ABSTRACT: The disturbed eruption process creates clinical situations that can be challenge for dental specialist. The spectrum of tooth eruption disorders include problems ranging from delayed tooth eruption (DTE) to failure of eruption. There are several local, environmental and genetic factors which altered normal physiologic eruption process – Active or Passive and create periodontal and esthetic problems. Altered passive eruption (APE) is a situation where gingival margin is located more incisal to CEJ, creating a gummy smile because of Short Tooth Syndrome (STS). Thyroid is a hormone, critical for maintenance of metabolic activity of the body including oral cavity. Prolonged or untreated hypothyroidism lead to critical medical situation but a dentist by detecting the early signs and symptoms of hypothyroidism can refer the patient for treatment and avoid potential complications with uncontrolled disease. This case report presents a case with diagnosed hypothyroidism who sought dental care due to DTE and STS and a justified treatment plan was made.

1 2 3 4Surbhi Garg, Rohit Chauhan, Sachit Anand Arora, Shivjot Chinna, 5 6 1,2 3 4Sneh Nidhi, Kumar Saurav, Reader, Professor and Head, Professor, 5,6Senior Lecturer Department of Periodontics, ITS Dental College, Greater Noida. Uttar Pradesh,

INTRODUCTION : Eruption of deciduous teeth, their

exfoliation followed by eruption of permanent dentition is

sequential and age specific event. Eruption is defined as the

movement of the tooth from its site of development to the

occlusal plane and comprises of two phases: an active

eruption which causes the tooth to emerge into the oral cavity,

and a passive eruption involving apical migration of the

dentogingival junction (DGJ) from the crown onto the root

surface just apical to cement-enamel junction (CEJ).[1]

Active eruption occurs due to forces originating from root

formation, increase in hydrostatic pressure at periapical level,

selective bone resorption and deposition around the tooth and

the contraction capacity of the periodontal ligament fibers.

Bone resoption is mediated by osteoclast cells and this

follows the gubernacular canal above each tooth to allow the

crown to move through the alveolar bone.[2 Tooth eruption

begins when 3/4 of its final root length is established.

However, mandibular canines and second molars show more

advanced root development than the expected [3]/4th of the

final root length.[3] Active eruption is completed when the

tooth reaches in functional occlusion and proceded by passive

eruption. Several local factors[4] and systemic factors

(genetic and environmental)[5] (Table-1) can modify the

mechanism of eruption (active or passive) so that tooth do not

erupt at the time of mean eruption age despite the formation of

2/3rd or more of the root length, known as Delayed Tooth

Eruption (DTE).[3]

Table 1- Etiology of Delayed Tooth Eruption5

SHORT TOOTH SYNDROME ASSOCIATED WITH DELAYED TOOTH ERUPTION - A PERIODONTICS – ORTHODONTICS CHALLENGE

Journal of Dental Sciences

University

Key words : Delayed tooth eruption, Altered passive eruption, Short tooth syndrome, Hypothyroidism

Source of support: NilConflict of interest : Nil

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University J Dent Scie 2015; No. 1, Vol. 3

Clinical Papers

Variation in physiology of eruption (active or passive)

involving more coronal placement of peridontium as

compared to CEJ referred as Altered Passive Eruption

(APE)6 that results in Short Tooth Syndrome(STS)[7] which

is esthetically unpleasant. More coronal positioning of gums

produce square shaped crowns, flattened gingival festooning

and gummy smile.[8] APE classified into two types- I, II9

according to the location of the mucogingival junction with

respect to the bone crest and two subtypes-A,B (Table-2,

Figure-1) in reference to the position of the bone crest with

respect to CEL.

Figure 1- Type and subclass of Altered Passive Eruption9

Table 2 - Classification of Altered Passive Eruption7

Hypothyroidism is thyroid hormone insufficiency frequently

found in women, increases with age and exhibits familial

tendency. Thyroid hormone have regulatory effects on bone

development and metabolism and also show impact on

developing teeth.[10] Dental characteristics of

hypothyroidism are: vertical facial growth, small jaw, thick

lips, macroglossia, anterior open bite and fanned-out anterior

teeth. Primary and permanent dentition presents eruption

retardation, although teeth reach normal size. The present

article report a clinical case of teenager male patient taking

treatment for hypothyroidism and have been diagnosed DTE

associated with STS secondary to hypothyroidism.

CASE REPORT: An11year old male patient reported with a

chief complaint of retained milk teeth and compromised

esthetics. The patient was of normal build and had no relevant

family history. Patient also had undergone surgery for hernia

5years. Suddenly, before one year he diagnosed for

hypothyroidism and was taking treatment since then. The

patient was advised for complete hemogram, T4, TSH and

Vitamin D level. Complete hemogram showed normal

picture. Thyroid hormone levels were compatible with

hypothyroidism: TSH=7.2µUI/mL (reference: 0.7–6.2); free

T4=0.8ng/dl (0.9–1.6).

On intraoral examination, total 23 teeth were present in the

patient's oral cavity. The patient had 15 retained deciduous

teeth (52, 53, 54, 55, 62, 63, 64, 65, 72, 73, 74, 75, 83, 84, 85)

with 8 permanent teeth (16, 21, 26, 31, 36, 41, 42, 46). All

erupted permanent teeth showed incomplete eruption with

short clinical crowns. Gingiva was thick & fibrous and

macroglossia was evident. (Figure-3b) The OPG of the

patient showed neither anodontia nor supernumerary teeth.

(Figure-2a) The roots of unerupted permanent teeth were not

fully formed and the roots of deciduous predecessors showed

incomplete resorption, indicating an imbalance between the

processes of deciduous root resorption and root formation.

Based on clinical and radiographic features, diagnosis of

Delayed Eruption associated with Short Tooth Syndrome

secondary to hypothyroidism was made.

Patient recalled after 12 months, when he achieved normal T3

& T4 level. This dental visit revealed absence of 52, 62 and 72

but no eruption of successor of maxillary LI. At 12yrs of age

OPG of the patient had shown complete root formation with

apex closure of all molars (16, 26, 36 and 46). (Figure-2b) To

facilitate the eruption of maxillary lateral incisors crestal

incision was given and partial eruption occurred after

3months. (Figure- 3a, c) Patient was not convinced for

intensive dental treatment, so he was kept on recall visits.

Fig 2 OPG at the age (a)11years (b)12 years (c)13 years (d) 14 years

Fig 3- At 12years of age

(a) (b) (c)

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(a) 3months after crestal incision for maxillary lateral incisors

(b) Mandibular arch and macroglossia

(c) Oclussal view of Maxillary arch

At 13 yrs of age patient had shown mobility of 33 and 43 and

extraction was done. There was formation of tooth bud in

relation to all third molars. (Figure-2c) Right lateral and left

lateral view of dentition showed thick fibrotic gingiva with

increased overbite. (Figure-4) At the age of 14 yrs, no

evidence of eruption in relation to permanent canine and

premolars which is greater than 2 standard deviation (SDs)

from the expected eruption time. (Figure-2d)

Fig 4 – At 13years of age (a) Right and Left lateral view

DISCUSSION : Hypothyroidism can be primary, where the

defect is intrathyroid or secondary (acquired), where

lowering of hormone levels are due to other causes such as

childhood hypothyroidism (cretinism), idiopathic (no known

cause can be established), iatrogenic (due to radiation therapy

or surgical procedures) or autoimmune Hashimoto's

thyroiditis. Understanding of thyroid dysfunction is

important to the dentist because the dentist may be the first

person to suspect a serious thyroid disorder and once such

patients are under good medical care, no expected problems in

dental treatment, except for malocclusion and enlarged

tongue.10

The diagnosis of our cases was based on medical history,

clinical and radiographic characteristics and undergone

sequential examination of tooth eruption. First, we examined

and correlate the patient's age with present dentition and

found that the eruption time was greater than 2 SDs from the

mean expected eruption time known as Chronologic Delay

Tooth Eruption.5 Second step includes determining the factor

(surgery leading to iatrogenic hypothyroidism) that adversely

affects tooth eruption. The third step is to consider the

patient's dental age as evidenced by root formation. Normal

biologic eruption time is defined as tooth eruption that occurs

when the dental root is approximately 2/3 its final length.

However in this case there is no eruption of lateral incisors

and canines even after >2/3rd of the root formation has been

completed, so diagnosed as delayed biologic eruption due to

hypothyroidism. This positive co-relation between DTE and

congenital hypothyroidism have been reported in several

studies 10-14 but this was a case of iatrogenic hypothyroidism

associated with DTE.

The eruption process requires continuous adaptation from the

periodontal membrane and the active movement of the crown

follicle, destroying overlying bone via odontoclasts. T

lymphocytes produce receptor activator of nuclear kappa B

ligand (RANKL) which plays an important role in the

regulation of bone cell and bone mass biology. Periodontal

ligament cells secrete osteoprotegerin (OPG) which inhibits

osteclastogenesis.15 Balance between RANKL and OPG

regulate odontoclastogenesis since ligament cells derived

from primary roots during the physiological resorption

process express increased levels of RANKL. In contrast,

during the phases that precede resorption, the ligament

expresses OPG, and not RANKL.16 This RANKL/OPG

system is regulated by several hormones (growth hormone,

thyroid hormones, glucocorticoids), vitamin D and cytokines

(interleukin 1, 4, 6, 11, 17 and TNF delta).

This should be differentiated from cases of Primary Failure of

Eruption(PFE). PFE17 refer to those cases where non-

ankylosed teeth fail to erupt because of malfunction of

eruption mechanism, suggesting an alteration of metabolism

or of the blood flow in the periodontal ligament. It should be

differentiated from DTE as PFE affected teeth is impossible

to erupt even after application of any orthodontic force.

The association between hypothyroidism and the presence of

APE is not infrequent.18 Volchansky et al6 reported the

presence of APE associated with acute necrotizing ulcerative

gingivitis, suggesting that deep gingival sulcus creates an

anaerobic environment for the development of infection.

Tab. 3 Etiology, Diagnosis & Treatment for Altered Eruption

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Treatment for such cases is team work of periodontist and

orthodontist which includes elimination of obstacles to

eruption, exposure of affected teeth (gingivectomy) with or

without orthodontic traction and control of the systemic

disease.19 (Table-3) Exposure of the tooth delayed in

eruption at the time of surgical removal of barrier would be

done in this case so that orthodontic traction van be applied.

Moreover STS affected tooth would be corrected by crown

lengthening as sufficient amount of attached gingival is

present. This facilitates the suitable positioning of gingival

margin relative to the lip.

CONCLUSION:

Variation in the normal eruption of teeth is a common finding

but significant deviations from established norms should alert

the clinician to further investigate the patient's health and

development Multidisciplinary approach would be the

appropriate choice as treatment involves esthetics, functional,

and oral health problem.

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CORRESPONDING AUTHOR

Dr. Surbhi Garg

39, Burj Mohalla, Hapur, Ghaziabad.

Reader,Department of Periodontics, ITS Dental college.

Email id- dr.surbhi80@gmail.com

Phone N.- 09680470707

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