Oral hygiene Posts

Dental Bleaching
Natascia Raciti Fabio Cozzolino

Dental hypersensitivity
Natascia Raciti

Dental Bleaching

Dental Bleaching


The natural tooth color is determined by an inherent component associated with the enamel and dentin light absorption and diffusion optical properties and is influenced by the presence of surface or internal colour differences. Tooth bleaching is a highly conservative aesthetic treatment, with a favourable cost-advantage ratio, allowing the removal of all the organic components responsible of the pigmentations staining the teeth. It needs a preliminary clinical intraoral examination and a correct diagnosis and supervision by the dentist. Fundamental elements for the successful outcome of the treatment, patient related (personal needs, age, expectations, means) and operator related (product availability, knowledge of materials science), concur to the planning of a well suited therapeutic plan. Visible tooth pigmentations are not only an aesthetic problem but can also become a physical handicap and go further on and generate a self-image distortion with subsequent lack of confidence. Because of these reasons tooth bleaching has widely spread, becoming one of the most popular and successful aesthetic treatments. The growing public interest for smile beauty has been supported by a development and distribution of specialized and differentiated commercial products along with new application methodologies and dental bleaching procedure in the dentists’ clinical practice.



Intrinsic factors: they include irreversible dischromia depending on chromogenic molecule absorption by enamel and dentin, in the course of dental development or after tooth eruption. They depend on pulp chamber lesions (intrapulpal bleeding, necrosis, calcification with tertiary dentin deposit), endodontic therapy, congenital diseases (phenylketonuria, cystic fibrosis, congenital hyperbilirubinemia, amelogenesis and dentinogenesis imperfecta), medical drug use (tetracycline, fluorine).

Extrinsic factors: they include yellow-brown surface pigmentations affecting exclusively the enamel. They are connected to eating, drinking, smoking, poor dental hygiene, ageing (enamel thinning and dentin increase).

Active ingredient: Hydrogen peroxide, carbamide peroxide (organic molecule that releases hydrogen peroxide and urea; 10% is equivalent to 3.5% hydrogen peroxide), sodium perborate (monohydrate, trihydrate and tetrahydrate mixed with hydrogen peroxide) and calcium oxide.

Mechanism of action: oxidation of the double bonds of the chromophores conjugated chains (chemically stable long chain organic molecules) absorbed by the dental hard tissues (enamel and dentin) with subsequent brightness increase and chrome reduction. More specifically, hydrogen peroxide releases HO2(peroxide anion) and free radicals, responsible for the chromogenic molecules destruction; carbamide peroxide in aqueous solution releases hydrogen peroxide and urea, able to denaturise dental tissues’ organic matrix proteins.

Adverse reactions

1. Temporary low/moderate increase in dental sensitivity found during and after the treatment in 2/3 of the patients who underwent vital teeth bleaching, due to a reversible pulpitis caused by the whitening agent and amplified by dental dehydration. It can be treated using topical fluoride prophylaxis (dentinal tubules occlusion and dentinal fluid reduction) or applying potassium nitrate that has an analgesic effect on the transmission of the nervous impulses.

2. Enamel microhardness reduction: the enamel exposed to the whitening agents presents a clinically non relevant reduction of its microhardness which spontaneously recovers after contact with saliva (saliva electrolytes). Studies on 10% carbamide peroxide have demonstrated that applying whitening agents on the enamel surface causes local microstructural modifications similar to those present in the initial stages of caries and that the amount of calcium ions lost by the enamel is around 1mcg/ mm2 – a neglectable amount from the clinical point of view.

3. Soft tissues irritation: concentration greater than or equal to 10% hydrogen peroxide can cause cellular damage, gingival ulceration and mucosa and skin burning. It is clinically possible to observe an initial reddish area leaving the place to a light coloured lesion that tends to heal rapidly without leaving any permanent harm. Soft tissues protection is thus mandatory.

4. Taste alteration. The patient may report the presence of a metallic taste after the whitening for several hours.

5. Intrapulpal temperature increase. A significant variation of the temperature, associated with a photothermal effect and possible pulp damage, is observed in the course of the bleaching treatment using hydrogen peroxide when activation sources (halogen lights, LED, laser) are used to speed up the process. Light sources increase hydrogen peroxide decomposition and thus the release of free radicals able to oxidise the dark pigments. Heat-producing activation sources may determine expansion of dentinal tubules fluid, causing pulp hyperemia and post-whitening hypersensitivity. Heat induces a more pronounced teeth dehydration and, subsequently, an increased post-whitening hypersensitivity. The free radicals chemical action, moreover, can make the pulp tissues damage worse.

6. Alteration of the composite fillings superficial texture and of the enamel-composite interface: a study on dental elements affected by Black class V carious lesions restored with composite and subsequently treated with 35% hydrogen peroxide (seven 30 min. treatments) proved that whitening determines alterations in the teeth surface topography with prevalence of depression areas that facilitate plaque build-up and increase the risk of caries and periodontal disease. The enamel-composite interface, analysed with the help of profilometric analysis and SEM, on the contrary, shows no alteration after the whitening treatment.

7. Cervical resorption associated with non-vital tooth bleaching in the case a correct isolation is not set up.


Fluoride-based whitening products

The whitening power of fluoride fortified products does not seem to be compromised in respect to traditional products, nor post-whitening fluoride prophylaxis is able to negate the treatment itself. Remineralisation of the enamel treated with whitening agents happens more rapidly and the loss of hard substance is inferior; therefore the teeth exposed to fluoride-based whitening show more resistance to acid dissolution (caries) than non-whitened teeth. The topic preliminary application of fluoride-based varnishes can, by itself, reduce dentin dehydration during the whitening process and the subsequent hypersensitivity.



The safety parameters of bleaching agents are defined according to the effects observed on the dental hard tissues, the pulpodentinal organ, oral soft tissues and in the case of swallowing the product in the course of a vital tooth extracoronal whitening. As far as soft tissues, the attention is mostly directed to the possible toxic effects of the free radicals released by the peroxides and able to react with proteins, lipids and nucleic acids, causing cellular damage. Hydrogen peroxide is thus a molecule that, at 10% concentration or more, may result cytotoxic ad be potentially harmful for the mucosa and the skin, causing a burning sensation. The risks connected with these lesions are mostly observable in the case of chairside professional treatment, usually performed with products releasing hydrogen peroxide at a concentration of 25% or more, when an adequate protection of the gingival tissues is not set up. On the other hand, no risk for oral and systemic health comes from professional home bleaching performed using ADA approved products made up of 10% carbamide peroxide (equivalent to 3.5% hydrogen peroxide). In the case of hard tissues, the risks include a temporary increase in dentinal sensitivity observable in the first phases of the bleaching, whose entity varies depending on peroxide concentration and duration of contact. It is worth remembering, that peroxide easily crosses both enamel and dentin after the first 5-15 minutes of application. Nonetheless, there is no evidence of long-term damage to the pulpodentinal organ (enzymatic inactivation) when the technique is performed correctly. The occurrences and the severity of the sensitivity seem to depend on product quality, chosen technique and on the individual response to the bleaching.


Bleaching results

The length of the treatment and the expectations on the outcome depend on the aetiology of the stains (genetic defects or development problems, age-related changes, extrinsic pigmentations, intrinsic aspects) and on the diagnosis, as well as on the chosen product and how it is applied. In general, dark pigmentations respond well to whitening, while white spots are not affected, although they result less evident since there is less contrast with the adjacent teeth. Using the trays technique (individual trays), the teeth normally whiten up within 3 days to 6 weeks. Nicotine stains can take 1-3 months to disappear while tetracycline stains 2-6 months or even more of night use. The kind of stain and the initial tooth colour are to be taken in consideration; pigmentations localized on the neck of a tooth, dark grey or blue and important tetracycline-induced discromies are hard to treat.

-Preliminary investigations: an intraoral clinical examination along with all the necessary X-rays is the tool that lets us make a correct diagnosis and use whitening products in perfect safety: therefore, it must always come before the bleaching treatment. Collecting useful information (past or present dentinal hypersensitivity, presence of reconstructions, temporomandibular disorders, latex, silicone and whitening substances allergy) can help us choose the best methodology for each patient.

-Product choice: the ideal whitening agent should be designed with a neutral pH. Carbamide peroxide has proven more effective at night-time since urea induces the pH increase to the desired levels. Hydrogen peroxide has a low pH and is short-acting. For these reasons whitening formulations containing hydrogen peroxide require shorter contact but more applications while those containing carbamide peroxide take few days but require longer contact. Product choice, then, has to be compared to the patient’s habits and lifestyle, not to mention the possible dentinal hypersensitivity, the type of stains and the presence of carious lesions.

-Subsequent treatment: the need of a second treatment can greatly vary, ranging from 1-3 years to more than 10 years after the initial bleaching.


Vital teeth bleaching

External bleaching (extracoronal) is performed applying the active ingredient to the surface of the tooth to be treated, so that it can diffuse into the hard tissues without causing any enzymatic damage to the pulpodental organ. After a careful isolation of the soft tissues, the whitening agent can be fitted to the surface to be treated.

In the following pictures you can see a case of a maxillary-arch-only home whitening using 15% carbamide peroxide for 3 nights in order to highlight the chromatic improvement; afterwards the patients, happy with the achieved results, decided to have the same treatment performed on the mandibular arch.

Dental hypersensitivity

Dental hypersensitivity


Dentine hypersensitivity represents a dental pathology of relevant clinical interest. It is characterized by pain, usually localized in one or more dental elements presenting a gap of the dentinal tissue, evoked by different stimuli (temperature, tactile, chemical and osmotic) which act in lack of other dental pathologies. Chronic traumas such as friction, abrasion, erosion acting on vital dental elements may remove the enamel or the cement that normally protect dentin causing gaps and consequently the direct contact between external intra-oral milieu and the pulp dental tissue (because of an anatomic variability, in some patients there cannot be a contact at a cervical level between the dental enamel and the cement). Pain can affect every dental element and any patient at any age although female patients age 20- 40 are typically affected (1, 2). Dentine hypersensitivity most frequently affects patients with periodontal diseases (3, 4), and can transitorily appear in patients under deep scaling, root planning, or periodontal surgery therapy (5) and patients undergoing teeth whitening or receiving conservative therapies (6). The role of the bacterial plaque in this disease is however controversial. The plaque accumulates on the radicular surfaces and its demineralizing effect on the dental structure can be associated to the opening of the orifices of the dentinal tubuli(7). According to some investigators patients maintaining a good plaque control have a low risk to develop a dentinal hyper sensitivity (8). On the contrary, many patients presenting gingival recessions together with plaque accumulation, have dental hyper sensitivity symptoms(9,10).

Definition: Brief but intense pain sensation caused by physical or chemical stimuli not induced by other dental pathologies (11).

Etiology: The association between dentinal tubuli and pain is based on the well known Brannstrom’s hydrodynamic theory. The application of a stimulus can cause a perturbation of the dentinal fluid contained in the tubuli (contraction, expansion, movement) which mechanically activates baroreceptors of the nerve endings of the dentinal pulp organ (A-D fibres) causing pain. The generation of the potential of action in the intra-dental nerve is responsible for the sense of pain (12, 13). In particular, temperature drop, loss of hydration caused by water jet, evaporation and application of an osmotic stimulus (sugar, acid, salt etc.) may cause the centrifugal movement of the tubular fluid. Therefore, it can activate the nerve endings more efficiently compared to other stimuli (tactile and temperature rise) inducing fluid movement towards the pulpe (14,15). A 75% of patients with dentine hyper sensitivity feel, in fact, pain when in contact with a thermic stimulus (cool) (16)

Initial lesion: the opening of the external end of dentinal tubuli appears when the smear layer or the intra-tubular substance are removed (17) mechanically (abrasion) or chemically (erosion). Acid erosion seems to be the main causal factor(18).

Lesions site: the cervical edge is affected in more than 90% of cases both on the vestibular and the lingual-palatal side (16). The loss of enamel and moreover, a gingival recession are fundamental elements in the etiology of the dental gap (18)).

Prevalence: The significant differences among the populations studied and the investigation methods used by different authors cause a large range of prevalence values (4-57%) (19, 20). The dental hyper sensitivity prevalence ranges from 60 to 98% in patients with a periodontal disease (3). The incidence top is at the end of the third life decade and decreases during the fourth and the fifth decade (1,2), The age dependent reduction of dentinal permeability and nerve sensibility, the secondary dentinal production, the extended use of toothpastes and mouthwashes containing fluorine can in fact occlude the exposed dental tubuli and reduce sensibility (21).

Distribution : superior premolar, first superior molar and superior and inferior incisives are the dental elements frequently involved in the dental hyper sensitivity phenomena (22,23). There seems to be a light predilection for the female sex (22,1,24).

Differential diagnosis:

· caries lesions affecting dentinal tissue

· pulp hyperemia

· cuspids’ fracture

· infiltrated restores

· palatal-gingival ploughs

· dental breaks or chips (25,26)

· elements prosthetically prepared without definitive cements

Clinical diagnosis: the diagnosis may be defined following personal anamnesis collection, clinical and X-ray examination and after exclusion of other pathological conditions (see differential diagnosis). The typical temporary pain which appears after a stimulation of the dental element affected, can be provoked by the operator by using a dental drill or an air stream to register the patient’s personal answer to the disturb severity and to follow it up (11,27).

Symptoms: dentinal hyper sensitivity can be present as an uncomfortable and unpleasant sensation. The pain described by the patient can be defined as soft or intense, vague or specific, intermittent or constant (28).

Risk factors:

· wrong brushing techniques

· wrong inter-dental floss use

· use of highly abrasive toothpastes

· presence of acid materials of external or internal origin in the oral cavity

· chronic traumas due to wrong habits (grinding teeth in stress situations)

· small dental breaks

· dental substance loss in the dental collar presumably associated to near occlusive trauma

· periodontal surgery operations

· dentinal gaps in the dental collar associated to the adherent gingival loss

· defect in the development of enamel and dentin

· broken fillings

· prosthetic preparations (generating gaps of 70000 tubuli per mm2).

Professional therapy: it is a more complex treatment indicated when hyper sensitivity affects one or more dental elements. The following are some substances contained in commercially available products to control dentinal hyper sensitivity:

· fluoride: sodium fluoride made toothpaste or concentrated solution and stannous fluoride in water solution or gel made by glycerin and carboxi-methyl-cellulose reduce the dentinal permeability in vitro (29) perhaps through precipitation of insoluble calcium fluoride on the dentinal surface promoting obliteration of exposed tubuli (7).