A Review on Various Reasons for Teeth Discolouration

 

Rakhi Menon*

II B.D.S Student, Saveetha Dental College, Chennai, India

*corresponding author e-mail: rakhimenon1@gmail.com

 

ABSTRACT:

Teeth discoloration is mainly a cosmetic problem that occurs when the enamel (the hard, outer surface of the tooth) or the dentine (the layer below the enamel) become discoloured or stained. The teeth can become discoloured by stains on the surface or by changes within the tooth.

 

Tooth stains can cause great embarrassment and keep people from smiling. So what causes tooth discoloration and how can you prevent it from happening to you? There are two types of tooth stains: extrinsic and intrinsic. Extrinsic stains are known as surface stains. These are caused when outside elements affect the surface of the tooth. Intrinsic stains result when the interior sections of the tooth have darkened due to various reasons.

 

KEYWORDS: Teeth discoloration, tooth stains, tetracycline staining, dental fluorosis, tooth bleaching, Enamel hypoplasia, ageing, root resorption.

 


INTRODUCTION:

Discoloration can be caused by: 

·         External factors cause staining of the outer layer of the tooth and include smoking, beverages such as coffee, wine, cola or foods such as apples and potatoes.

·         Internal factors cause the inner structure of the tooth (the dentin) to darken or get a yellowish tint and may be caused by:

·         excessive exposure to fluoride during early childhood

·         Using tetracycline antibiotics during the second half of pregnancy and children 8 years old or younger.

·         Dental trauma tooth in a young child causing damage to the developing permanent tooth.

·         Systemic disease/illness during tooth formation such haemolytic disease of the newborn

·         Age-related discoloration is due to dentin turning yellow naturally with ageing and the stained dentin makes the teeth look discoloured.

·         Dentinogenesis imperfecta is a rare condition in which children are born with gray, amber or purple discolorations in the teeth.

·         Loss of vitality secondary to trauma or infection (dental caries) results in greyish discoloration.

 

·         Amelogenesis imperfecta is a genetic condition in which enamel formed during tooth development is abnormal and causes discoloration of teeth.

 

The prognosis is very good for teeth stains caused by external factors. However, stains caused by internal factors may be more difficult or take longer to remove.

 

TETRACYCLINE STAINING:

Tetracycline’s (TCN) were introduced in 1948 as broad-spectrum antibiotics that may be used in the treatment of many common infections in children and adults. One of the side-effects of tetracycline is incorporation into tissues that are calcifying at the time of their administration. They have the ability to chelate calcium ions and to be incorporated into teeth, cartilage and bone, resulting in discoloration of both the primary and permanent dentitions. This permanent discoloration varies from yellow or gray to brown depending on the dose or the type of the drug received in relation to body weight. Minocycline hydrochloride, a semi synthetic derivative of tetracycline often used for the treatment of acne, has been shown to cause pigmentation of a variety of tissues including skin, thyroid, nails, sclera, teeth, conjunctiva and bone. Adult-onset tooth discoloration following long-term ingestion of tetracycline and minocycline has also been reported. The remarkable side-effect of minocycline on the oral cavity is the singular occurrence of "black bones", "black or green roots" and blue-gray to gray hue darkening of the crowns of permanent teeth. The prevalence of tetracycline and minocycline staining is 3-6%. The mechanism of minocycline staining is still unknown. Most of the reviewed literature consisted of case reports; longitudinal clinical trials are necessary to provide more information on the prevalence, severity, aetiology and clinical presentation of tetracycline and TCN-derivative staining in the adult population.

 

Systematic (IUPAC) name:

(4S,6S,12aS)-4-(dimethylamino)-1,4,4a,5,5a,6,11,12a-octahydro-3,6,10,12,12a-pentahydroxy-6-methyl-1,11-dioxonaphthacene-2-carboxamide OR (4S,6S,12aS)-4-(dimethylamino)-3,6,10,12,12a-pentahydroxy-6-methyl-1,11-dioxo-1,4,4a,5,5a,6,11,12a-octahydrotetracene-2-carboxamide
Clinical data

Trade names     Sumycin

Routes oral, topical (skin and eye), intramuscular, intravenousPharmacokinetic data

Bioavailability 60-80% oral, while fasting

<40% intramuscular

Metabolism      Not metabolized

Half-life       6-11

 

MECHANISM:

Tetracycline binds to the 30S subunit of microbial ribosome. It inhibits protein synthesis by blocking the attachment of charged aminoacyl-tRNA to the A site on the ribosome. Thus, it prevents introduction of new amino acids to the nascent peptide chain. The action is usually inhibitory and reversible upon withdrawal of the drug. Mammalian cells are less vulnerable to the effect of tetracycline, as these contain no 30S ribosomal subunits (only prokaryotes have 30s subunit), but tetracycline also may bind to the eukaryotic 80S ribosome.


Tetracycline Antibiotics Stain the Teeth?

Tetracycline is an antibiotic is used to target bacterial infections. Those who are diagnosed by doctors to have Urinary Tract Infections, Acne, Pneumonia or even some skin infections could possibly be prescribed tetracycline.


The Side Effect of Tetracycline on the Teeth:

Despite tetracycline being prescribed by doctors, what many people don’t realize are the side effects or tetracycline on the teeth. Sure, it is a powerful antibiotic that works well in fighting infections however; the adverse effects on both developing and adult’s teeth can be catastrophic.


However, teeth staining in children can be caused by other factors too–for example, ingesting too much fluoride from toothpaste can cause discoloration as well. To prevent this, it’s a good idea to let them use toothpaste without fluoride.


Another side effect of tetracycline on the teeth is that the teeth can become disfigured. This is less likely but much more serious a problem. If you ever notice your children’s teeth changing in shape or becoming sensitive in anyway then you should book an appointment with your children’s dentist immediately.

Adults can also be affected by this side effect of tetracycline however, this is only likely when taking daily doses of more than 100mg.


Tetracycline staining only occurs in approximately 5% of people who are prescribed this antibiotic but despite this, you should be aware that if you fall into this 5% your teeth could be severely affected. From a cosmetic point a view, the appearance of the teeth can be devastated and you will have a mottled effect instead of nice white teeth. If a doctor wants to prescribe you this medication, it is important that you discuss this side effect of tetracycline with him and perhaps ask him/her to suggest an alternative medication.


How does Tetracycline cause teeth staining?

When teeth are still growing, the enamel is also developing. This means that a young person’s teeth are particularly vulnerable to discoloration. Tetracycline can cause teeth stains in children when it becomes stuck in the gum line.


One thing to note is that tetracycline stains are permanent, but one of the ways to cover them is by getting veneers. However, it is much easier to avoid them in the first place, so do consult your doctor to find an alternative antibiotic.


Doctors in developed countries don’t tend to prescribe this drug to children under 8 anyway, since they are aware of the consequences that can happen to the colour and structure of the teeth. However, years ago, the detrimental effects of tetracycline on the teeth were unknown and so there are some people who have to live with the side effect of tetracycline staining.


Unfortunately, because intrinsic teeth stain are the most difficult to remove, most conventional whitening treatments won’t have a huge effect effect on discoloration caused by tetracycline. Brite White Teeth can treat clients with Tetracycline staining, however as the results achieved in cosmetic teeth whitening will not be as effective, we cannot guarantee a 100% white teeth. This is also specified on our consultation and consent forms. We will also advise a client with tetracycline staining to visit their dentist for a consultation prior to treatment with us.


Use of Tetracycline is contradictory in case of:

Use of tetracycline during pregnancy after the fourth Month can cause staining of the deciduous teeth, but will not have a permanent effect on permanent teeth. In general, tetracycline should not be given to women who are pregnant or to young children.


Use cautiously in clients with liver and renal disease. Doxycycline and minocycline may be used in clients with renal disease.

 

Tetracycline discoloration is classified according to the extent, degree and location of the staining [2]:

1      First degree, Mild tetracycline staining. This staining is minimal expression of tetracycline. , varies from yellow to grey with no banding.

2      Second degree. Moderate tetracycline staining. Yellow-brown to dark grey banded staining.

3      Third degree. Severe tetracycline staining. Blue grey or black with significant banding across the tooth.

4      Fourth degree. Extended and more severe staining.


Minocycline, a tetracycline derivative used for the treatment of Acne vulgaris, respiratory diseases and rheumatoid arthritis, has also the ability to cause pigmentation of skin, nails, bone and teeth [2]. The picture varies from a green-grey to blue-grey post-eruptive discoloration [3]. Minocyline is well absorbed from the gastro-intestinal tract and chelates with iron ions to form complexes that are insoluble and may cause the discoloration [2].


There are two other theories of the mechanism of staining; the extrinsic and intrinsic factors. “The extrinsic theory is based on that minocycline is excreted in a high concentration in the gingival fluid”, and can stain the enamel “by diffusing through the pulp or by affecting odontogenesis”. The intrinsic theory proposes that minocycline is absorbed and bound to plasma proteins and distributed to tissues with high affinity for minocycline [2]. This discoloration appears to happen in 3-6% of patients who are on long-term minocycline therapy with more than 100 mg per day. The onset of staining can vary from one month to many years after the start of therapy [3].


Ciprofloxacin:
Ciprofloxacin is a synthetic antibiotic of fluoroquinolone drug class introduced in 1981 [3]. It is used in treatment of infections with Klebsiella (can cause pneumonia) [3]. According to a case report from 1991 [3] ciproflaxacin has association with greenish discoloration of teeth.

 

FLUOROSIS:
An excess ingestion of fluoride that induces multiple changes in the developing enamel [4].


Amelogenesis:

The ameloblasts pass through several stages of differentiation and the pre-secretory ameloblasts differentiate into secretory ameloblasts.


The secretory ameloblasts deposit a protein matrix, which acts as a temporary protein platform on which the enamel crystals can form. An aprismatic thin layer of enamel is first deposited against the dentin. Fully differentiated secretory ameloblasts with Tomes' processes deposits the bulk (inner) layer of the enamel. Protein matrixes, predominantly amelogenins, are secreted into the enamel space by these cells. The ameloblasts lose their Tomes' process and deposit a layer of aprismatic enamel with small crystals. The cells transform into maturation ameloblasts and the enamel matrix proteins are gradually removed from the matrix during this stage.



In the maturation stage, matrix proteins are removed from the extracellular space, and mineralization increases progressively until the tooth erupts [4].


The ingestion of fluorides is particularly important in infants as dental fluorosis can only originate during the tooth development [4]. There are various sources of fluoride in the environment and fluorides can be delivered through water, supplements, milk and salt or through oral care products as toothpastes, gels, varnishes, paint-on applications and mouth rinses. Fluorides occur naturally, usually at very low doses in water supplies, mostly less than 0.5-0.7 mg/l. If a mother has a high intake of fluoride, it is poorly transported from plasma to milk, but a child may ingest high amounts of fluoride through milk formulas, if these are prepared with fluoride-containing water. The limit value for fluoride is 1.5 mg/l in water supply in Norway. Plants exposed to fluoride in the soil or water supplies containing high levels of fluoride may also contain significant amounts of fluoride. Fresh water fish and tea are other examples of fluoride sources. A cup of tea may contain a fluoride concentration of 0.5-4 mg/l partly depending on the water that is used. It is important to think of the total intake of fluoride that (adults and) especially children ingest through water, food and dental products [4].


Fluoride is highly reactive and reacts rapidly with mineralizing tissues. One can say that fluoride will gradually be incorporated into the crystal lattice structure in the form of fluorohydroxyapatite, and be stored in bones and teeth. The higher the dose of fluoride occurring during the tooth development, the higher the concentration of fluoride is to be found in enamel» [4]. The amount of fluoride exposure is reflected in the different layers of the enamel.

There have been various explanations for the mechanisms behind dental fluorosis. Based on present evidence, a slight excess of fluoride ions affects the rates at which enamel matrix proteins break down and/or the rates at which the by-products from this degradation are withdrawn from the maturing enamel[4]. Interference with removal of the enamel matrix could inhibit crystal growth during maturation and this in turn could lead to incomplete mineralization. The enamel organ cells and their proliferation and differentiation are, however, not affected.


According to a review, Aoba and Fejerskov (2002), fluoride may modulate the kinetics of enzymic degradation of the matrix proteins in the extracellular environment and may indirectly interfere with protease activities by decreasing the free calcium ion concentration in the mineralizing environment [4].


Disturbances in the formation of the enamel may be seen as opacities reflecting the porosities of the fluorosed enamel. These are seen as “thin, white, opaque lines corresponding to the perikymata running across the tooth surface” [4]. The enamel porosity, which is a result of a hypo mineralization of the enamel, is seen along the stria of Retzius. Posteruptively, this chalky white enamel may change to more severe forms of fluorosis depending on the degree of hypo mineralization which is a result of post eruptive mechanical damage such as mastication, attrition and abrasion [4].


Thylstrup and Fejerskov (1988) have classified fluorosis according to the scored severity from 0 to 9.

Pulpal haemorrhagic products, pulp necrosis, pulp tissue remnants after endodontic therapy and their possible effect on tooth color.

 

Tooth discolorations can be caused by blood components, by-products from haemolysis of red blood cells, pulpal tissue remnants, filling materials or sealer remnants that penetrate deep into the dentinal tubules.


Trauma, crown preparation or vibrations from the bur that cause a rupture of the blood vessels and the accumulation of haemoglobin or other haematin molecules can result in discoloration of the tooth substance (6) If pulp remnants remain inside the pulp chamber after endodontic treatment, this can cause a coronal discoloration due to a gradual disintegration and flow into the dentinal tubules [6].


When filling materials and sealer remnants or medicaments containing tetracycline that are not completely removed from the pulp chamber after endodontic treatment are in contact with dentin over time, they can penetrate into the dentin tubules and discolour the tooth.


An internal bleeding directly after a full crown preparation is characterized by a pink discoloration of a tooth with a vital pulp. This intrapulpal bleeding with blood cells penetrating the dentin can also be caused by vibrations created by, for example, an eccentrically rotating bur [5].


The discoloration of a necrotic tooth caused by a trauma will become more severe over time. If the trauma does not cause a pulpal necrosis, the discoloration can be reversed. If the tooth becomes revascularized the pinkish hue that was seen initially after a trauma might disappear in 2-3 months [6].

On the other hand: If a colour change of a tooth crown is yellow, this can be a sign of excessive dentin formation and narrowing of the pulpal space. It can often be seen after a minor trauma, mainly luxation injuries) [5].


ROOT RESORPTION:

Root resorption is a removal process, pathologic or physiologic, of tooth structure by odontoclasts [6]. This process can be classified based on location, internal if the root resorption begins at the pulpal aspect, and it is known as external if the process is started from the outside of the root.

The aetiology of root resorptions requires two phases: injury and stimulation. Injury is related to the non-mineralized tissues; cementum or dentine, and may be a consequence of a dental trauma, surgical procedures, and excessive pressure from orthodontic treatment or from an impacted tooth or tumour [5].


Injured tissues are then colonized by multinucleated cells, osteoclasts that begin a localized inflammatory response and the resorption process. Whether the active resorption process will continue or not, it depends on a stimulation factor of osteoclasts, either in form of infection or pressure. The process will stop without further stimulation of the resorption cells. In about 2-3 weeks the repair with cementum-like tissue will take place, and no treatment is needed. If the damage on the root surface is severe the osteoclasts will be able to attach to the dentine of the root before the cementum-producing cells, resulting in  ankylosis [5].

 

The most common stimulation factor is a pulpal infection. Due to injury to the cementum or dentine, dentinal tubules become infected, and this can stimulate the inflammatory process with osteoclastic activity in the peri-radicular tissues, leading to external or internal root [5]


resorption. The treatment for the internal resorption is pulpectomy, removing the resorbing cells (of pulpal origin) and their blood supply [5].


If there is an external root resorption it is important to control the pulpal bacteria that act as stimulation factor. It is recommended to treat the tooth endodontically with calcium hydroxide for 6-24 months in order to arrest the resorption process [6]. The reason is that calcium hydroxide has an antibacterial effect and low solubility, giving a long-term effect in the root canal, and a removal the stimulation from the canal [5].


External root resorption may occur after an injury to the cementum, apical to the area of the bacterial stimulation originating from the periodontal sulcus [5]. Internal root resorption takes place within the pulp cavity or root canal and involves the dentinal wall. The result is that the pulp space becomes bigger. It happens that the enlarging pulp perforates the dentine and enamel becomes involved. It may appear clinically as a pink spot [6].

 

AGEING:
As a person gets older, secondary dentine naturally gets deposited in the tooth, and the enamel can become thinner. When the enamel gets thinner, more colour of the darkened dentine reflects. This can result in a gradual darkening of the colour of the teeth with age [1].

 

ENAMEL HYPOPLASIA:

Enamel hypoplasia is a condition of deficient amelogenesis, resulting from an injury to the formative cells, the ameloblasts. A consequence of this is less quantity of enamel formation than normal. The prevalence varied from 3 to 15% of young adults having EH in the permanent   teeth [7].

 

Hypoplasia of primary teeth is rarely as severe as in the permanent teeth [8]. Enamel hypoplasia may be localized or generalized [1]. Trauma and localized infections in the primary dentitions are the most common reasons to EH [7]. Turner´s hypoplasia is a common term for EH where an apical localized infection in the deciduous dentition has caused disturbances of the normal amelogenesis. The infection destroys the enamel epithelium, and the inflammation interferes with normal calcification [8].


Generalized EH may be the result of any disturbance caused by foetal or maternal conditions such as maternal vitamin D deficiency, rubella infection, drug intake during pregnancy or paediatric hypocalcaemic conditions. These defects are related to the degree of the systemic upset, and are chronologically laid down in the teeth according to the time of interferences [11].


The quantitative defects of EH on the tooth surface appear as thin, or pitted - single or multiple, shallow or deep, or scattered or arranged in horizontal rows, or grooved – single or multiple, narrow or wide, or evident as partial or total absence of enamel over substantial areas [9]. The pits and grooves are exposed to extrinsic staining of the enamel and it often becomes internalised [11]. The thickness of the enamel is reduced, and may be translucent or opaque [9].


Another interesting developmental dental defect in this context is molar-incisor hypo mineralization, MIH, which has a different clinical appearance. MIH presents as demarcated opacities, resulting from incomplete mineralization and is a qualitative defect, in the permanent first molars and incisors. Demarcated opacities have a clear and distinct boundary to the near areas of normal enamel. They vary from white, yellow to brown in colour, and do not always appear symmetrically. The number of affected teeth also varies. In addition, the affected teeth at times undergo post-eruptive break-down due to soft and porous enamel [9].


EH and MIH can be difficult to differentiate diagnostically if the affected molars have a post-eruptive break-down caused by caries or trauma from masticatory forces. EH and MIH can occur together, especially at a histological level [11].


TOOTH WEAR AND GINGIVAL RECESSION:

Tooth wear is a progressive loss of the outer layers of the enamel and dentine caused by erosion, abrasion and (or) attrition [11], while gingival recession is a condition characterized by retraction of the gingival margins, which expose the root surface of the tooth. Gingival recession is usually associated with pathological alveolar bone loss at that site [11].


As the enamel gets thinner the teeth become darker. The colour of the dentine becomes more apparent and if the enamel fractures, secondary attrition can occur faster, the dentine will be exposed and the colour changes to a darker degree in this area. Other factors that might change the colour of the teeth are fractures, loss of enamel or enamel cracks, as stains are included into the body of the tooth [10].


Some factors that contribute to tooth wear are causes that naturally occur as a result of ageing. Examples can be attrition and erosion that also are stimulus that can initiate the formation of tertiary dentin. Secondary dentin is naturally formed and deposited as a result of age. This increased thickness of dentin will gradual darkens the teeth. Therefore, is aging itself is a factor that will influence on tooth colour.


Gingival recession:

When a tooth has a gingival recession, the cervical area will be exposed. The enamel layer is thin in this area, so the dentin underneath the enamel is showing through the enamel and influences more on the tooth colour. The teeth become darker as the enamel thins. The cementum covering the exposed root will be lost over time. Once the dentine is exposed, the inclusion of chromogens in the tooth substance increases [11].


Treatment:
If a patient wants to treat discolorations of his/her teeth, and bleaching can give a good aesthetic result, this will also be the most conservative treatment (plan) we can offer.


A BRIEF HISTORY OF TOOTH BLEACHING:

In 1916, the use of hypochloric acid was used to treat fluorosis by Adams. A technique used by Ames in 1937 to treat mottled enamel (fluorosis), was done over 5 to 25 visits. A mixture of hydrogen peroxide and ethyl ether on cotton, heated with a metal instrument for 30 minutes was applied on the tooth. The same technique was used in 1942 by Younger to treat dental fluorosis on 40 children [10]. Since 1930 the use of concentrated hydrogen peroxide and heat has been an accepted treatment. The combination of hydrochloric acid and hydrogen peroxide for removing brown stain from mottled teeth was used in 1966. In 1970 a method for whitening tetracycline-discoloured dentin was published and this was the first publication indicating that there is chemical penetration of hydrogen peroxide to the dentin to whiten teeth [3, 12].


A custom-fitted night guard with proxigel (which also contain 10% carbamide peroxide) was made by Klusmeier in 1972, and ”the walking bleach technique” for whitening non vital teeth with the use of 35% hydrogen peroxide and sodium perborate was introduced in 1976.

 

10 % carbamide peroxide was introduced and commercially available in 1989. The first study with the “night guard vital bleaching” technique using 10% carbamide peroxide was published by Haywood and Heymann in 1989 [3, 12].

 

REFERENCE:

1      Mehta, Akul (2011-05-27). "Mechanism of Action of Tetracycline", Pharmaxchange.info. Retrieved 2012-06-07.

2      Kenneth Todar, Antimicrobial Agents in the Treatment of Infectious Disease. Online Textbook of Bacteriology. 2012.http://textbookofbacteriology.net/antimicrobial_4.html

3      Chopra I, Roberts M (June 2001). "Tetracycline Antibiotics: Mode of Action, Applications, Molecular Biology, and Epidemiology of Bacterial Resistance". Microbiol. Mol. Biol. Rev. 65 (2): 232–260. doi:10.1128/MMBR.65.2.232-260.2001. PMC 99026. PMID 11381101.

4      Connell SR, Tracz DM, Nierhaus KH, Taylor DE (December 2003). "Ribosomal Protection Proteins and Their Mechanism of Tetracycline Resistance". Antimicrob. Agents Chemother. 47 (12): 3675–3681. doi:10.1128/AAC.47.12.3675-3681.2003. PMC 296194. PMID 14638464.

5      Klajn, Rafal, Chemistry and chemical biology of tetracyclines, retrieved 20 June 2007. Jukes, Thomas H. Some historical notes on chlortetracycline. Reviews of Infectious Diseases 7(5):702-707 (1985).

6      Hochstein, F. A.; Stephens, C. R.; Conover, L. H.; Regna, P. P.; Pasternack, R.; Gordon, P. N.; Pilgrim, F. J.; Brunings, K. J. et al. (November 1953). "The structure of terramycin". Journal of the American Chemical Society 75 (22): 5455–75.

7      George Armelagos (May 2000). "Take Two Beers and Call Me in 1,600 Years - use of tetracycline by Nubians and Ancient Egyptians". American Museum of Natural History. Retrieved 2007-12-19.

8      Riordan,Jan."Breastfeeding and Human Lactation",Jones and Bartlett,2010 p.179 a b FDA Adverse Events Reporting System Retrieved on January 14, 2011

9      Lippincott's Illustrated Reviews: Pharmacology, 4th ed. Harvery RA, Champe, PC. Lippincott, Williams and Wilkins, 2009

10    The Johns Hopkins Medical Institutions. > Tetracycline Labeling Last updated January 8, 2001.Olson CA, Mitchell KD, Werner PA (October 2000). "Bait ingestion by free-ranging raccoons and nontarget species in an oral rabies vaccine field trial in Florida". J. Wildl. Dis. 36 (4): 734–43.

11    William J. Cromie (February 10, 2000). "Researchers Switch Cancer Off and On -- In Mice". Harvard Gazette. Retrieved 2008-10-25.

12    Conal Urquhart (15 July 2012). "Can GM mosquitoes rid the world of a major killer?". The Observer. Retrieved 2012-07-15.

 

 

 

 

 

 

Received on 26.03.2014                  Modified on 01.06.2014

Accepted on 06.06.2014                  © RJPT All right reserved

Research J. Pharm. and Tech. 7(7): July  2014 Page 815-820