permanent dentition.
• Terminal plane relationship: The distal surfaces of the maxillary and mandibular second primary molars form a relationship — the terminal plane — that predicts the future Class I, II, or III molar occlusion. A flush terminal plane (molars flush) typically develops into a Class I permanent molar relationship with the mesial step of the first permanent molars as they erupt. A mesial step predicts Class I; a distal step predicts Class II; an exaggerated mesial step predicts Class III.
• Overbite and overjet: Primary teeth have a greater overbite than permanent teeth, and a small positive overjet is normal. An anterior open bite in the primary dentition is frequently associated with digit-sucking or dummy (pacifier) habits.
• Wear facets: Physiological attrition of primary teeth is normal and expected.

Mixed Dentition

The mixed dentition stage spans from approximately age 6 — when the first permanent molars and central incisors begin to erupt — to approximately age 12, when the last primary teeth are shed. Both primary and permanent teeth are present simultaneously.

The mixed dentition is divided into an early mixed dentition (age 6–9, first molars and incisors erupting) and a late mixed dentition (age 9–12, canines and premolars transitioning).

Critical orthodontic concepts in the mixed dentition include:

• The ugly duckling stage: A normal transient phase during eruption of the maxillary permanent incisors (approximately age 7–9) characterised by divergence of the central incisor crowns due to the unerupted canines pressing on the lateral incisor roots. Parents are frequently alarmed. The spacing self-corrects when the canines erupt — no treatment is required if this is the sole finding.
• Leeway space: The combined mesiodistal width of the primary canine, first molar, and second molar is larger than their permanent successors (canine and two premolars). The difference — the leeway space — is approximately 1.5 mm per side in the maxilla and 2.5 mm per side in the mandible (Nance, 1947). This space is normally used by the permanent first molar drifting mesially as primary teeth are shed, converting a flush terminal plane into a Class I molar relationship. Loss of leeway space through early extraction of primary teeth without space management is a common cause of permanent tooth crowding.
• Mixed dentition space analysis: Predicts whether there is adequate arch space for all erupting permanent teeth. Methods include the Moyers mixed dentition analysis (using probability tables based on lower incisor width to predict unerupted canine and premolar sizes) and the Tanaka-Johnston method (a simpler formula). These analyses guide decisions about early extraction, space maintenance, or arch expansion.
• Eruption sequence: The normal sequence of eruption is important — deviations (canines erupting before second premolars, or laterals failing to erupt) are clinical flags. In the maxilla the typical sequence is: 6 → 1 → 2 → 4 → 3 → 5 → 7 (using FDI number notation for permanent teeth). In the mandible: 6 → 1 → 2 → 3 → 4 → 5 → 7.

Permanent Dentition

The permanent dentition consists of 32 teeth (including third molars) or 28 (excluding third molars). Excluding third molars, the permanent dentition is complete by approximately age 12–13. Third molars erupt variably between age 17 and 25 (or may be impacted, absent, or require extraction).

Key features of the developing permanent dentition relevant to orthodontics include:

• Eruption timing of the maxillary canine: The maxillary permanent canine has the longest and most complex eruption path of any tooth — it begins its journey high in the maxilla and must descend over a considerable distance. It is the most commonly impacted tooth after third molars. Any absence of a visible canine bulge in the buccal sulcus by age 10–11 warrants radiographic investigation.
• Late lower incisor crowding: A well-documented phenomenon in which the lower anterior teeth develop crowding in the late teen years and early adulthood, even in patients with previously well-aligned dentitions. It is multifactorial — late mandibular growth, pressure from erupting third molars (controversial), soft tissue maturation, and periodontal changes all contribute. It is a primary driver of long-term retention protocols.
• Third molar development and eruption: Third molars begin calcifying at age 8–10 and erupt between 17–25 years — the last teeth to develop. Their eruption is highly variable; impaction rates are approximately 25–35% in the general population. Their role in late incisor crowding remains debated, but their management (retain, monitor, or extract) is a common clinical decision point in the late adolescent and young adult patient.

Clinical Considerations

• Assess growth stage, not just age: Chronological age is a poor proxy for biological maturity. Two patients of the same age can differ by 2–3 years in skeletal maturity. Always assess growth stage with CVM or equivalent before committing to growth-dependent treatment timing.
• Growth modification has a window: Orthopaedic treatment (e.g., Class II functional appliances, Class III facemask therapy) is only effective while significant growth remains. Starting too late produces dental rather than skeletal change — the outcome is less stable and more relapse-prone. For Class III facemask treatment, the earlier the better: most effective before age 10, and of limited benefit after age 12.
• Sexual dimorphism in growth timing: Males grow later and for longer than females. A 14-year-old male may still have 3–4 years of significant mandibular growth remaining. A 14-year-old female is often near or at growth completion. Treatment timing decisions must account for this dimorphism.
• Manage the mixed dentition proactively: The mixed dentition offers the greatest opportunity for interception — space maintenance after premature primary tooth loss, expansion of a constricted maxilla, correction of functional shifts, and guidance of erupting canines. These interventions, timed correctly, can simplify or prevent the need for comprehensive treatment.
• Plan for soft tissue changes: The soft tissue profile continues to change after skeletal growth is complete — the nose and chin in particular continue to develop into early adulthood. Treatment planning for aesthetic outcomes must account for anticipated soft tissue changes, particularly in young patients.
• Document growth with serial records: When growth status is uncertain, serial cephalometric records (taken 6–12 months apart) and comparison of CVM stages is more reliable than a single snapshot. Superimposition of serial cephalograms is the gold standard for documenting growth direction and amount.

Common Mistakes & Misconceptions

• Misconception: “The condyle is the only growth centre of the mandible.”
  Correction: The condyle is the primary growth site, but the entire mandible remodels through periosteal apposition and resorption. The coronoid process, ramus posterior border, and symphysis all undergo active remodelling. Calling the condyle the sole “growth centre” oversimplifies mandibular development.
• Misconception: “Menarche signals the start of the growth spurt in girls.”
  Correction: Menarche typically occurs after peak height velocity — the growth spurt has already peaked by the time menstruation begins. A patient who has recently experienced menarche has passed the optimal window for growth modification, not entered it.
• Misconception: “Rapid maxillary expansion can be done at any age.”
  Correction: RME is most effective before mid-palatal suture closure — ideally before age 14–16. Beyond this, the suture begins to interdigitate and eventually fuses. In adults, surgically assisted rapid palatal expansion (SARPE) or Le Fort I osteotomy is required for meaningful transverse correction.
• Misconception: “Spacing in the primary dentition means the child will need orthodontic treatment.”
  Correction: Generalised spacing and primate spaces in the primary dentition are entirely normal and actually desirable — they accommodate the wider permanent successors. A closed, tightly packed primary dentition is a risk factor for crowding, not spacing.
• Misconception: “Once orthodontic treatment is complete, the result is permanent.”
  Correction: Orthodontic results are inherently unstable without retention. Late mandibular growth, soft tissue pressure, periodontal fibre recoil, and occlusal forces all act to move teeth back toward their original positions. Lifelong retention — at minimum for the lower anterior segment — is increasingly recognised as the standard of care.

Related Topics

Growth and development is foundational to all areas of orthodontics and connects directly to cephalometrics, functional appliances, and interceptive treatment.

References & Sources

This article draws on foundational textbooks and landmark studies in craniofacial biology and orthodontics.

1. Proffit WR, Fields HW, Sarver DM (2018). Contemporary Orthodontics, 6th ed. Elsevier Mosby.
2. Enlow DH, Hans MG (1996). Essentials of Facial Growth. W.B. Saunders Company, Philadelphia.
3. Baccetti T, Franchi L, McNamara JA Jr (2002). An improved version of the cervical vertebral maturation (CVM) method for the assessment of mandibular growth. Angle Orthodontist, 72(4):316–323.
4. Nance HN (1947). The limitations of orthodontic treatment I: mixed dentition diagnosis and treatment. American Journal of Orthodontics, 33(4):177–223.
5. Bjork A (1968). The use of metallic implants in the study of facial growth in children: method and application. American Journal of Physical Anthropology, 29(2):243–254.
6. Tanaka MM, Johnston LE (1974). The prediction of the size of unerupted canines and premolars in a contemporary orthodontic population. Journal of the American Dental Association, 88(4):798–801.
7. Graber LW, Vanarsdall RL, Vig KWL, Huang GJ (2017). Orthodontics: Current Principles and Techniques, 6th ed. Elsevier.
8. Moss ML, Salentijn L (1969). The primary role of functional matrices in facial growth. American Journal of Orthodontics, 55(6):566–577.

Summary

Growth and development in orthodontics is the biological foundation on which every treatment decision is built. The craniofacial skeleton grows through endochondral ossification at the condyle and cranial base synchondroses, intramembranous surface remodelling of the facial bones, and reactive sutural growth. The maxilla grows downward and forward primarily by displacement; the mandible grows downward and forward primarily by condylar growth, with the crucial distinction that mandibular growth continues later — and longer — than maxillary growth. The pubertal growth spurt, assessed most reliably using cervical vertebral maturation, is the key window for growth modification. The dentition transitions through primary, mixed, and permanent stages, each with distinct space, timing, and interceptive implications. Failure to account for remaining growth — and the certainty of post-treatment change — is one of the most common sources of orthodontic relapse. Growth is not merely a backdrop to orthodontic treatment; it is an active biological force that the orthodontist must understand, predict, and work with.

About the Author

Dr. Andries Smith

Founder, Dental Panda

Dr. Andries Smith founded Dental Panda in 2020. As an immigrant to the United States, he had to take the INBDE exam, even though he was practicing dentistry for over 10 years. This revealed an opportunity. Andries noticed that INBDE prep course companies were putting profit over students. With his expertise and experience in dentistry, he created free dental wiki resources for students and the general public to have access to.