O R T H O D O N T I C S

Late Lower Arch Crowding:

The Aetiology Reviewed
MARGARET E. RICHARDSON

teeth, retroclination of anterior teeth or a

Abstract: This article reviews the causes of the crowding that commonly occurs, combination of both.
particularly in the lower arch, after eruption of the second permanent molars. Factors
discussed include mesially directed forces, in treated and untreated subjects, distally
directed forces, occlusal changes, direction of eruption, tooth morphology, periodontal
MESIALLY DIRECTED
forces, and degenerative connective tissue changes.
FORCES
Dent Update 2002; 29: 234–238 Mesial migration of human teeth has
been recognized since the late 18th
Clinical Relevance: The general practitioner sees patients over a period of many century, when it was described by John
years, observes the changes in dental alignment that occur with time and needs to be
aware of the possible reasons for such changes.
Hunter,2 and has been demonstrated
more recently by the forward movement
of the first molars measured radiologically
in subjects examined at 13 and again at 18
years.3 There is evidence to support the
view that it is largely responsible for the

T he human dentition is in a dynamic

state, constantly changing
throughout life. Particularly noticeable
in this respect is alignment of the lower
arch, which may be crowded at the age
of 7–8 years as the permanent incisors
start to erupt, less so at 9–11 years and
crowded again in the early teenage
years. Recent research1 suggests that
the lower arch may be relatively stable in
the later part of the second and in the
third decade of life but crowding may
develop or increase thereafter. An ever-
increasing volume of literature reports
the development of post-retention
crowding in subjects treated
orthodontically with various regimes,
both extraction and non-extraction, and
using various retention protocols.
The causes of crowding in the lower
arch after eruption of the second
Margaret E Richardson, MA, MDentSci, FDS,
DOrth,Associate Specialist Orthodontist (retired),
Orthodontic Department, School of Clinical
Dentistry, Belfast.
permanent molars are complex and
controversial. Many factors may be
involved, acting singly or in combination,
with varying degrees of influence, in
different subjects and at different ages.
Much of the research on late crowding
has been performed on orthodontically
treated subjects. This introduces other
variables related to mechanical tooth
movement which may obscure those that
occur in untreated subjects. It is difficult
therefore to establish a cause and effect
relationship and negative findings should
not eliminate possible causes.
The orthodontic literature abounds
with statements to the effect that
increased crowding is due to a decrease
in arch length, which is a normal and
inevitable part of the process of
maturation. Obviously, if arch length
decreases crowding must increase,
unless there is a corresponding decrease
in tooth size, a feature not commonly
found in the modern human dentition.
The real problem is the cause of the
decrease in arch length. It must be due
either to forward movement of posterior
increase in crowding during the teenage
years.
Mesial migration may be caused by:

physiological mesial drift;

the anterior component of the force
of occlusion on mesially inclined
teeth;

the mesial vectors of muscular
contraction;

the contraction of the trans-septal
fibres of the periodontal ligament; or

the presence of a developing third
molar.
In 1979 a consensus conference4 on
third molars concluded: ‘...there is little
rationale, based on present evidence, for
the extraction of third molars solely to
minimize present or future crowding of
lower anterior teeth, either in
orthodontic or non-orthodontic
patients.’ Numerous review papers5–13
on the subject have arrived at more or
less the same conclusion.
In 1997, a team from the National
Health Services Centre for Reviews and

234 Dental Update – June 2002

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Dissemination, at the University of York
in the United Kingdom, set out to
evaluate published reviews on the
appropriateness of prophylactic removal
of impacted third molars. This
publication,14 based on second-hand
interpretation of the original
investigations and written by a team,
only one of whom appears to hold a
dental qualification, concluded that the
association between third molars ‘... is
not significant enough to warrant
removing third molars for the prevention
of incisor crowding.’ Statements such as
these diminish the role of the third molar
in the development of late crowding.
None of these reviews has considered
all the evidence: in some cases only one
or two references on the subject were
quoted. In this era of evidence-based
dentistry, the question ‘how and by
whom is the evidence evaluated?’ must
be asked.
Third-molar agenesis15,16 and extraction
studies17,18 and second-molar extraction
studies,19–24 which were not included in
any of the reviews, provide a body of
evidence to support the view that the
presence of a developing third molar
does indeed have some influence on
lower arch alignment during the teenage
years. In these studies, less crowding
was observed when the third molar was
congenitally absent, or when the third or
second molar was extracted, than in
subjects whose third molars were allowed
to develop in intact arches.
It should be stressed that it is eruption
of third molars that is likely to cause
increased crowding: the commonly held
opinion that it is only impacted third
molars that cause the problem is
erroneous. The eruption path of the
posterior teeth is in an upward and
forward direction, and a third molar that is
erupting or attempting to erupt in
reduced space will undoubtedly exert an
influence on the eruption vectors of the
second and first molars. Third molars that
increase their mesial inclination to
become horizontally impacted are unlikely
to cause much pressure on the lower
arch. The milder mesioangular and
vertical third molars may cause pressure
while they are trying to erupt, but once
they become impacted (and especially
Dental Update – June 2002
O RT H O D O N T I C S
once the apices close) they probably
cease to do so – as do the distoangular
impactions once they begin to tip distally.
Those third molars which force their way
into the arch and erupt are the ones most
likely to cause crowding.
Extraction of third molars, impacted or
not, does not solve the problem: in any
one individual the aetiology of late
crowding may be due to a combination
of factors.
DISTALLY DIRECTED
FORCES
Forces acting in a distal direction may
cause retroclination of the lower incisors,
with reduction in arch length and
consequent crowding.
Distally directed forces may be due to:

incisor uprighting;

complex growth patterns;

skeletal structure; or

soft tissue maturation.
Incisor Uprighting
The inter-incisal angle increases on
average during the teenage years.25,26
This may have the effect of retroclining
the lower incisors and reducing arch
length. Incisor uprighting is due to the
differential nature of late skeletal growth.
Mandibular prognathism increases
relative to maxillary prognathism,
resulting in straightening of the profile.27
B point, on alveolar bone, grows less
in a horizontal direction than gnathion
on basal bone, suggesting that alveolar
growth does not keep pace with skeletal
growth.28
So, if the lower jaw is growing forward
more than the upper, and the lower basal
bone more than the alveolar bone, and
the lower incisors are not free to move
forward owing to the restraining
influence of the upper incisors, they
may become retroclined – and
consequently crowded.
Complex Growth Patterns
Extreme degrees of mandibular rotation
in a forward29,30 or backward direction29
could result in increased crowding.
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When the mandible rotates upwards and
forwards the paths of eruption are
displaced in a mesial direction, resulting
in what Björk29 called ‘packing of the
lower anterior segment’. In extreme
downwards and backwards rotation the
lower incisors become retroclined
through their functional relationship
with the upper incisors. The posterior
teeth are not guided distally in their
eruption – and crowding develops.
Skeletal Structure
A specific type of skeleton, which is
susceptible to crowding, and a specific
pattern of growth have been implicated in
the aetiology of late crowding.31
One study found crowding to be
associated with a high mandibular angle,
a retrognathic face and an increased
overjet.32 However, in another study,
analysis of measurements of various
cephalometric parameters representative
of skeletal morphology at age 13 years
in relation to increased crowding from 13
to 18 years could not conclusively
identify a particular skeletal type that is
susceptible to crowding.33
Soft-tissue Maturation
It is generally recognized that tooth
position is influenced by the oral soft
tissues. Although there is no direct
evidence of a relationship between soft-
tissue changes and increased crowding,
there is some indirect evidence:
1. A reduction in mandibular arch
length found in an untreated control
group was prevented in subjects
treated with the Functional
Regulator.34 The researchers argued
that the vestibular shields of the
appliance favourably influenced the
sagittal development of the
mandibular dental arch by
eliminating the restraining forces of
the external muscular environment.
2. The lower incisors of children who
were mouth breathers were more
retroclined and crowded than in
controls35 and proclined after
adenoidectomy and changes to the
mode of breathing that altered the
235
 O RT H O D O N T I C S
muscular environment.36
These studies show that lower arch
alignment can improve after the removal
of adverse muscle forces, and suggest
that the reverse may also be true. There
are various ways in which the perioral
musculature may change over time:

Late mandibular growth changes
may bring the lower incisors into a
different soft-tissue environment.

Soft-tissue growth continues up to
19 years37 and may not proceed at
the same rate as skeletal growth.

Teenagers with incompetent lips,
becoming more aware of their
appearance, may make a conscious
effort to hold their lips together and
cause an increase in perioral pressure.

Orthodontic treatment involving
changes in incisor position may alter
the pressure environment of the teeth.
OCCLUSAL FACTORS
Alterations in functional occlusion may
produce a different pattern of masticatory
forces or an occlusion with premature
contacts. Occlusal changes may be due to:

tooth loss;

restorations;

development of parafunctional
habits;

orthodontic treatment.
Children with Class II division 1
malocclusion treated by extraction of
upper first premolars and fixed appliances
showed a significantly greater increase in
lower arch crowding (2.0 mm) than
untreated children.38 This was thought to
be due to the transmission of reciprocal
forces through functional tooth contact
to the lower arch. Alternatively, with
reduction of the overjet and
establishment of tooth contact, occlusal
forces and soft-tissue pressures may be
transmitted through the upper incisors to
the lower ones, causing them to become
retroclined and crowded.
Canine guidance in lateral excursion
may produce a lingually directed force
on the lower canines, causing narrowing
of the arch in the canine region with
consequent crowding.
236
A high inter-incisal angle at the end of
orthodontic treatment may result in a
more lingually directed retroclining force
to the lower incisors.
DIRECTION OF ERUPTION
The concept of continuous eruption of
teeth to maintain occlusal equilibrium is
fundamental to orthodontic theory and
practice. The amount and direction of
eruption may vary in relation to
mandibular growth.
It has been suggested that the axial
inclination of teeth is indicative of the
direction of eruption and that there may
be favourable and unfavourable
relationships between the axial
inclinations of molars and incisors,
contributing to a decrease or increase in
lower arch crowding during the change
over from the mixed to the permanent
dentition.39 Mesially inclined molars and
distally inclined incisors that continue
to erupt in the same direction would
result in reduction in arch depth and
increased crowding.
No relationship between axial
inclinations and increased crowding
could be demonstrated in older children
in the early teenage years:40 in fact, the
axial inclinations tended to change and
were not always indicative of the
direction of eruption. However, this
does not preclude the possibility of an
unfavourable direction of eruption
resulting in increased crowding in
individual cases.
TOOTH MORPHOLOGY
Well aligned lower incisors are smaller
mesiodistally and larger labiolingually.41
The broad areas of contact created by the
large labiolingual dimension seem to
provide a buttressing effect, making the
teeth more resistant to perioral pressures
than the slender contact points of teeth
that are narrow labiolingually, which will
more readily slip under pressure to
become overlapped and crowded.
PERIODONTAL FORCES
The presence of a continuous
periodontal force acting to maintain
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interproximal contacts in a state of
compression has been demonstrated in
humans,42 and significant correlations
between interproximal force and
mandibular anterior malalignment have
been found.43 Thus, periodontal forces
could contribute to the development of
lower arch crowding. It is difficult to see
how periodontal forces alone could
initiate crowding but in combination
with other factors they may well
exacerbate the process.
DEGENERATIVE TISSUE
CHANGES
Bone and periodontal membrane are
thought to be biologically labile in
response to the hormonal changes that
occur during adolescence. Elongation of
clinical crowns as a result of gingival
recession and bone loss is a well
recognized part of the ageing process,
and can be hastened or exaggerated by
periodontal disease. The resultant
weakening of the supporting tissues will
render the teeth more susceptible to
pressures that they were previously able
to resist. In the upper arch, the incisors
frequently become spaced and in the
lower more crowded. In a group of adults
examined at age 18 and again at 50
years,44 all except two had some increase
in lower arch crowding and all showed
some degenerative change, ranging from
lengthening of clinical crowns to active
periodontal disease. These degenerative
changes are more likely to be the cause of
crowding that develops in later life.
There is evidence that orthodontic
tooth movement causes root resorption
and reduced bone levels.45–53 In most
cases, these changes are small and
scarcely detectable clinically, but they
may be large enough to allow the teeth to
move under perioral pressures which
they previously resisted. It seems that
orthodontic tooth movement may create
a situation of premature ageing, which
may account for the high incidence of
post-retention crowding.
ORTHODONTIC
TREATMENT
Teeth that have been moved
Dental Update – June 2002
 O RT H O D O N T I C S
orthodontically have a natural tendency
to return to their original (crowded)
positions. This is particularly true in the
case of rotations. Inadequate distalization
of canine roots and excessive arch
expansion in the canine region have a
strong tendency to relapse.
CONCLUSION
The evidence on the aetiology of late
crowding remains inconclusive, which is
not altogether surprising in view of its
multifactorial nature. Some factors may
have more influence than others. They
may act in various combinations in
different individuals at different stages of
development. More information is
required on changes in the untreated
dentition after the age of 20 years.
Further post-retention studies of
subjects with similar malocclusions,
treated at the same age, reviewed at
regular intervals and compared with
untreated controls over the same age
range would contribute to a better
understanding of the problem.
REFERENCES
1. Richardson ME. A review of changes in lower arch
alignment from seven to fifty years. Semin Orthod
1999; 5: 151–159.
2. Hunter J. The Natural History of the Human Teeth,
2nd ed. London: Johnson, 1778; p.81.
3. Richardson ME. Late lower arch crowding: Facial
growth or forward drift? Eur Orthod J 1979; 1:
219–225.
4. Consensus. Removal of Third Molars. National
Institute of Health Consensus Development
Conference Summary, New York 1979; 2, 11.
5. Stephens RG, Kogon SL, Reid JA. The unerupted or
impacted third molar – a critical appraisal of its
pathological potential. J Can Dent Assoc 1989; 55:
201–207.
6. Bramante MA. Controversies in orthodontics. Dent
Clin North Am 1990; 34: 91–102.
7. Vasir NS, Robinson RJ. The mandibular third molar
and late crowding of the mandibular incisors – A
review. Br J Orthod 1991; 18: 59–66.
8. Mercier P, Precious D. Risks and benefits of
removal of impacted third molars. Int J Oral
Maxillofac Surg 1992; 21: 17–27.
9. Peterson LJ. Rationale for removing impacted teeth:
when to extract or not to extract. J Am Dent Assoc
1992; 123: 198–204.
10. Southard TE.Third molars and incisor crowding:
when removal is unwarranted. J Am Dent Assoc 1992;
123: 75–79.
11. Sands T, Pynn B, Nenniger S.Third molar surgery:
current concepts and controversies. Part 1–II. Oral
Health 1993; 83: 11–30.
238
12. Toth B. The Appropriateness of Prophylactic Extraction
of Impacted Third Molars. A Review of the Literature.
Bristol: Healthcare Evaluation Unit, University of
Bristol, 1993.
13. Tate TE. Impactions: observe or treat? J Can Dent
Assoc 1994; 22: 59–64.
14. Song F, Landes DP, Glenny A-M, Sheldon TA.
Prophylactic removal of impacted third molars: an
assessment of published reviews. Br Dent J 1997;
182: 339–346.
15. Bergstrom K, Jensen R. The significance of third
molars in the aetiology of crowding. Trans Eur
Orthod Soc 1960; 84–96.
16. Vego L. A longitudinal study of mandibular arch
perimeter. Angle Orthod 1962; 32: 187–192.
17. Schwarze CW. The influence of third molar
germectomy – A comparative long term study.
Transactions of the Third International Orthodontic
Congress, London, 1975; pp.551–562.
18. Lindqvist B,Thilander B. Extraction of third molars
in cases of anticipated crowding in the lower jaw.
Am J Orthod 1982; 81: 130–139.
19. Brenchley ML, Ardouin DGF. Investigations into
changes in some mandibular arches in the
postdeciduous dentition. Trans Br Soc Study Orthod
1968; 50–58.
20. Schwarze CW. Nachuntersuchungsbefunde bei
Patienten mit Extraktion zweiter Molaren. Fortschr
Kieferorthop 1980; 41: 105–128.
21. Richardson ME. The effect of lower second molar
extraction on late lower arch crowding. Angle
Orthod 1983; 53: 25–28.
22. Richardson ME, Mills K. Late lower arch crowding:
the effect of second molar extraction. Am J Orthod
Dentofac Orthop 1990; 98: 242–246.
23. Hart AJ, Springate SD. Mandibular permanent
second molar extraction: effect on lower incisors.
Br Soc Dent Res Abs 1989; 98.
24. Orton HS, Battagel JM, Ferguson R, Ferman AM.
Distal movement of buccal segments with the ‘en
masse’ removable appliance: Its value in treating
patients with mild Class 11, Division 1 malocclusion.
Part 11:The model measuring system and results.
Am J Orthod Dentofac Orthop 1996; 109: 379–385.
25. Humerfelt A, Slagsvold O. Changes in occlusion and
craniofacial pattern between 11 and 25 years of age.
Eur Orthod Soc Trans 1972; 113–122.
26. Siatkowski RE. Incisor uprighting: Mechanism for
late secondary crowding in the anterior segments
of the dental arches. Am J Orthod 1974; 66: 398–
410.
27. Björk A, Palling M. Adolescent age changes in sagittal
jaw relation, alveolar prognathy and incisal
inclination. Acta Odontol Scand 1954; 12: 201–232.
28. Lande MJ. Growth behaviour of the human bony
facial profile as revealed by serial cephalometric
roentgenology. Angle Orthod 1952; 22: 78–90.
29. Björk A. Prediction of mandibular growth rotation.
Am J Orthod 1969; 55: 585–599.
30. Perera PSG. Rotational growth and incisor
compensation. Angle Orthod 1987; 57: 39–49.
31. Sakuda M, Kuroda Y, Wada K, Matsumoto M.
Changes in crowding of the teeth during
adolescence and their relation to growth of the
facial skeleton. Eur Orthod Soc Trans 1976; 93–104.
32. Meng HP, Gebauer U, Ingervall B. Die Entwicklung
des Engstandes der unteren Inzisiven im
Zusammenhang mit Veranderungen der Zahnbogen
und des Gesichtsschadels bei Individuen mit guter
Okklusion von der Puberat bis zum
Erwachsenenaeter. Schwiez Mschr Zahn 1985; 95:
Downloaded from magonlinelibrary.com by 128.243.044.244 on March 23, 2018.
762–777.
33. Richardson ME. Late lower arch crowding: The role
of facial morphology. Angle Orthod 1986; 56: 244–
254.
34. Fränkel R, Loffler U. Functional aspects of
mandibular crowding. Eur J Orthod 1990; 12: 224–
229.
35. Woodside DG, Linder-Aronson S, Stubbs DO.
Relationship between mandibular incisor crowding
and nasal mucosal swelling. Proc Finn Dent Soc 1991;
87: 127–138.
36. Linder-Aronson S, Woodside DG, Hellsing E,
Emerson W. Normalisation of incisor position
after adenoidectomy. Am J Orthod Dentofac Orthop
1993; 103: 412–427.
37. Vig PS, Cohen AM.Vertical growth of the lips: a
serial cephalometric study. Am J Orthod 1979; 75:
405–415.
38. Owman G, Bjerklin K, Kurol J. Mandibular incisor
stability after orthodontic treatment in the upper
arch. Eur J Orthod 1989; 11: 341–350.
39. Sanin C, Savara BS. Factors that affect the alignment
of the mandibular incisors:A longitudinal study. Am J
Orthod 1973; 64: 248–257.
40. Richardson ME. Late lower arch crowding in
relation to the direction of eruption. Eur J Orthod
1996; 18: 341–347.
41. Peck S, Peck H. Crown dimensions and mandibular
incisor alignment. Angle Orthod 1972; 42: 148–153.
42. Southard TE, Southard KA, Tolley EA. Periodontal
force: A potential cause of relapse. Am J Orthod
Dentofac Orthop 1992; 101: 221–227.
43. Southard TE, Behrents RG, Tolley EA. The anterior
component of occlusal force. Part 2. Relationship
with dental malalignment. Am J Orthod Dentofac
Orthop 1990; 97: 41–44.
44. Richardson ME. A preliminary report on lower
arch crowding in the mature adult. Eur J Orthod
1995; 17: 251–257.
45. Sjolien T, Zachrisson BU. Periodontal bone support
and tooth length in orthodontically treated and
untreated persons. Am J Orthod 1973; 64: 28–37.
46. Zachrisson BU, Alnaes L. Periodontal condition in
orthodontically treated and untreated individuals. II.
Alveolar bone loss: radiographic findings. Angle
Orthod 1974; 44: 48–55.
47. Hollender L, Rönnerman A, Thilander B. Root
resorption, marginal bone support and clinical
crown length in orthodontically treated patients. Eur
J Orthod 1980; 2: 197–205.
48. Hamp SE, Lundström F, Nyman S. Periodontal
conditions in adolescents subjected to multiband
orthodontic treatment with controlled oral hygiene.
Eur J Orthod 1982; 4: 77–86.
49. Kennedy DB, Joondeph DR, Osterberg SK, Little
RM. The effect of extraction and orthodontic
treatment on dentoalveolar support. Am J Orthod
Dentofac Orthop 1983; 84: 183–190.
50. Polson AM, Reed BE. Long-term effect of
orthodontic treatment on crestal alveolar bone
levels. J Periodont 1984; 55: 28–34.
51. Sharpe W, Reed B, Subtelny JD, Polson A.
Orthodontic relapse, apical root resorption, and
crestal alveolar bone levels. Am J Orthod Dentofac
Orthop 1987; 91: 252–258.
52. Øgaard B. Marginal bone support and tooth lengths
in 19-year-olds following orthodontic treatment.
Eur J Orthod 1988; 10: 180–186.
53. Bondemark L. Interdental bone changes after
orthodontic treatment.A 5-year longitudinal study.
Am J Orthod Dentofac Orthop 1998; 114: 25–31.
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