Introduction
Understanding the different etiological factors of staining and discoloration in primary
teeth will lead to better management approaches and quality of dental treatments,
meeting children's rights and improving their quality of life. Dental treatment can
make a positive impact on the psychological and social aspects of a child's life.[1]
[2] For pediatric dentists, it is essential to provide parents with information regarding
the preventive methods to avoid deciduous teeth discoloration. Increasing population
knowledge about tooth discoloration etiology, especially systemic diseases that can
cause discoloration, the importance of oral hygiene, pregnancy and infancy care, and
preventing injury to deciduous teeth should be a priority.[3]
Teeth color is influenced by a combination of presence of any extrinsic stains that
may form on the tooth surface and their intrinsic color.[4] Teeth discoloration is defined as the variation from normal color, and this phenomenon
can significantly affect the child's personality.[5] Color variations can be present in an individual tooth from the incisal edge to
the darker cervical area around the gingiva.[6] Among the millions of color varieties, ∼100,000 can be found in natural human teeth.[7] Color is a combination of the psychophysiological response to the physical interaction
of light energy with an object and the subjective experience of an individual observer.[8] In 1981, Munsell described color using the following three terms: chroma, hue, and
value.[9] The value reflects the lightness of the color and the chroma is the brightness reflecting
its degree of strength and intensity. The hue enables the individual to differentiate
between the different families of color.[10] Within the same dentition, tooth color can vary between different types of teeth,
where canines are usually darker in color than others.[11] For the tooth to appear in its total color, a combination of light will be created
and then it will be scattered and reflected by different layers of enamel and the
dentin underneath.[6] The perception of color is influenced by three different factors: the object, the
observer, and the light source.[12] Other factors to be considered are the time of day and the angle of the tooth.[13] As a result, a tooth will exhibit different colors when viewed under different conditions
due to the differences in wavelength of the light source.[14] According to Kim and Simmer, A1, A2, and B1 are the most common color shades in
primary dentition.[15]
Primary teeth develop earlier than permanent teeth. An accurate chronology of primary
teeth calcification is clinically significant to dentists.[16]
[17] All primary teeth develop throughout the embryonic stage, starting from around 6
weeks and undergoing five stages of the tooth life cycle, including the following:
initiation, proliferation, histodifferentiation, morpho-differentiation, apposition,
and calcification. It is common to have a defect that includes primary teeth discoloration
and staining as a result of a disturbance to any stages.[16]
[17] Multiple variations have been found when comparing primary and permanent teeth.
These are important to understand, as it is essential to address the difference in
response to a condition affecting them and how to deliver an evidence-based treatment.
There is a difference in the enamel and dentin thickness between primary and permanent
teeth, in addition to a difference toward the enamel rods. A study compared both dentitions'
mineral content, the thickness of the enamel, and enamel rods, and concluded the following:
the primary enamel structure showed a lower calcium and phosphorus level, less thickness,
and higher numerical density of rods.[18]
Finn, Nelson, and Ash identified 12 differences between deciduous and permanent teeth;
deciduous teeth are smaller than their successors in all dimensions, a thinner layer
of enamel and dentin thickness is noted with a wider pulp chamber having the pulp
horns (specially the mesial horn) closer to the occlusal surface when compared with
permanent molars. In addition, the crown of primary teeth is wider mesiodistally and
the roots are longer and narrower.[19]
[20] In staining, some conditions commonly affect permanent teeth, such as molar incisor
hypomineralization.[5] In contrast, other conditions affect primary teeth more severely, such as dentinogenesis
imperfecta (DGI).[21]
Nondental primary care providers can improve children's oral health. There is a growing
international interest in the role of pediatricians in children's oral health,[22] especially considering the high caries rate affecting children with primary teeth
(∼33% of 5 years old). While recent findings demonstrate limited knowledge regarding
oral health, pediatric awareness of the risk factors and etiology of dental conditions
will lead to a timely referral system and cost-effective dental management. A study
of dental awareness among pediatric postgraduate physicians in the United Kingdom
concluded that collaboration with dentists should be done to ensure that education
programs include information about the oral health of children.[22]
[23]
Since the United Nation convention on children's rights in 1987, research has shifted
toward increasing involving children in decision making, including in dental treatments.[24] Meeting patients' aesthetics demands is proven to motivate patients to adhere to
preventive measures and to keep their teeth healthy.[3] In addition, the psychological concerns of children and their parents or caregivers
have been reported. A study of 1,140 adolescents concluded that multiple dental disorders,
including caries, tooth loss, and dental trauma affected their self-esteem.[25] Another study asked 40 children affected by amelogenesis imperfecta (AI) about the
single most important feature they wanted following their dental treatment; the results
show that more than 60% of children hoped for color improvement in their teeth. Furthermore,
most children started to notice a difference in their teeth color at around 6 years
of age due to a defect.[26]
The purpose of this study is to review the literature on the etiology of primary teeth
staining and discoloration as there has been little mention in literature.[27]
Classification of Tooth Discoloration
The crown of the tooth is composed of the following three layers: enamel, dentin,
and pulp. Any disturbance that occurs within these layers may affect the appearance
and color of the tooth, caused by the light transmission and reflection properties
of these layers. Teeth discoloration is classified as intrinsic and extrinsic based
on the stain location, where each can be further classified into the subcategories
shown in [Fig. 1].[14]
Fig. 1 Classification of teeth discoloration.
Intrinsic Discoloration Factors
Intrinsic discoloration occurs due to a change in the structural composition or thickness
of the dental hard tissues, both the enamel and dentin. This means that the chromogenic
material becomes incorporated within the dental hard tissue: either during tooth development
(pre-eruption), such as dental fluorosis, tetracyclic stain, inherited development
defects of enamel and dentin without any systemic features and hematologic disorders,
or during the post-eruptive phase of tooth development, such as pulpal necrosis. These
stains can be localized on one or several teeth, through trauma, inadequate or improper
endodontic treatment, and staining due to restoration (amalgam staining).[28]
The treatment of intrinsic tooth discoloration staining conditions will depend on
the cause, severity of the condition, and age of the child. However, appropriate management
should include establishing prevention, pain and sensitivity control, improve the
aesthetic, and using different behavior management techniques. Both partial (resin
composite and glass ionomers) and full coverage (preformed crown) are used to restore
defected primary teeth.[29]
Dental Fluorosis
Dental fluorosis causes generalized intrinsic staining due to excessive exposure to
fluoride in both prenatal and postnatal periods. It is the most common cause of intrinsic
stain, especially in areas where drinking water has fluoride concentrations above
optimal levels. Furthermore, the high prevalence may be due to the high availability
of fluoride in multiple sources other than water.[30]
[31]
The severity differs based on the dose, duration of exposure, stage of ameloblastic
activity, and variation in personal susceptibility.[32]
[33] This excessive or chronic ingestion of fluoride during the enamel formation will
cause hypomineralization or the porosity of this layer. In severe cases, the porosity
will extend to the amelodentinal junction, which may lead to the breakdown of the
enamel after tooth eruption.[27] High concentrations of fluoride have an effect on the activity of the ameloblasts,
with more clinical effect during the formation of the anterior teeth.[34]
The clinical appearance of dental fluorosis ranges from mild, gentle accentuation
of perikymata pattern, to white opaque spots or streaks on the surface enamel, extending
to brown pitting patches, to a more severe case of almost complete loss of the enamel
layer. This phenomenon is less aggressive in primary teeth than permanent teeth and
this can be attributed to shorter maturation and formation periods of primary teeth
or the thinner enamel layer in them.[27]
Tetracycline Stain
Tetracycline stain was first reported in the mid-1950s. The Food and Drug Administration
announced in 1963 the harm of such antibiotics to pregnant women and young children.[35] The most critical time for tetracycline staining is during tooth formation (i.e.,
between the 2nd trimester intrauterine and 8 years of age). Deposition of tetracycline
stain in the bone of the fetus will affect bone growth. If large amounts of tetracycline
are consumed during the calcification stage, this will result in hypoplasia of dental
hard tissues (i.e., enamel or dentin).[36]
The pattern of deposition occurs on the incremental lines of both dentin and enamel,
giving the whole tooth a stained appearance. The mechanism of deposition is explained
by the chelation action of the tetracycline molecule with the calcium present in the
hydroxyapatite crystals that form a complex named tetracycline-calcium orthophosphate
complex.[36]
[37] Having a larger surface area of hydroxyapatite crystals, such in dentin, makes it
susceptible to absorb a higher load of the tetracycline. After the administration
of tetracycline, its chromogen is permanently present in the dental hard tissue; it
can even be released throughout the normal bone remodeling. This constant release
of tetracycline circulates freely in the bloodstream to reenter and be incorporated
into other distant tissues undergoing calcification.[38]
The extent and severity of the stain depend on the time and duration of the drug's
administration and the dosage used, affecting the extent, color, depth, and location
of the stain ranging from light yellow to blue or brown in more severe cases.[38] Minocycline, a tetracycline analog, may cause serious discoloration in teeth for
both children and adults when taken for as short as 1 week.[39]
Diagnosis of the tetracycline stains is based on history, clinical presentation, and
the fluorescence appearance under ultraviolet light (at ∼360 nm). The labial surface
of the anterior teeth is usually the first to get a darker color, whereas the more
protected posterior teeth maintain a yellowish color for a longer period.[40] When comparing the effect on both primary and permanent teeth, permanent teeth are
less intense but more diffused compared with the primary teeth.[41]
Inherited Development Defects of Enamel and Dentin Without Any Systemic Features
AI is caused by gene mutation or altered expression. The term used when a group of
hereditary conditions affects the tooth enamel appearance and structure, frequently
associated with changes in other intraoral and/or extraoral tissues. The teeth are
sensitive, fragile, and discolored, and are characterized by hypomineralization or
hypoplasia. When a child's teeth are affected by AI, the clinical appearance and structure
of all or the most of primary and secondary dentitions will be affected. The prevalence
of AI differs depending on region or country of origin; however, the average global
prevalence is less than 1 in 200.[42] Aldred et al proposed a classification of AI based on different aspects that includes
molecular basis, mode of inheritance, phenotype (appearance), and biochemical outcome.[43] Depending on the appearance, the types of AI vary from the relatively mild hypomature
“snow-capped” enamel to the more severe hereditary hypoplasia with thin, hard enamel,
which has a yellow to yellow–brown appearance[14] as shown in [Fig. 2].
Fig. 2 Amelogenesis imperfecta.
Fig. 3 Deciduous molar hypomineralization.
The etiology of AI is attributed to multiple fetal or maternal conditions. For example,
a disturbance in the development of the tooth germ, such as deficiency of maternal
vitamin D, infections (i.e., rubella), drug intake during pregnancy, and in pediatric
hypocalcemia conditions.[44] The time at which the interference in development is very important where it characterizes
the degree of the systemic uptake.
Deciduous molar hypomineralization is another enamel defect leading to yellow–brown
staining. The significance of this condition comes from the second primary molars
develop in the same period of the first permanent molar. As a result, children with
primary molars hypomineralization are at a greater risk of molar incisor hypomineralization;
therefore, regular monitoring of these patients is recommended ([Fig. 3]).[45]
Enamel hypoplasia in primary teeth has been widely reported in the literature. An
association was found between enamel hypoplasia and premature birth, where it was
the most frequently reported outcome.[46] Opacity and hypoplasia are two outcomes of prematurity, referred to as “developmental
enamel defects,” where another study established a significant difference between
exposed and nonexposed subjects.[47]
Heredity dentin disorder is a genetic group of autosomal dominant conditions including
DGI and dentin dysplasia (DD). These conditions affect the dentin structures of primary
teeth or both dentitions. DGI is more common than DD, the incidence is 1 in 6,000
to 8,000 and 1 in 100,000, respectively. The defects cause teeth staining, which may
vary from normal to amber, gray, or purple to bluish translucent discoloration. In
addition to the discolored teeth caused by these conditions, the teeth are translucent
and often roughened with severe amber discoloration, structural defects such as a
radiographically small pulp chamber and bulbous crowns. The defect in the mineralization
process increases the potential of the enamel layer shearing that subsequently leads
to wear in the dentinal layer.[48]
Shields classified DGI into three types and DD into two subcategories.[49] DGI type I is the most common and the only type associated with genetic disorders
that affect bones known as osteogenesis imperfecta. Radiographically, the roots of
the teeth are short, constricted, and associated with dentin hypertrophy. Therefore,
teeth experience pulp canal obliteration after or before their eruption. Clinically,
it affects both dentitions with significant tooth surface loss. The color is translucent
and typical amber. Other types include DGI type II, also called hereditary opalescent
dentin, and the Brandywine isolate type III, found most commonly in Brandywine in
the United States.[50]
Hematologic Disorders
Hematological disease, such as erythroblastosis fetalis and icterus gravis neonatorum,
might produce jaundice in the newborn. This can cause a yellow–green discoloration
and enamel hypoplasia in deciduous teeth. The reason for this yellow color is due
to the deposition of bilirubin in the dental hard tissue during the developmental
stage. Congenital erythropoietic porphyria is another disorder that causes purplish–red
or reddish–brown discoloration to both deciduous and successor teeth. The discoloration
is caused by the deposition of porphyrin pigments in bone and dentin. Diagnostically,
the affected teeth can be detected with ultraviolet light under red fluorescence.[27]
Trauma
When children start to crawl, walk, and run, they are subject to unintentional falls
and collisions that may result in trauma to the primary teeth, most commonly in children
between 2 and 6 years of age.[51] Some types of trauma will cause necrosis to the primary teeth. Keeping these teeth
untreated will lead to resorption of both primary teeth and the supporting bone, this
phenomenon will lead to early loss of primary teeth and early eruption of the successor.[52]
The color change of traumatized teeth is an early common sign witnessed by parents
or guardians.[53] Furthermore, discoloration is also considered an early sign of pulpal degeneration.[54] When the pulp degenerates without hemorrhage, a stain of grayish–brown will appear
caused by protein degeneration.[55] The trauma causes a rupture of the blood vessels present in the pulp chamber, causing
a breakdown of the blood and hemolysis of the erythrocytes that produce hemoglobin.
Hemoglobin then gradually degrades to iron that shows as a bluish–black stain of the
tooth,[52]
[56] as shown in [Fig. 4].
Fig. 4 Trauma for upper left primary central incisor.
Although it has been suggested that the gray discoloration of the crown is a sign
of pulp necrosis,[57] studies have shown that traumatized primary teeth might stay discolored (having
a discolored gray crown) for several years with no other clinical or radiographic
sign of pulpal degeneration or necrosis.[54] Inadequate or improper endodontic treatment following trauma may lead to dark discoloration,
which may occur due to incomplete removal of the pulpal tissue or incomplete removal
of root canal filling material from the pulp chamber.[27]
Amalgam Staining
The demand for high aesthetics dental filling and the significant increase of minimal
intervention of restorative approaches, considering the amalgam as a material of choice
for primary teeth, has been reduced.[58] The use of amalgam has been controversial due to concerns related to its mercury
release. An in vivo study that included 20 primary molars indicated that amalgam causes
bluish discoloration because of copper release. The grayish–black stain could be a
result of an amalgam filling, which may occur due to the corrosion of amalgam, leading
to the formation of silver sulfide.[58]
[59]
Root Resorption
The physiological pattern of root resorption of primary teeth occurs on the root surface,
either within the pulp or from the periodontal ligament (i.e., in the form of internal
or external root resorption). The exact location of resorption is hard to detect until
the lesion reaches a certain size. Clinically, it is asymptomatic, but occasionally
it may appear as pink discoloration of the amelocemental junction.[14]
[60]
Dental Caries
Dental caries involves microorganisms excreting acid resulting in changes in dental
tissue hardness and color. Dental caries is diagnosed by the change in color and may
indicate the stage of the disease and lesion activity. The initial change in color
due to caries is an opaque white spot as a result of increased enamel layer porosity
due to acid production by the microbial metabolism of sugar.[61] When caries develop further, a brown discolored dentin layer will be present, but
the cause of discoloration remains controversial in the literature.[62] However, particularly for primary teeth, the color and hardness of carious lesions
are two clinical criteria used for the diagnosis of the progression degree of the
disease. An active caries tends to be light yellow/beige, whereas slowly progressing
or arrested caries lesions are usually darker.[63]
Erosion
Tooth erosion is defined as the loss of dental hard tissue by nonbacterial chemical
mechanical processes, resulting in loss of superficial enamel and visible by yellow
tooth coloration. Recent lifestyle changes and the increased consumption of acidic
foods and beverages have led to an increase in the prevalence of dental erosion worldwide.
High prevalence of tooth erosion in 5-year-old children (from 30 to 98%) has been
reported.[64] Due to lower mineralization levels and thinner primary teeth enamel compared with
permanent teeth, the process of erosion is expected to be faster in children. A comparative
study evaluated 60 primary and permanent teeth focusing on the erosive potential due
to different type of beverages consumed and showed that surface microhardness was
lower for primary teeth than for permanent teeth.[65] Darker color can occur due to prolonged exposure of the underlying dentin as the
enamel thins.[14]
Extrinsic Discoloration
Extrinsic discoloration is outside the tooth substance and lies on the tooth surface
or in the acquired pellicle.[66]
Stains
Black stains affect 2.4 to 16% of primary teeth.[67] It starts as early as age 2 and can significantly affect the parents and have an
influence on the child's personality as well as the child's self-confidence. It is
a form of dental plaque characterized by high calcium and phosphate levels in addition
to insoluble iron salts.[68] The black stain is ferric sulfide from the interaction of hydrogen sulfide arises
with gingival fluids or saliva. Another etiological factor reported is the association
with some bacterial strains like Lactobacillus and Actinomyces.[69] The strength of the adhesion is still under investigation; however, attractive forces,
including hydrophobic interaction, electrostatic, and hydrogen bonds, have been reported.[68] Different criteria have been proposed to establish a diagnosis. Koch et al considered
the presence of dark dots, linear discoloration, and changes to the smooth surfaces
of two or more different teeth.[70] On the other hand, Koch et al relied on the presence or absence of the dental plaque
as follows: (1) no line, (2) incomplete coalescence of pigmented dots, or (3) continuous
line formed by pigmented spots.[70]
It is essential to state that there is a relationship between the prevalence of dental
caries and the presence of black stain. A recent meta-analysis that included 13 studies
concluded that individuals experiencing black stain had lower caries experience in
comparison to those without the condition.[71]
Iron deficiency affects more than two billion people in the world and is one of the
most common nutritional deficiencies. Iron can be found in dental hard tissue, including
enamel and dentin.[72] The most common cause of iron deficiency is the insufficient intake of iron in the
diet. This is mostly treated by food and syrup supplements that contain iron salts.[73] Black stain is a type of complication that results from oral iron supplements to
help children fight anemia.[74]
Green stain is a type of stain of unknown etiology that affects more male children
than female. However, it has been reported that it is an action of chromogenic bacteria.
The most common teeth affected are the maxillary central incisor, especially on the
gingival third labially. Mouth breathing is also considered as a contributing factor.[27]
The orange stain is less frequent when compared with previously mentioned black and
green stains, and can be removed more easily. Types of chromogenic bacteria, including
Serratia marcescens and Flavobacterium lutescens, have been reported as potential etiology in combination with poor oral hygiene. Orange
stain is mostly noted on the gingival third of the tooth.[75]
As it is not possible to remove extrinsic stains by daily oral care, professional
cleaning is usually required to meet the child aesthetic demands. Brushing with pumice
powder following simple scaling is usually enough; however, the stain tends to recur.
As a result, the enamel beneath the stain might be affected, resulting in initial
demineralization or roughness.[27]
[68]
Stannous Fluoride Pigmentation
Research done by Muhler in 1946 reported the efficiency of using stannous fluoride
(SnF2) on reducing dental caries. The study compared two groups receiving 2 and 4%
of SnF2, respectively, with a control group showed that children received SnF2 had
experienced 37% reduction in new caries surface.[76] Upon applying 8% SnF2 solution, certain areas of the tooth become discolored, ranging
from light brown to black depending on the depth and involvement of caries. Furthermore,
pigmentations affect caries and precarious enamel following stannous fluoride application.[77]
Silver Diamine Fluoride Stain
Silver diamine fluoride (SDF) is one of the recently recommended materials to prevent
and arrest dental caries owing to the low cost of using SDF.[78] SDF is a colorless alkaline solution containing silver and fluoride, which forms
a complex with ammonia. The ammonia ions combine with silver ions to produce a complex
called the diamine–silver ion.
Several studies have demonstrated the efficacy use of this type of fluoride in treating
carious primary dentition.[79] Thus, SDF usage could increase the cost-effectiveness of health care and improve
oral health, ultimately reducing the need for urgent care.[80] Since the 1940s, silver components have been developed and used for caries prevention
and it has been used in Japan for more than 40 years. Moreover, in Hong Kong and China,
a trial compared the effect of 38% SDF and 5% sodium fluoride varnish and found that
the SDF is more effective arresting primary teeth caries.[78] Other studies have reported a caries arrest rate of 81%.[81] SDF application is affected by the concentration used and the number of times applied
per year, showing that 38% SDF treatment is more recommended than 12% SDF, especially
when applied twice a year.[81]
Regarding the mechanism of action, the antimicrobial effect is a result of silver
particles acting on proteins. Moreover, the black stain of carious dentin and enamel
resulting from SDF silver particles is included in [Fig. 5]. A recent scoping review stated that “The aesthetic perception of black staining
associated with SDF is not directly related to acceptability and satisfaction of patients
and parents but related to a lower professional's acceptance.”[82]
Fig. 5 Stain following silver diamine fluoride application.
