Aesthetics is a major topic in modern dentistry. majority of patients presenting to the dental clinic today are concerned about their smile. A holistic dental care must encompass restoring function, anatomy and a confident smile.

1. TOOTH
DISCOLORATION
Dr. Akinrodoye S.T.
BDS (IB)

2. Outline
 Introduction
 Aetiologies
 Predisposing factors
 Pathogenesis
 Extrinsic tooth discoloration
 Intrinsic tooth discoloration
 Management
 Prevention
 Treatment
 References

3. Introduction
 Primary teeth are whiter compared to the
permanent teeth.
 Permanent teeth have a range of color which
is normal and must be differentiated from
pathological discoloration.

4. Aetiologies
 The causes of tooth discoloration are
classified according to the location of the stain
 Extrinsic: Located on the outer surface of the
tooth structure
 Intrinsic: Deposits incorporated into dental tissues

5. Extrinsic stains
 Dental plaque and calculus
 Foods and beverages (coffee, tea)
 Habitual chewing of kolanuts, betel nuts, pan
 Tobacco
 Metallic compounds
 Chromogeneic bacteria
 Topical medicaments

6. Nathoo classification system of
extrinsic dental stain
 Nathoo type 1 (N1)
 N1-type colored material binds to the tooth surface
 The color of the chromogen is similar to that of dental
stains caused by tea, coffee, wine, chromogenic bacteria,
and metals.
 Nathoo type 2 (N2)
 Changes color after binding to the tooth.
 The stains actually are N1-type food stains that darken
with time.
 Nathoo type 3 (N3)
 N3-type colorless material or prechromogen binds to the
tooth and undergoes a chemical reaction to cause a stain.
 Caused by carbohydrate-rich foods (eg, apples, potatoes),
stannous fluoride, and chlorhexidine.

7. Predisposing factors
 Enamel defects
 Salivary dysfunction
 Poor oral hygiene.
 Microscopic pits, fissures, and defects
 Local disease (eg, salivary obstructions and
infections)
 Systemic disease (eg, Sjögren syndrome)
 Head and neck radiation therapy for cancer
 Chemotherapy
 Anticholinergics, antihypertensives,
antipsychotics, antihistamines

8. Causes of intrinsic stains
 Dental materials (eg, tooth restorations)
 Dental conditions and caries
 Trauma
 Infections
 Medications
 Nutritional deficiencies and other disorders
 Complications of pregnancy
 Anemia and bleeding disorders
 Bile duct problems
 Acid reflux (Anorexia, Bullimia nervosa)
 Genetic defects and hereditary diseases
 Those affecting enamel and dentin development or
maturation

9. Intrinsic stains
 Inherited enamel defects: Mainly presents as
enamel hypoplasia
 Localised to the teeth
Amelogenesis imperfecta
 Inherited dentine defects
 Dentinogenesis imperfecta
 Dentine dysplasia

10. Intrinsic stains
 Associated with systemic disease
 Epidermylosis bullosa
 Hurler’s syndrome
 Tricho-osseous dental
 Oculo-dental digital
 Pseudohypoparathyroidism (AD)
 Chondroectodermal dysplasia
 Hypophosphatasia
 Vitamin D resistant ricket

11. Intrinsic stains
 Acquired enamel defects
 Generalized
 Prenatal
 Neonatal
 Postnatal
 Localized (Turners tooth)
 Trauma
 Infection
 Gunshot
 Surgery
 Irradiation

12.  Generalised causes
 Prenatal (presents as chronological enamel
hypoplasia affecting the deciduous teeth)
 Rubella
Congenital syphilis
Toxaemia in pregnancy
Drugs intake by mother - tetracycline,
thalidomide
Gastroenteritis of mother
Vitamin D deficiency

13.  Neonatal
 Presents as chronological enamel hypoplasia
affecting the deciduous teeth and early
permanent teeth)
 Rhesus incompatibility
 Neonatal hypocalceamia
Prematurity
Cerebral palsy
Asphyxia neonatorium

14.  Postnatal
 Presents as chronological enamel hypoplasia
affecting the permanent teeth
 Measles
 Scarlet fever
 Whooping cough
 Pneumonia
 Vit A,C & D deficiency
 Vit D intoxication
 Hypoparathyroidism
 Cancer chemotherapy
 Gastroenteritis
 Fluorosis > 1ppm
 Herbs
 Antibiotics of the tetracycline family (e.g. tetracycline,
minocycline)1

15. • CEH in a 14 year old who suffered from
malnutrition resulting in prolonged
hospitalization around the age of 1-2 years.
 Chronologic enamel
hypoplasia

16. Iatrogenic causes
 Use of Grey MTA (GMTA) as cervical sealing
material in endodontic procedures.
 Tripple antibiotic paste (TAP) in Regenerative
Endodontic Procedures

17. Amelogenesis imperfecta
 An inherited developmental abnormality of
enamel
 It is purely ectodermal
 Both primary and permanent dentitions are
affected
 Most of the enamel on all teeth are affected

18.  AI is generally characterized by tooth
discoloration, tooth sensitivity, increased caries
risk, anterior open bite, increased calculus
formation, as well as wear and erosion.
 AI can be clinically classified into hypoplastic,
hypocalcified (hypomineralized) or hypomature
types depending on the stage of enamel
formation that is affected by the genetic defect.

19. Inherited dentin defects
 Dentinogenesis imperfecta
 Type I
 Type II
 Type III
 Dentine dysplasia
 Type I
 Type II

20. Molar-incisor
hypomineralization
 Permanent molars and incisors show
demarcated areas of hypomineralization or
opacities which may be coloured yellow or
brownish. There is high susceptibility to caries,
tooth sensitivity and difficulty in achieving
adequate anaesthesia
 Clinically, the hypomineralized enamel
appears to be soft, porous and look like
discoloured chalk or Old Dutch cheese.

21.  Sometimes, posteruptive enamel breakdown
can occur so rapidly after eruption that it
seems as if the enamel was not formed
initially.
 Some studies hypothesize that, in the case of
MIH, the ameloblasts are affected in the early
maturation stage, or maybe even earlier at the
late secretory phase.

22.  A case of MIH in an 8
year old child due to
a chicken pox
infection at the age of
2

23. Fluorosis
 It is characterized by faint white flecking of
enamel
 White patches / striations
 Severe cases appear yellow, black or brown
 Occur during the maturation stage of tooth
development due to excessive ingestion of
fluoride

24. Pathogenesis of extrinsic tooth
discoloration
 Chromogeneic bacteria
 Produce green and black stains on the labial
surfaces of maxillary teeth in children.
 Medicaments
 Chlorhexidine mouthwashes cause protein
denaturation of salivary pellicle on teeth surface.
This in turn favours retention of stains. Thus, its
use should be discontinued after two weeks to
avoid stains.

25.  Beverages
 Deposition of tannins causes brown stains

26. Stain Location Organism Composition
Black Gingival margin Actinomyces sp Ferric sulfide
Green Maxillary anterior
teeth
Fluorescent bacteria
Penicillium
Aspergillus sp
Orange Serratia marcescens
Flavobacterium
lutescens.

27. Stain Metallic compounds
Black Iron
Manganese
Silver
Blue-green Mercury
Lead
Green–to–blue-green
stain
Copper
Nickel
Deep orange stain Chromic acid fumes
Brown Iodine solution
Stannous fluoride
Violet-black stain Potassium permanganate
Cetylpyridinium chloride

28. Pathogenesis of intrinsic
discoloration
 Localized discoloration may be a result of
either preeruptive or posteruptive processes
 Widespread involvement indicates a deviation
in normal tooth formation

29. Overview of Amelogenesis
 The process of enamel development is known as
amelogenesis and enamel producing cells are known
as ameloblasts.
• Stages
 Presecretory
 Secretory
 Transition
 Maturation
 The enamel organ consists of an outer enamel
epithelium (OEE), a layer of stellate reticulum
sandwiched between the OEE and the stratum
intermedium. This is followed by the inner enamel
epithelium

30.  Presecretory stage:
1. Deposition of predentin by Odontoblasts
2. Secretion of enamel matrix proteins by
ameloblasts
 Secretory stage:
1. The first enamel crystals formed grow between
the dentin crystals
2. Development of Tomes’ processes and secretion
of large amount of AMELX, AMBN, ENAM, and
MMP20 that form long, thin, mineral, crystallite
ribbons.

31.  Transition stage: Final coating of aprismatic
enamel
 Maturation stage: Removal of excess
secreted and partially hydrolyzed matrix
proteins from the enamel layer so that the rod
and interrod crystallites can expand in volume
to occupy as much space as possible within
the enamel layer.

33. Pathogenesis of intrinsic tooth
discoloration
 Can be classified into three parts
 Changes in the structure/ thickness of hard dental
tissues.
 Diffusion of pigments into the dental hard tissues
after formation.
 Incorporation of pigments into the hard dental
tissues during formation.

34. Changes in the structure / thickness of
dental hard tissues
 Enamel Hypoplasia: failure of the
ameloblasts to produce normal volume of
matrix. Colour ranges from opaque to yellow
to brown
Types:
 Localised: Single tooth (e.g. Turners tooth)
 Chronological: affecting teeth that develop at
the same time
 Generalised: affecting all the teeth

35. Tooth wear lesions
 Attrition in a 75-year
old patient showing
the natural yellow hue
of the dentine

36. Diffusion / incorporation of
pigments after tooth formation
 Brown color is attributed to the formation of
 Maillard pigments (reaction between proteins and
small aldehydes produced by cariogenic bacteria)
 Melanins
 Lipofuscins
 Various food colors and bacterial pigments

37.  Necrosis
 Pulp necrosis is often a cause of tooth
discoloration
 Following haemorrahage in the pulp chamber
there is lysis of erythrocytes
 Leads diffusion of the derivatives of haemoglobin
into the dentine
 Initial colour is pink following trauma (pink tooth)
 Tooth becomes grey or bluish black over time

38. Pigments incorporated during
formation of dental tissues
 Congenital Hyperbilirubinaemia (neonatal
jaundice)
 Severe cases of neonatal jaundice results in
deposition of bile pigments in calcifying enamel
and dentine of developing teeth.
 Discoloration is often confined to neonatal lines
 Affected teeth can be green, yellow or brown in
colour.

39.  Congenital Porphyria
 Autosomal recessive disorder
 Associated with an inborn error of Porphyrin
metabolism
 Excretion of porphyrin pigments in urine
 Circulating porphyrin in blood is deposited in bone
and teeth.
 Affected teeth appear pink or brown in colour
 Teeth affected have a red fluorescence under UV
light
 Associated bullous lesions on exposed skin &
photosentivity

40. Tetracycline pigmentation
 Tetracycline, minocycline,
doxycycline
 Due to systemic
administration of the drug
during tooth development
(4mth – 8 yrs)
 There is deposition of the
drug in teeth & bone
 Affected teeth can be yellow,
brown or grey in colour
 It gives a yellow fluorescence
under UV light

41.  Degree of discolouration depends on
 Type of tetracycline taken (Vibramycin stains the
teeth least while Tetracycline stains most)
 Dosage of drug taken
 Age of patient at the time administration of drug

42.  It can cross the placenta and it is also present in
breast milk
 Thus it should not be given to pregnant women &
lactating mothers.

43.  Minocycline binds to the calcium ions present
in the dentin by means of chelation, being
incorporated into the dentin matrix and
inducing a change in the color of the dental
structure1.
 Discoloration induced by minocycline normally
occurs in the first 24 hours after its use,
promoting a bluish-grey staining, clinically
perceivable .
 Usually, this alteration is more evident in tooth
crown, and in the cervical third of the root

44.  MTA can also lead to a change in the tooth
color due to the oxidation of abundant
minerals present such as iron, magnesium,
aluminium as well as bismuth oxide, its
radiopacifier component.
 Silver sulfide, pins, composites, and glass
ionomer and acrylic restorations
 Eugenol, formocresol, root canal sealers, and
polyantimicrobial pastes

45. Management
 Appropriate history taking and examination
should be done to determine the cause of the
discoloration
 Reassure the patient if it’s the natural hue of
his/her teeth
 Scaling and polishing should preceed any
treatment for tooth discoloration

46. Prevention
 To avoid crown discoloration, the dentinal
tubules of the pulp chamber should be sealed
with bonding agent prior to the use of TAP as
intracanal medication
 Replacement or elimination of minocycline
from TAP composition. Use of cefaclor,
amoxicillin or clindamicine instead of
minocycline
 Use of white MTA (WMTA) due to less amount
of metallic ions

47. Treatment
 Treatment of discolored teeth is limited to
anterior teeth that are obvious when the
patient smiles
 Extrinsic stains
 Scaling and polishing & OHI
 Diet and habit modification
 Toothbrushing

48.  Intrinsic stains – can be treated through the
following approaches
 Etching & Abrading
 Enamel microabration
 Bleaching
 Veneering
 Crowning

49. Etching & Abrading
 Indicated for hypomineralization and fluorosis
 Steps
 Clean affected tooth
 Prepare two thick pastes
1. pumice powder added to 18% HCl
2. sodium bicarbonate added to water
 Isolate the tooth with rubber dam. Flow copal
varnish around it to get a good seal
 Place some sodium bicarbonate on the rubber
dam around the tooth to neutralized any acid
misplaced accidentally

50. Etching & Abrading
 Apply the pumice HCl paste using wooden
spatula on the tooth.
 Rub gently over the discoloured tooth, absorb
dripping HCl on absorbent cotton wool
 Avoid the use of prophylaxis brush or rubber
cup as this may cause a splatter
 After rubbing for 5 sec, rinse thoroughly with
water for 10 sec. The water must be sucked
away.

51. Treatment
 Bleaching:
 Indicated for tetracycline stains of yellow
discoloration
 Clean affected tooth
 Isolate the tooth with rubber dam.
 Apply 30% hydrogen peroxide on pledgets of
cotton wool to the palatal and labial surfaces of the
teeth.
 Activate the hydrogen peroxide using heat at a
temp patient can tolerate for 30 min keeping the
pledget moist throughout

52. Treatment
 Tooth bleaching: Internal bleaching technique
with sodium perborate or sodium perborate
associated to hydrogen peroxide
 According to Santos LG et al., application of
10% carbamide peroxide, inside the pulp
chamber and on the outer surface of the
crown, was enough to make the color of the
teeth similar to the original one2.

53.  Veneering
 Crowning

54. References
 Luciane Geanini Pena dos Santos et al. Alternative to Avoid
Tooth Discoloration after Regenerative Endodontic
Procedure: A Systematic Review. Brazilian Dental Journal
(2018) 29(5): 409-418. http://dx.doi.org/10.1590/0103-
6440201802132. ISSN 0103-6440
 Santos LG, Felippe WT, Souza BD, Konrath AC, Cordeiro
MM, Felippe MC. Crown discoloration promoted by materials
used in regenerative endodontic procedures and effect of
dental bleaching: spectrophotometric analysis. J Appl Oral Sci
2017;25:234-42.
 Tomasz Zyla et al. Black Stain and Dental Caries: A Review
of the Literature. BioMed Research International. Volume
2015, Article ID 469392, 6 pages.
http://dx.doi.org/10.1155/2015/469392

55.  Luciane Geanini Pena dos Santos et al. Alternative to Avoid
Tooth Discoloration after Regenerative Endodontic
Procedure: A Systematic Review. Brazilian Dental Journal
(2018) 29(5): 409-418 http://dx.doi.org/10.1590/0103-
6440201802132
 Tomasz gyBaet al. Black Stain and Dental Caries: A Review
of the Literature. Hindawi Publishing Corporation BioMed
Research International Volume 2015, Article ID 469392, 6
pages http://dx.doi.org/10.1155/2015/469392
 Dharti N Patel. Tooth Discoloration Clinical Presentation.
https://emedicine.medscape.com/article/1076389-clinical#b1