Management Of Tetracycline Discoloration
INTRODUCTION
Tetracycline broad-spectrum antibiotics were introduced in 1948 and quickly found favor in the treatment of a multitude of commonly occurring childhood and adult infections. All tetracycline compounds consist of four fused cyclic rings, hence the name tetracyclines. More than 60 years later they are still commonly used in the treatment of acne, and in addition there has been a resurgence of interest in them as a result of their beneficial use in combination therapy for bone metastasis (Saikali and Singh 2003) as well as in the treatment and prophylaxis of tuberculosis, anthrax, and malaria. Although they possess undoubted therapeutic benefits, tetracycline compounds have, nevertheless, also been found to exhibit a number of significant systemic side effects. These include hepatic damage in pregnant women (Madison 1963) as well as toxic, damaging effects on the developing fetus as a result their ability to cross the placenta. They are clearly, therefore, contraindicated during pregnancy.
EFFECTS OF TETRACYCLINES ON TEETH
One of the most obvious side effects of tetracycline use (and in particular minocycline [Minocin], which is a semisynthetic tetracycline derivative) is its incorporation as a fluorescent pigment into tissues that are calcifying at the time of administration (Cheek and Heymann 1999). It has the ability to chelate calcium ions and to be incorporated into teeth, cartilage, and bone, to form a tetracycline-calcium orthophosphate complex (Eisenberg and Bernick 1975) resulting in discoloration and enamel hypoplasia of both the primary and permanent dentitions if administered during the period of tooth development. The ability of tetracycline to intrinsically stain teeth during odontogenesis has been well known and documented for almost five decades (Schwachman and Schuster 1956, Davies et al. 1962) and usually causes affected patients considerable distress as well as posing a number of problems for dentists charged with the task of improving the appearance of such teeth.
The severity of the discoloration is considered to be related to dose, frequency, duration of therapy, and, critically, the stage of odontogenesis. The calcification of deciduous teeth begins at approximately the end of the fourth month of gestation and ends at approximately 11–14 months of age. Permanent teeth begin calcifying after birth and are not affected by exposure to tetracycline during the prenatal period. The calcification of permanent teeth is completed at 7–8 years of age with the exception of the third molars (Mello 1967, Jackson 1979). Therefore, in addition to the reasons stated earlier, the administration of tetracycline to pregnant women as well as to children up to 8 years of age must be avoided because it may result in discoloration (see Figure 12.2) and enamel hypoplasia (Conchie et al. 1970). Enamel hypoplasia (see Figure 12.1) can, of course, also be the result of childhood disease, hereditary defects in enamel formation, or prematurity of the child—all of which are known to cause enamel defects. Tetracyclines are excreted in urine and feces, with the urinary route being the most important for the majority of these drugs. The drugs should not be given to nursing mothers because they are also excreted in human milk (van der Bijl and Pitigoi-Aron 1995). Adult-onset tooth discoloration after long-term ingestion of tetracycline has also been reported (Di Benedetto 1985). The prevalence of tetracycline discoloration has ranged from 0.4–6% in various studies (Martin and Barnard 1969, Suckling and Pearce 1984, Berger et al. 1989), the actual figure clearly being a reflection of the prevailing prescribing habits of medical practitioners in any particular region at any given time. For example, King and Wei (1989) reported a prevalence of over 16% in Hong Kong’s population.
The ensuing discoloration is permanent and varies from yellow or gray to brown depending on the dose or the type of the drug received in relation to body weight. After tooth eruption and exposure to light, the fluorescent yellow discoloration gradually changes over a period of months and years to a nonfluorescent brown color. The labial surfaces of yellow-stained anterior teeth will darken in time, whereas the palatal surfaces and buccal surfaces of posterior teeth will remain yellow. These changes are thought to be the result of an oxidation product of tetracycline, which is light induced (Bevelander et al. 1961, Atkinson and Hartcourt 1962). A further complication, and one that adds to the stigma associated with tetracycline-discolored teeth, is that tetracycline will fluoresce bright yellow under ultraviolet light in a dark room.
Minocycline hydrochloride, a semisynthetic 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 (Rosen and Hoffmann 1989). A further side effect of minocycline on the oral cavity is the occurrence of “black bones,” “black” or “green roots,” and blue-gray to gray darkening of the crowns of permanent teeth. Minocycline differs from other tetracyclines in that it is well absorbed from the gastrointestinal tract and chelates with iron to form insoluble complexes, and this may provoke the tooth staining. It is best to try to avoid the long-term use of minocycline because this discoloration can be the most difficult to bleach. It is also important to discuss this complication with the patient’s medical practitioner so that he or she can administer a different medication.
DIAGNOSIS
It is important to recognize other causes of tooth staining to discriminate among tetracycline staining, minocycline staining, and other extrinsic or intrinsic tooth-staining problems (Table 12.1).
TREATMENT
Nowhere does the old adage that “an ounce of prevention is better than a pound of cure” apply better than with the prescription of tetracycline, not only from the patient’s point of view but also from that of the clinician, especially when one takes into account possible medico-legal implications. Indeed, a legal precedent was set in 1982 when tetracycline was alleged to have caused discoloration of the teeth of two children with an ensuing, successful, legal action being brought against the prescribing general medical practitioner (Medical Protection Society 1982).
Extrinsic factors |
Characteristics |
Chromogenic bacteria stains |
Green, black-brown, and orange |
Tobacco |
Black, brown |
Amalgam |
Black, gray |
Medicaments |
Silver nitrate: gray, black |
Stannous fluoride: black, brown |
|
Chlorhexidine: black, brown |
|
Foods and beverages |
Coffee, tea, wine, berries, and others: color of food item |
Iron |
Black cervical discoloration |
Intrinsic factors |
Characteristics |
Dentinogenesis imperfecta |
Yellow or gray-brown |
Amelogenesis imperfecta |
Yellow-brown |
Dental fluorosis |
Opaque white to yellow-brown patches |
Sulphur drugs |
Black staining |
Tetracyclines: |
|
Chlortetracycline |
Gray-brown hue |
Oxytetracycline |
Brown-yellow to yellow |
Tetracycline hydrochloride |
Brown-yellow to yellow |
Dimethylchlortetracycline |
Brown-yellow to yellow |
Minocycline |
Blue-gray to gray |
Doxycycline |
No change |
Dental trauma |
Transiently red through to black |
Hyperbilirubinemia |
Yellow-green to blue, brown, and gray |
Erythropoietic porphyria |
Red or brown |
Ochronosis |
Brown |
When actual treatment is sought—and this is almost always for esthetic reasons—there are a number of possible treatment options. These are as follows (in increasing degrees of invasiveness):
1. Tooth bleaching only.
2. Tooth bleaching and composite bonding, full or partial, over discolored areas (Figure 12.1).
3. Combination treatment starting with tooth bleaching and continuing to direct veneers (Figure 12.2).
4. Indirect laminate veneers (with or without prior tooth bleaching).
5. Full-coverage restorations.
When considering which of these options one should pursue, Dietschi has wisely observed that “Clinicians should correct restorative challenges by selecting a progressive treatment concept that begins with the most conservative restorative option and progresses to more invasive procedures only as required.”
TOOTH BLEACHING
The treatment of tetracycline staining with tooth bleaching has been used with varying degrees of success for the last 40 years. Haywood et al. (1997) were the first to show that carbamide peroxide, applied in trays and used overnight, can be effective in the treatment of tetracycline-stained teeth. Since then, other studies have confirmed the beneficial effects of combining in-office bleaching with home use of carbamide peroxide (Fiedler and Reichl 2000) and of hydrogen peroxide within bleaching strips (Kugel et al. 2002). A 90-month follow-up of Haywood’s 1997 study has been published and highlights the effectiveness of tray bleaching in reducing discoloration for an extended period of time (Leonard et al. 2003). The success of such treatment largely depends on the depth, severity, and degree of the discoloration; to make a well-informed prediction of likely treatment outcome, it is advisable to grade the degree of discoloration in terms of the following classification as devised by Jordan and Boksman (1984):
1. First degree: mild tetracycline staining. This is yellow to gray with no banding and is uniformly spread throughout the tooth. See Figure 12.1.
2. Second degree: moderate tetracycline staining. This is yellow-brown to dark-gray staining.
3. Third degree: severe tetracycline staining. This is blue-gray or black and is accompanied by significant banding across the tooth. See Figure 12.2.
4. Fourth degree: intractable staining is staining that is so severe that bleaching is ineffective.
5. A fifth degree of severe staining with enamel deficiency (such as white spots and ridges) has also been described (see Chapter 13).
Normally, bleaching can be successful in the first three types—namely, mild, moderate, and severe—and in each the best option is usually to bleach the teeth first and then review the need for further, more invasive, treatment. Types of bleaching treatment for tetracycline staining are as follows:
1. Home bleaching. This is the most predictable option to try.
2. Combination bleaching or deep bleaching (Chapter 15). This may work using both home and chairside treatments.
3. Power bleaching (Chapter 7). This approach will offer limited success for patients with tetracycline staining and may require multiple visits because the bleaching gel is usually unable to penetrate the dentin sufficiently deeply during the 1-hour power bleaching session.
4. Intentional devitalization (Chapter 8) and internal nonvital bleaching. This method has been recommended (Abou-Rass 1982) for severe tetracycline staining and consists of devitalizing the teeth and thereafter undertaking nonvital bleaching using hydrogen peroxide. Clearly, such a radical approach is controversial and it is now very rarely indicated given the success of home bleaching.
THE TREATMENT REGIMEN FOR BLEACHING TETRACYCLINE TEETH
Haywood et al. (1997) showed that it takes longer to bleach tetracycline-stained teeth in comparison with teeth yellowed with age and normal wear and tear and it is therefore necessary to set up a well-considered treatment program for these patients. Patients should be seen for an initial assessment during which photographs and radiographs are taken and a full detailed intraoral examination is performed. Tooth discolorations should be classified in terms of severity. All the various options ranging from bleaching and bonding (Haywood and Pohjola 2004) through to more extreme approaches such as porcelain veneers and full-coverage crowns should be discussed, and treatment should be planned to take place in a coordinated, sequential manner. Should bleaching be the preferred option, patients are advised that, according to research, treatment can take up to 3, 6, 9, or 12 months depending on the severity of the condition and its response to treatment. Given this, it is usually a wise precaution to underestimate the likely time taken to achieve a result and even the potential for improvement itself. Once the decision has been made to undertake bleaching, a review is normally set for around 2 to 3 weeks after the start of treatment to assess how much lightening has been achieved in that amount of time. Normally the upper teeth are bleached first using the home bleaching tray. This allows skeptical patients the opportunity to compare directly the treated upper teeth against the untreated lower ones. Patients are instructed about the treatment options for self-managing any possible sensitivity (Chapters 4 and 20). The lower bleaching tray is dispensed at this review appointment and the next review date set. The patient is given a 1-month supply of material, sufficient to treat both upper and lower teeth. Low concentrations of carbamide peroxide (10%) are used initially to prevent the patient from terminating treatment because of sensitivity. If the patient has experienced no sensitivity, the patient may then be given 15% carbamide peroxide gel to use. Matis et al. (2006) described the effects of bleaching using two of three different bleaching concentrations (10%, 15%, and 20% carbamide peroxide used overnight) for a 6-month period and found that bleaching could be accomplished with any of the three concentrations used. They also found that more than 55% of tooth lightening occurred within 1 month and that after 5 years, more than 65% of the maximum tooth bleaching remained for all three concentrations. Finally, the study revealed that cervical staining is the most difficult to correct.
Most of the home gels incorporate desensitizers such as potassium nitrate, fluoride, or amorphous calcium phosphate to reduce the incidence of sensitivity. At the 1-month review appointment the degree of improvement is assessed using the Vita porcelain shade guide and photographs taken. Depending on the result, the patient is then seen 1 month later and thereafter once a month until the bleaching treatment is completed. Often much of the initial lightness can be seen within the first 6 weeks, and thereafter the bleaching process may be a little slower. Further treatment may need to be undertaken; these decisions should be made together with the patient. In most instances patients are delighted with the result.
LAMINATE VENEERS
Indirect laminate veneers (usually ceramic, but occasionally composite) are one of the most commonly used ways of treating tetracycline-discolored teeth by restorative means. Directly applied composite is usually inadequate to mask tetracycline discoloration in all but the most minimally affected teeth.
Ceramic veneers have been around now for three decades and in that time have become a very useful and relatively conservative way of improving esthetics. Their use has grown considerably in recent years in line with developments such as dentin bonding and ultra-thin veneer systems. Not all of these developments have, however, been received entirely favorably, and concerns have been expressed about the widespread proliferation of ceramic veneers (Christensen 2006). When they were first introduced in the early 1980s it was recommended that veneers be restricted to those cases in which a predominantly enamel substrate was available, accompanied by minimal crowding, a favorable occlusion, and relatively little underlying tooth discoloration. Over time, though, these recommendations have increasingly been ignored, with the result that veneers are being used in ever more challenging circumstances. A growing number of “cosmetic” dentists display a worrying willingness to cut veneer preparations deeper than ever before into dentin to (1) mask extreme discolorations; (2) provide a bulk of ceramic capable of withstanding heavier occlusal loading; and (3) correct crowding, so-called “instant orthodontics.” The consequences of this are that first, the veneer suddenly ceases to be a particularly conservative treatment option, and second, retention of the restoration becomes almost entirely dependent on the strength and integrity of the bond between the luting cement and the dentin substrate. However, as Swift and Friedman (2006) observed, “Recent reports of 50% failure at 6 years and 34% fracture are disturbing when compared with 93% to 100% success rates of 15 years observation in the 1980s, i.e., at a time when veneers were universally bonded almost entirely to enamel.” This view is reinforced by recent data from the United Kingdom indicating a success rate for veneers placed within the General Dental Services in England and Wales of just over 50% at 10 years (Burke and Lucarotti 2009): “These results give a strong message to all clinicians who raise a rotating bur to a tooth, namely that, despite their intended minimal invasiveness, the tooth prepared for a veneer becomes compromised and may be replaced by a more invasive restoration which, in turn, increases the likelihood of pulpal involvement and/or tooth fracture.”
CLINICAL STUDIES
A number of clinical trials involving ceramic veneers are shown in Table 12.2 (Clyde and Gilmoure 1988, Reid et al. 1988, Calamia 1989, Jordan et al. 1989, Strassler and Nathanson 1989, Rucker et al. 1990, Christensen and Christensen 1991, Karlsson et al. 1992, Dunne and Millar 1993, Nordbo et al. 1994, Jager et al. 1995, Pippin et al. 1995, Strassler and Weiner 1995, Walls 1995, Shaini et al. 1997, Friedman 1998, Kihn and Barnes 1998, Meijering et al. 1998, Peumans et al. 1998, Dumfahrt 1999, Dumfahrt and Schaffer 2000, Magne et al. 2000, Aristidis and Dimitra 2002, Peumans et al. 2004, Smales and Etemadi 2004, Fradeani et al. 2005, Murphy et al. 2005, Layton and Walton 2007, Burke and Lucarotti 2009). It can be seen that failure rates range from 0% at 4 years (Kihn and Barnes 1998) to as high as 50% over 5 years (Shaini et al. 1997). Different studies have considerably different criteria for success and failure, but, in general, failure is seen as a breakdown resulting in total or partial loss of the veneer such that it requires replacement (Newsome and Owen 2008b). In addition to the studies shown in Table 12.2 a meta- analysis conducted in 1998 (Kreulen et al. 1998) combined the results of multiple clinical studies of porcelain veneer outcomes and was able to quote a probable survival of greater than 90% only after 3 years. A review of the literature in 2000 (Peumans et al. 2000) reported rates of 0–5% over 0–5 years.
What comes out of these various studies is that veneers, when used appropriately, offer acceptably high levels of durability and extremely high levels of patient satisfaction. However, as Burke and Lucarotti (2009) have warned, “Despite the more minimally invasive nature of the veneer preparation, as compared with a crown, the tooth that is veneered still enters onto a cycle of restorative dentistry which it cannot get off—a tooth which is restored with a porcelain veneer can never be whole again.”
CLINICAL CONSIDERATIONS
It is patently clear that great care must be taken in case selection, treatment planning, and clinical execution and that to get the very best out of the veneer technique a number of basic fundamental principles must be taken into consideration.
1. Bond to an enamel substrate wherever possible
The notion of etching enamel to accept resin luting cement is very well accepted and will be familiar to all dentists. It has taken more time, however, for the idea of dentin bonding to be accepted (Perdigao and Lopes 1999). In principle, for dentin bonding to be effective the dentin surface must be conditioned and then primed to form a hybrid layer onto which an adhesive is placed and which copolymerizes with the composite luting agent. The first bonding agents used a four-step process to etch enamel, etch dentin, and prime dentin, finally followed by the application of adhesive. This evolved into the so-called “total-etch” system in which the dentin and enamel are etched simultaneously but the prime and bond remained separate components. More recently “self-etch bonding” systems have been introduced that combine all the aforementioned steps. These have had a mixed reception (Tay 2005) despite the obvious convenience they represent and their possible role in reducing post-treatment sensitivity.
As far as ceramic veneers are concerned, the advent of dentinal adhesives has created the illusion that veneers bonded to dentin will be as successful as those bonded to enamel, thus encouraging dentists to use the technique in a wider range of clinical situations. Why is it that practitioners increasingly feel the need to extend veneer preparations into dentin and interproximally to the extent of breaking contacts with adjacent teeth? The main reasons would seem to be the ability of a thicker layer of porcelain to hide dark discolorations and to “correct” mild crowding of teeth, as well as greater ease of handling. Technicians also tend to find making thick ceramic veneers less challenging than very thin ones. As a result, tooth reduction into enamel alone can lead to bulky veneers, and so in many cases the dentist will cut further into the tooth to prevent overbuilding of the final restoration. Unfortunately, in spite of the considerable advances made in the field of dentin bonding, the longevity of a veneer continues to be a direct function of the amount of enamel substrate supporting it (Friedman 2001). There is an almost complete lack of clinical evidence to support the technique of bonding veneers to dentin as opposed to enamel, with Calamia and Calamia (2007) observing that “The key concept of preservation of enamel has gone by the wayside or is considered less important. This may be a huge mistake.”
Author |
No. of veneers |
No. of patients |
Observation period (years) |
Success rate (%) |
Clyde and Gilmoure 1988 |
200 |
Not specified |
1–2.5 |
99 |
Reid et al. 1988 |
217 |
50 |
4 |
79 |
Calamia 1989 |
115 |
17 |
2–3 |
97 |
Jordan et al. 1989 |
80 |
12 |
4 |
97 |
Rucker et al. 1990 |
44 |
16 |
2 |
100 |
Christensen and Christensen 1991 |
163 |
45 |
3 |
87 |
Karlsson et al. 1992 |
119 |
36 |
0.25–2.5 |
100 |
Dunne and Millar 1993 |
315 |
96 |
5.25 |
89 |
Nordbo et al. 1994 |
135 |
41 |
3 |
95 |
Jager et al. 1995 |
80 |
25 |
1–7 |
99 |
Strassler and Nathanson 1989 |
291 |
60 |
1.5–3.5 |
98 |
Pippin et al. 1995 |
120 |
60 |
5 |
100 |
Strassler and Weiner 1995 |
115 |
21 |
7–10 |
93 |
Walls 1995 |
54 |
12 |
5 |
72 |
Shaini et al. 1997 |
372 |
104 |
6.5 |
50 |
Meijering et al. 1998 |
56 |
Not specified |
2.5 |
Not specified |
Peumans et al. 1998 |
87 |
25 |
5–6 |
93 |
Kihn and Barnes 1998 |
59 |
12 |
4 |
100 |
Friedman 1998 |
3,500 |
— |
— |
— |
Dumfahrt 1999 |
— |
— |
— |
— |
Dumfahrt and Schaffer 2000 |
205 |
72 |
10.5 |
1 |
Magne et al. 2000 |
48 |
16 |
4.5 |
100 |
Aristidis and Dimitra 2002 |
186 |
61 |
5 |
98 |
Smales and Etemadi 2004 |
110 |
50 |
7 |
96 and 86* |
Peumans M et al. 2004 |
87 |
25 |
10 |
64 |
Fradeani et al. 2005 |
182 |
46 |
12 |
95 |
Murphy et al. 2005 |
62 |
29 |
5 |
89 |
Layton and Walton 2007 |
304 |
100 |
15 |
81 |
Burke and Lucarotti 2009 |
2562 |
1177 |
11 |
53 |
a This study specifically looked at preparation design; the 96% success rate refers to veneers with incisal coverage, whereas the 86% success rate refers to veneers without incisal coverage.