Pigmented lesions of the head and neck

Introduction

There is a wide spectrum of pigmented lesions which present an oral mucosa or skin in the head and neck area.  In the oral cavity some of the pigmented lesions are physiologic, but most are considered pathologic.  The clinical features of benign and malignant lesions of oral mucosa are, in most instances, virtually indistinguishable.  This makes it impossible for the clinician to arrive at a definitive diagnosis without biopsy and histopathologic examination of such lesions.

            Some of the pigmented lesions of oral mucosa and facial skin include:

            1.  Normal physiologic pigmentation

            2.  Ephelis

            3.  Lentigo

            4.  Melanotic macule

            5.  Melanoacanthoma

            6.  Nevi

            7.  Melanoma

            8.  Pigmentation secondary to pregnancy

            9.  Pigmentation secondary to some other pathologic condition

Melanocytic Lesions

 1.  Normal physiologic intra-oral pigmentation

            - observed in all racial groups, but to varying degrees

            - characterized by symmetry

            - virtually always asymptomatic

            - most common sites involved are gingiva and buccal mucosa

            - melanin pigment incontinence (spillage from epithelium into underlying

               connective tissue)

 2.  Ephelis

            - Freckle

-          Usually limited to sun exposed facial skin, but may involve lip mucosa.

-          Normal number of melanocytes in relation to keratinocytes.

-          Melanocytes have increased number of melanosomes in their cytoplasm hence more melanin is produced.

-          Physiologic response to protect epithelium from uv radiation in sunlight

-          Normal thickness of epithelium, no increase in keratinocyte population

 3.  Lentigo

            - 3 variants: simple, solar, and maligna

            - Simple lentigo features

                        a) no predilection for sun exposed skin

                        b) flat surface and uniform brown color

                        c) relative increased number of melanocytes as epithelial layer is

                            thicker (elongated rete ridges)

            - solar lentigo features

                        a) sun exposed skin

                        b) middle age or elderly population

                        c) multiple lesions of uniform brown color

            - lentigo maligna features

                        a) histopathologically atypical melanocytes limited to epithelium

                        b) melanoma in situ or precancerous melanosis

                        c) lacks invasion warranting diagnosis of lentigo maligna melanoma

 4.  Melanotic macule

            - flat (macular) surface

            - well circumscribed border

            - focal concentration of normal melanocytes in basal layer of epithelium

 5.  Melanoacanthoma

            - facial skin and oral mucosal lesions significantly different

            - facial skin lesion

                        a) elderly

                        b) caucasians

                        c) slow growth

            - oral mucosa lesion

           

                        a) young adults

                        b) blacks

                        c) rapid growth to large size (4 cm in 4 weeks)

                        d) oral lesion can frequently be associated with irritation or trauma

                        e) increased number of both normal appearing melanocytes and

                            keratinocytes, with melanocytes migrating through all layers of

                            epithelium which is also a feature of melanomas

                        f) potential for misdiagnosis and radical overtreatment

                        g) resolves following biopsy or removal of irritation

 6.  Nevi

            - congenital and acquired variants

            - may be flat, slightly elevated papillary, pedunculated (on stalk) or nodular

              (dome shaped)

            - usually well circumscribed

            - pigmented or amelanotic (non-pigmented)

            - congenital nevus

                        a) incidence 1% live births

                        b) usually larger than acquired nevi (>1.5 cm diameter)

                        c) considered giant nevus if >20 cm

                        d) often has shape of garment

                        e) can exhibit hair growth as well as pigmentation

                        f) malignant transformation 1%, if giant nevus 6-12%

                        g) excise if possible

            - intradermal nevus

                        a) most common oral variant (55%)

                        b) can have any surface morphology

                        c) nests and sheets of nevus cells within supporting connective tissue

                            (dermis) without epithelial melanocyte proliferation

                        d) neural nevus is a type of intradermal nevus in which nevus cells

                            assume a spindle shape and this lesion can be misdiagnosed by

                            pathologists as a neurofibroma

            - junctional nevus

                        a) usually presents as a flat (macular) lesion which relates to lack of

                            connective tissue involvement

                        b) nodule formation observed in intradermal or compound nevi or when

                            flat surface melanoma in situ invades connective tissue

                        c) melanocytes in basal layer of epithelium aggregate into clusters or

                            nests called theques

            - compound nevus

           

                        a) combination of intradermal and junctional nevus features, that is

                            nevus cells observed as islands in dermis and forming intra-epithelial

                            theques

                        b) some believe junctional activity decreases as lesion matures

            - blue nevus

                        a) second most common oral variant (35%)

                        b) characteristic blue-black color

                        c) common form <1 cm in diameter, cellular form >1 cm

                        d) melanocytes usually appear as pigmented spindle cells in deeper

                            connective tissue having failed to migrate to epithelium from neural

                            crest during embryogenesis

                        e) extremely rare malignant blue nevus reported

            - mongolian spot

                        a) bluish discoloration clinically resembling bruise at base of spinal cord

                        b) more common in black and asian population

                        c) presents at or near birth, resolves by early childhood in blacks, may

                            persist into adulthood in asians

                        d) results from delayed disappearance of dermal melanocytes

            - nevus of Ota

                        a) speckled blue-black pigmentation following distribution of trigeminal

                            nerve branches 1 and 2

                        b) may have synchronous skin and intra-oral lesions

            - nevus of Ito

           

                        a) associated with nevus of Ota

                        b) follows distribution of supraclavicular, scapular and deltoid nerves

            - epithelioid and spindle cell (Spitz) nevus

                        a) first reported in 1948 by Spitz as benign juvenile melanoma

                        b) pink skin nodule

                        c) clinically resembles pyogenic granuloma

                        d) most common in children but 25% are reported in patients over age 30

                        e) epithelioid and spindle shaped cells, clefting at the junction of

                            epithelium and supporting connective tissue and fibrosis

            - halo nevus

                        a) clinically pigment nevus of any variant surrounded by a zone of

                            depigmented epithelium

                        b) correlates with a prominent lymphocyte response surround nevus on

                            histopathologic examination

            - dysplastic nevus

                        a) first reported as lesion of BK mole syndrome describing familial

                            tendency of patients with multiple pigmented lesions to develop

                            melanoma

                        b) subsequently patients with single isolated lesions with this histo-

                            pathologic presentation failed to develop melanoma

                        c) large size (>5 cm diameter), ill defined border

                        d) irregular pigmentation, multinodular

                        e) clinically similar to superficial spreading melanoma

                        f) compound nevus with elongation of epithelial rete ridges

                        g) some consider a borderline or premalignant lesion

 7.  Melanoma

            - background information

                        a) incidence (US): 14/100,000 males and 10/10,000 females

                        b) 1995 ACS statistics: 34,100 new cases

                        c) 1995 ACS statistics:   7,200 deaths

                        d) predominantly caucasians (13:1)

                        e) incidence predicted to increase due to sun exposure and loss of

                            protective effect afforded by ozone layer

                            UVB (290-320 mm) being most carcinogenic

                        f) increased risk with fair complexion, tendency to sunburn rather

                            than tan, history of blistering sunburn in childhood

                        g) family history of melanoma increases risk eightfold

                        h) as incidence increases, so does improved prognosis

                        i) in oral cavity, metastatic melanoma significantly most likely than

                            primary disease

            - signs and symptoms

                        a) change in color or size of a pigmented lesion

                        b) satellite areas of pigmentation

                        c) bleeding or ulceration of lesion

                        d) inflammation surrounding lesion

                        e) pain and/or itching of lesion

            - classification of primary skin melanoma

                        a) lentigo maligna melanoma

                                    * acral lentiginous melanoma

                        b) superficial spreading melanoma

                        c) nodular melanoma

            - growth phases

                        a) horizontal (peripheral expansion) and vertical (downward invasion)

                        b) extent and duration of horizontal growth phase differs for each

                             variant of melanoma

                        c) prognosis after invasion similar for all variants

            - lentigo maligna melanoma

                        a) terminology

                                    * lentigo maligna: melanoma in situ

                                    * lentigo maligna melanoma: invasive melanoma

                        b) large size (4-6 cm average diameter)

                        c) flat surface

                        d) long horizontal growth phase averaging 10-15 years

                        e) earliest expected vertical growth phase is 2-4 after onset

            - acral lentiginous melanoma

                        a) observed on oral or genital mucosa and the extremities

                        b) essentially an aggressive form of lentigo maligna melanoma

                        c) prominent dendritic processes similar to melanoacanthoma

                        d) vertical growth phase lacks clinical warning sign of nodularity

                             from a previously flat lesion

                        e) exhibits multifocal invasion and widespread dissemination

            - superficial spreading melanoma

                        a) most common skin variant (70%)

                        b) predominant sites

                                    *males: head, neck and trunk

                                    *females: back of legs

                        c) typically smaller size than lentigo maligna melanoma with average

                            diameter of 2 cm

                        d) slightly elevated

                        e) shorter duration for horizontal growth phase before invasion

                            downwards, averaging 1 year from onset

            - nodular melanoma

                        a) rapid increase in size

                        b) very short horizontal growth phase before invasion, measured in

                            weeks

                        c) worst prognosis

            - primary oral melanoma

           

                        a) uncommon, 1% of all primary melanoma, oral cavity melanoma much

                            more likely to represent metastasis

                        b) most common sites: maxillary alveolar ridge and palate (80%)

                        c) male predominance (2:1)

                        d) middle age (average 55 years)

                        e) prognosis grave, 5 year survival < 10%

            - classification of oral melanoma

           

                        a) acral lentiginous (most common)

                        b) superficial spreading

                        c) nodular

            - biopsy considerations

                        a) melanocytic lesions are clinically indistinguishable making all, at

                            least potentially malignant melanoma; therefore, all require biopsy

                            and histopathologic examination to establish a definitive diagnosis

                        b) total excision as a first procedure is preferred

                        c) suggest referral to surgeon who will perform definitive surgery

                            rather than perform incisional biopsy with referral following

                            histopathologic interpretation

                        d) cervical lymph nodes following incisional biopsy may be clinically

                            enlarged and suggest metastasis, mandating surgical exploration of

                            the neck

                        e) if lesion is too large to excise for biopsy, sample from darkest or

                            most nodular area

            - treatment considerations

                        a) surgical

                                    * wide to radical tumor excision

                                    * therapeutic regional lymph node dissection for obvious

                                       metastasis, elective dissection in search of occult metastasis

                                    * tumor invasion < 0.75 mm predictably non metastatic

                                    * tumor invasion > 1.50 mm worrisome for occult metastasis

                                    * tumor invasion > 3.59 mm generally too late to prevent

                                       metastasis

                                    * 40% primary oral melanoma have metastasized when patient

                                       initially presents

                                    * distant metastasis associated more with uncontrolled disease

                                       at primary site (i.e.: inadequate initial surgery) than regional

                                       nodal metastasis

                                    * average interval to relapse following surgery 8.5 months

                        b) radiation therapy

                                    * high dose fractions 2400cGy over 21days had 53% partial and

                                       30% complete remission in one study

                                    * fast neutrons vis a vis orthovoltage

                                    * hyperthermia enhancement

                                    * radiosensitizers: boron (absorbs fast neutrons) combined with

                                      chlorpromazine (affinity for melanoma cells)

                        c) adjunctive chemotherapy

                                    * DTIC

                                    * cisplatin

                                    * nitrosurea

                                    * tamoxifen

                        d) immunotherapy

                                    * bacillus calmette-guerin (BCG) stimulation of immune system

                                       effective in early disease but has little positive effect (7%) once

                                       melanoma has metastasized

                        e) biologic response modifiers

                                    * high dose interleuken II stimulates tumor infiltrating

                                       lymphocytes (TIL) to attack melanoma cells

                                    * monoclonal tumor antibody vaccine

            - prognostic factors

                        a) histopathologic factors and clinical stage (extent) both considered

                            important in determining patient outcome

                        b) tumor thickness (volume) and depth of invasion are most important

                            histopathologic factors in determining patient outcome

                        c) Clark method measures tumor invasion utilizing anatomic layers

                        d) Breslow method measures tumor invasion in mm utilizing calibrated

                            microscope

                        e) mitotic index of >2 per 10 microscopic high power fields reduces 5

                            year survival 20%, all other factors being equal

                        f) ulceration due to ischemia (tumor growth outrunning its blood supply)

                            associated with reduced survival

                        g) increased patient age reduces prognosis

                        h) females have slightly better survival rate (7%) than men, all other

                            factors being equal

            - survival estimates based on depth of invasion

                        a) Clark method of determining depth of invasion

                                    Clark 1                        melanoma in situ (no invasion)

                                    Clark 2                        tumor in papillary dermis

                                    Clark 3                        tumor to junction of papillary and reticular dermis

                                    Clark 4                        tumor in reticular dermis

                                    Clark 5                        tumor in subcutaneous tissues

                                    Level               5 Year             10 Year

                                        1                  100%                  96%

                                        2                     92%                 96%

                                        3                     65%                 90%

                                        4                     54%                 67%

                                        5                     48%                 26%

                        b)  Breslow method of determining depth of invasion

                                    Breslow 1        0.00 - 0.75 mm invasion

                                    Breslow 2        0.76 - 1.69 mm invasion

                                    Breslow 3        1.70 - 3.50 mm invasion

                                    Breslow 4        3.60 mm or greater invasion

                                    Level               5 Year             10 Year

                                       1                     99%                  98%

                                       2                     94%                  89%

                                       3                     81%                  67%

                                       4                     49%                  43%

            - survival estimates based on staging

                        a) TNM method

                                    stage 1             lesions without metastasis

                                    stage 2             lesions with metastasis to only 1 regional

                                                            lymph node

                                    stage 3             disseminated metastasis

                                    TNM               5 Year             10 Year

                                    stage 1               89%                    81%

                                    no recurrence                                88%

                                    local recurrence                             42%

                                    stage 2                61%                   47%

                                     1 node                45%

                                     2 nodes              28%

                                     3 nodes                9%

                                    stage 3                  2%                    0%

            - metastatic melanoma to the oral cavity based on 800 cases NIH study

                        a) 3% of skin melanoma metastasize to oral cavity

                        b) primary is usually in the head or neck area

                        c) male predilection (3:2)

                        d) average age 40 years

                        e) average interval between primary and metastatic lesion is 4.2 years

                        f) most common metastatic sites: tongue, cheek, parotid gland, alveolus

                        g) metastatic melanoma to parotid gland lymph nodes commonly from

                             primary in scalp

                        h) metastatic melanoma may be non-pigmented

                        i) symptoms may include tooth mobility, non-healing extraction sites

                            and tumor expressing from extraction socket

 8.  Pigmentation secondary to pregnancy

            - probable association with increased ACTH during pregnancy

            - ACTH mimics chemical structure of HSH (melanin stimulating hormone)

            - chloasma: (pregnancy mask) irregular, flat areas of pigmentation on facial

               skin of women during 2^nd and 3^rd trimesters

            - melasma: circumoral pigmentation at vermilion border may also been

              observed in women taking birth control pills

 9.  Pigmentation secondary to Acanthosis Nigricans

            - thickened skin and oral mucosa

            - seen in childhood as a benign process

            - cutaneous marker for internal malignancy in adults, chiefly gastrointestinal

              carcinoma

            - oral lesion may exhibit papillary surface and/or pigmentation

10.  Pigmentation secondary to Peutz-Jegher syndrome

            - syndrome characterized by circumoral pigmentation and multiple intestinal

              polyps

            - polyps can involute (intusseption) and obstruct causing surgical emergency

            - malignant transformation very low in comparison to polyposis of Gardner’s

              syndrome

11.  Pigmentation secondary to neurofibromatosis

            - multiple neurofibroma of skin and oral mucosa

            - multiple areas of skin pigmentation known as café au lait spots (coffee with

              cream color)

            - low potential (2%) for malignant transformation of benign neurofibroma

               into neurogenic sarcoma

            - Von Recklinghausen’s disease of skin

12.  Pigmentation secondary to chronic adrenocortical insufficiency

            - primary form of condition due to autoimmune destruction of adrenal cortex

            - pituitary gland continues to secrete ACTH as biofeedback mechanism to

              terminate process cannot be performed by affected adrenal cortex

            - ACTH stereochemically similar to MSH (melanin stimulating hormone)

            - excess ACTH causes bronzing of skin and oral pigmentation

            - Addison’s disease

13.  Pigmentation secondary to malignant tumors

            - oat cell carcinoma of the lung produce ectopic ACTH which may elicit oral

              pigmentation

            - generalized melanosis of skin observed in patients with disseminated

              metastatic melanoma

14.  Pigmentation secondary to vitamin deficiency

            - pellegra (niacin deficiency) can produce a skin rash and hyperpigmentation

              of exposed facial skin

            - oral lesion is an enlarged beefy red tongue

15.  Pigmentation secondary to therapeutic drugs

            - oral contraceptives

            - chloroquinine used as anti-malarial and control of lupus erythematosus

            - tetracycline administered over long duration can alter oral microflora and

              enhance conditions for development of brown or black hairy tongue

            - thorazine used in the treatment of psychosis

            - minocine antibiotic causes blue gray discoloration of bone

            - quinibrine used as anti-helminthic causes yellow discoloration of skin and

              oral mucous clinically similar to jaundice

            - over the counter preparations such as laxatives taken in excess can cause

              pigment deposition in mucosa

16.  Pigmentation secondary to Albright’s syndrome

            - polystotic (multiple site) fibrous dysplasia

            - café au lait colored skin and oral mucosal pigmentation

            - in females, precocious puberty

17.  Neonatal pigmentation secondary to tumor

            - neuroectodermal tumor of infancy

                        a) most common site is anterior maxilla

                        b) melanin pigmentation deposition in mucosa

                        c) radiographic presentation is well circumscribed radiolucency

                            surrounding developing tooth

                        d) vanillymandelic acid (VMA) from metabolism of excess

                            catecholamines (epinephrine and norepinephrine) found in urine

18.  Pigmentation secondary to systemic intoxication (poisoning) by heavy metals

            - lead poisoning

                        a) lead sulfate deposition in gingival sulcus (Burton’s line)

                        b) excessive salivation (ptyalism)

                        c) peripheral neuropathy and learning defects associated

                        d) treat with chelating agents

            - mercury

            - bismuth

            - arsenic

            - gold

19.  Pigmentation secondary to foreign body implantation

            - amalgam tattoo

                        a) most common sites are gingiva and buccal mucosa

                        b) radiographic discovery may allow clinical correlation precluding

                            necessity for biopsy and histopathologic examination

                        c) focal argyrosis

            - graphite

                        a) most common sites are palate, floor of mouth and lip

                        b) history of accidental puncture by pencil may be recounted

20.  Pathologic conditions which mimic melanocytic lesions

            - hematoma

                        a) secondary to trauma

                        b) recurrent lesions suggest abuse

            - hemangioma

                        a) most common mesenchymal tumor in childhood

                        b) dioscopy test positive

                        c) treat by a variety of modalities

           

            - varix

                        a) vascular anomaly often with thrombus

                        b) essentially a varicose vein

           

            - Kaposi sarcoma

                        a) usually red to purple in color but may exhibit a brown hue

                        b) malignant blood vessel tumor

                        c) incidence of oral lesion in AIDS 50%

                        d) predisposing factors ???

                        e) treat with intralesion vinca alkyloids or interferon

            - thrombocytopenia

                        a) blood platelets < 100,000/ cc

                        b) marrow suppression due to infection, leukemic infiltrate, aplastic

                             anemia

            - seborrheic keratosis

                        a) middle aged to elderly

                        b) head, neck, trunk

                        c) sharply demarcated plaques with rough surface

                        d) in African Americans, dermatosis papulosa nigra 35% incidence

21.  Depigmented Lesions

            - vitiligo

                        a) autoimmune destruction of melanocytes

                        b) autoantibody to melanocytes formed inkeratinocytes

                        c) scalp lesions common

            - albinism

                        a) melanocytes are inactive but not destroyed

22.  Yellow and Orange Lesions

            - Fordyce granules

                        a) multiple small elevated asymptomatic papules

                        b) ectopic sebaceous glands

                        c) buccal mucosa most common location

                        d) increase at puberty

            - parulis

                        a) dento-alveolar abscess with purulent drainage

                        b) may be painful until drainage occurs

                        c) strep, staph, actinomyces

            - lymphoepithelial inclusion cyst

                        a) lymph appears yellow clinically

                        b) embryologically entrapped epithelium in lymphoid aggregates

                        c) superficial floor of mouth location common

                        d) conservative excision

            - lipoma

                        a) common to skin, uncommon to mucosa

                        b) tongue, buccal mucosa, labial mucosa most common sites

            - lymphonodular pharyngitis

                        a) multiple aggregates in Waldheyer’s ring area

                        b) coxsackle A10 virus

                        c) 5 day incubation followed by sore throat, fever, headache

                        d) 2 week course

                        e) supportive therapy

            - jaundice

                        a) secondary to organ dysfunction or drug therapy

                                    * viral hepatitis

                                    * sickle cell or hemolytic anemia

                                    * congestive heart failure

                                    * renal failure

                                    * hepatocellular carcinoma or metastatic tumor to liver

                                    * quinacrine therapy

                        b) liver metabolism of hemoglobin breakdown to bilirubin

                                    * liver capacity to metabolize bilirubin 2.0 mg/dl

                                    * unconjugated bilirubin brought to liver bound to albumin

                                    * liver conjugates to water soluble form for excretion in bile

                        c) excess rbc breakdown overwhelms hepatic capacity in hemolytic

                            anemia

                        d) hepatitis and cirrhosis prevent conjugation to water soluble state

                        e) obstruction by tumor or gallstones prevents excretion of bile once

                            conjugated

            - Tangier’s disease

                        a) hereditary high density lipoprotein deficiency

                        b) Tangier’s island inhabitants - consanguinity allows autosomal

                            recessive trait to be expressed

                        c) gingival enlargement and deposition of cholesterol in tonsillar

                            tissue producing orange discoloration

                        d) loss of protective effect from high density lipoprotein results in

                            higher than expected incidence of atherosclerosis and arteriosclerosis

Tooth Whitening and History, Safety, and Effectiveness of current Bleaching Techniques and applications of the Nightguard Vital Bleaching Technique

What is tooth whitening?

Whitening is any process that will lighten the existing natural colour of your teeth without removing any of the tooth surface. This can be achieved in two ways;

A product can bleach a tooth, which means that it actually changes the natural tooth colour. Bleaching products contain peroxides that help remove deep (intrinsic) and surface (extrinsic) stains.

Non – bleaching whitening products can be used which contain agents that work by chemical or physical action to help remove surface stains only.

How long has tooth whitening been used?

Tooth whitening has been practised by dentists for over 100 years. The history of “modern day” tooth bleaching, however, began in 1989 and is credited to Haywood and Heymann who introduced the nightguard method of vital tooth bleaching. At the same time, Omnii International (USA), working with a dentist named John Munro, developed and marketed the first commercially available home-bleaching product to be used under dentist supervision.

Interestingly enough, this system was initially discovered quite by accident by an orthodontist named William Klusmier. He instructed a patient to use an oral antiseptic containing 10% carbamide peroxide in an orthodontic positioner, which the patient wore at night, in an effort to facilitate tissue healing. The patient returned with improved tissue health and, after using the product for an extended period of time, his teeth were significantly lighter in colour. He began using this technique to lighten teeth. From 1970 to 1975, Klusmier presented his findings at several dental meetings. Haywood and Haymann attended one of these meetings and initiated their clinical and laboratory investigations on the technique as a result.

Why might I want my teeth whitened?

As with hair and skin colour, the colour of our teeth is genetically determined and therefore varies between individuals. Our teeth tend to naturally darken as we get older.

Teeth can be stained on the surface by food and drinks such as tea, coffee and red wine. Tobacco smoking can also stain teeth. Acidic drinks and foods such as fizzy drinks, fruit juice and yoghurt can cause the teeth to appear more yellow as they cause erosion of the outer enamel layer allowing the underlying yellow dentine to shine through.

Discolouration can also be caused by illness or the use of tetracycline antibiotics while the teeth are forming. Minocycline, a tetracycline antibiotic, can cause staining in adult teeth.

Deposits of calculus (tartar) that form around the necks of teeth can pick up unsightly stains.

Who should decide if my teeth are suitable for whitening?

A  thorough oral examination, performed by a dentist, is essential to determine whether you are a candidate for tooth whitening and what type of whitening system would provide the best results. If tooth bleaching is the treatment of choice the dentist will then administer or supervise the use of bleaching agents within the context of a comprehensive, appropriate treatment plan.

Only a trained clinician can diagnose the type of stain present. In some cases, it may be sufficient to whiten teeth by removing surface stains with a thorough prophylaxis which involves polishing teeth with pumice.

What are the different options for tooth whitening?

Whitening products may be administered or dispensed by dentists or purchased over the counter. Professional bleaching is the most common and effective form of tooth whitening. There are two techniques available for professional bleaching;

Dentist monitored home bleaching techniques.

In surgery bleaching techniques.

What do the different options for tooth whitening involve?

Home Technique

With this technique you bleach your teeth at home, under the supervision of your dentist, using a tooth bleaching gel, usually 10% -20% carbamide peroxide, which is held next to the teeth in a mouthguard.

Impressions of your teeth are taken by the dentist and a custom made bleaching tray is constructed. The tray is lightweight, clear and fits closely around the teeth to ensure that the bleaching gel can be applied to the teeth without touching the gums. The dentist will show you how to put a small amount of the bleaching gel into the tray and will demonstrate how to slide it over your teeth.

You will then continue the treatment at home. The tray is worn for several hours, usually at night time or when it is most convenient. A course of treatment usually takes two weeks but may vary dependant on the concentration of bleaching agent used. In cases of heavily stained teeth the duration of treatment may be as much as six months.

Disposable trays pre-filled with 9% hydrogen peroxide gel which can be adapted to fit around the teeth without the need for impressions have also become recently available.

In Surgery Technique

This technique involves using either light-activated units for ‘power bleaching’ or lasers while you sit in the dental chair.

The dentist will apply a rubber dam or a gel to protect the soft tissues, and a bleaching agent, usually containing 15-35% hydrogen peroxide, is then applied onto your teeth.  A light or laser is then shone on the teeth to activate the chemical so that it acts more quickly on the discolouring molecules within the tooth. The actual tooth whitening procedure will take about one hour.

Before these tooth bleaching techniques are carried out the dentist will make 

a note of your baseline tooth shade using a guide so that it can be compared with the shade after bleaching on your follow up appointment.

The success of these techniques is determined by the initial colour of the teeth. Generally, bleaching easily removes yellow with dark brown and grey stains being more resistant to the process. As younger teeth are more porous it has been suggested that they would be easier to bleach than older ones. With the home bleaching technique it is important to remember that patient compliance with the dentists instructions plays a crucial role in the success of the treatment.

What are the active ingredients in professional bleaching gels and how do they work?

Bleaching gels contain either hydrogen peroxide or one of its precursors, notably carbamide peroxide.  Carbamide peroxide breaks down into hydrogen peroxide and urea, with hydrogen peroxide being the active ingredient.

The success of any bleaching treatment is based on the ability of the bleaching agent to permeate tooth structure to the source of the discolouration. Hydrogen peroxide has a low molecular weight and therefore passes easily through enamel and dentine. Bleaching is an oxidation of the discolouring molecules within the tooth. Peroxides release free radicals which interact chemically with large organic pigment molecules contained in enamel and dentine. These molecules are reduced into smaller, less pigmented molecules.

How long does tooth whitening last?

Some individuals experience better effects from tooth whitening than others. Tooth whitening should last for approximately 18 months to 3 years. At this point you may chose to have a touch up treatment and the colour will usually change to the optimal shade readily. The effect is less likely to last as long if you smoke, or eat or drink products that can stain teeth.

Is tooth whitening safe?

The evidence on safety published to date tends to suggest that bleaching is a relatively safe procedure.

Hydrogen peroxide breaks down into water and oxygen. Urea breaks down into carbon dioxide and ammonia. Normal body processes easily handle all four products.

 It has been suggested that peroxides are mutagenic and can boost the effects of known carcinogens. The American Dental Association (ADA), however, has found no evidence that when used as directed, tooth whiteners increase cancer risk or cause other problems. The ADA have acknowledged that bleaching products are abused by some members of the public.

What are the side effects?

The most commonly observed side effects to hydrogen or carbamide peroxide are tooth sensitivity to cold and occasional irritation of the soft tissues in the mouth, particularly the gums.

Tooth sensitivity often occurs in the early stages of bleaching treatment. In most cases, gum irritation is caused by an ill fitting bleaching tray rather than the actual bleaching agent. Both of these conditions are usually temporary and disappear within a few days of the treatment finishing. The use of desensitising agents containing fluoride or different bleaching gel formulations can address the sensitivity problem.

If you encounter any of these side effects you should consult your dentist.

Will tooth whitening damage my teeth?

Over bleaching can cause teeth to become chalky and translucent.

Several studies have been carried out to investigate the reaction of the pulp, which contains the nerve and blood supply to the tooth, to the bleaching process. Evidence shows that bleaching may either have no effect or may cause an initial, mild, localised pulp reaction which is reversible several weeks post treatment.

There are no reports in the literature indicating that bleaching may exert a negative impact on existing restorations. Defective restorations should, however, be replaced before bleaching to minimise potential sensitivity.

How much does tooth whitening cost?

Whitening treatments are not available from your dentist on the NHS. Private charges will vary between practices and between regions. In surgery bleaching techniques tend to be more expensive than dentist supervised home techniques.

Patients are advised to contact their dentist to determine costs.

Existing crowns and fillings on the front teeth may also need to be changed following the bleaching procedure which increase the overall cost.

How can I look after my teeth during and after whitening?

Personal habits may need to be modified to achieve and maintain the desired goal of whiter teeth.

Teeth should be dry and cleaned of debris before any bleaching agent is applied. During bleaching teeth may be slightly dehydrated and consumption of food and drinks which can cause staining should be kept to a minimum. These foodstuffs should also be kept to a minimum after tooth whitening. Stopping smoking will also prevent staining of teeth.

What about whitening products bought ‘over the counter’?

Although cheaper, over the counter bleaching kits often contain an insufficient concentration of hydrogen peroxide to be effective. Some may contain acetic or citric acid as active ingredients. These acids have too low a pH (too acidic) and can cause significant structural damage to enamel when used for extended periods of time and worsen the discolouration through erosion. Bleaching trays provided are not made to fit your mouth and can therefore cause increased leakage and soft tissue irritation.

Whitening toothpastes do not affect the natural colour of teeth but may be effective at removing surface (extrinsic) staining because they contain abrasives.

Before you use a tooth whitening product you should consult your dentist.

Are there any people for whom tooth whitening is not a good idea?

Individuals with a history of extreme sensitivity to hot and cold food or drink, fracture lines in their teeth, large dental pulps, and severe loss of enamel may not be suitable candidates for tooth whitening as the procedure may precipitate sensitivity.

Decay, periapical lesions, and gum disease should be treated before any tooth whitening procedure is carried out. Tooth whitening should not be carried out on individuals with a peroxide allergy. 

When might tooth whitening not work?

Tooth whitening only works on natural teeth and will therefore have no effect on fillings, crowns, and veneers. If you have white fillings in your front teeth, these should be replaced approximately 2 weeks post - bleaching to ensure a good colour match and bond strength.

Very severe tetracycline stained teeth may not respond or have a limited response to tooth whitening. In these cases, porcelain veneers may be the treatment of choice. Mild to moderate tetracycline staining does, however, tend to respond to extended bleaching regimes of 3-6 months. White fluorosis spots do not tend to bleach but will become less obvious as a result of lightening of the surrounding tooth area.

Can a single tooth which has been root filled be whitened?

Sometimes teeth become discoloured by the breakdown of tissue inside the root canal when the nerve dies.  It is hypothesised that the blood in the pulp chamber undergoes haemolysis, which releases haemoglobin. The iron in the haemoglobin then combines with hydrogen sulphide, produced by bacteria to form iron sulphide, which is a very dark pigment.

Provided a satisfactory root filling, hydrogen peroxide or sodium perborate can be placed inside the tooth (internal bleaching) under a temporary dressing. After a week, the bleach is removed and a permanent filling placed to reseal the tooth. Internal bleaching can also be combined with external bleaching.

Can I whiten my teeth while I am pregnant?

The effect of the bleaching gel on the foetus is unknown. You will swallow some of the gel while you are bleaching with home kits. It is now generally accepted to avoid unnecessary medical interventions during pregnancy in order to minimise any possible risks to the health of the foetus.

History, safety, and effectiveness of current bleaching techniques and applications of the nightguard vital bleaching technique

Introduction

The purpose of this article is to evaluate the safety of the various techniques for bleaching teeth in general, and the newer nightguard vital bleaching technique specifically, as well as provide examples of some of the applications of the nightguard vital bleaching technique. Bleaching techniques may be classified by whether they involve vital or nonvital teeth and by whether the procedure is performed in the office or has an at‑home component.

Hydrogen peroxide, in various concentrations, is the primary material currently used by the profession in the bleaching process. Current in‑office techniques for vital teeth and the "walking bleach" technique for nonvital teeth typically use a 30% to 35% concentration of hydrogen peroxide. The majority of the products currently on the market for the nightguard vital bleaching technique use a 10% carbamide peroxide solution. A 10% carbamide peroxide degrades into 3% hydrogen peroxide and 7% urea, and hydrogen peroxide can be considered its active ingredient.The urea may provide some beneficial side effects, because it tends to raise the hydrogen ion concentration (pH) of the solution.Some products marketed directly to consumers, over the counter (OTC), use 6% hydrogen peroxide solutions in a gel form.

Hydrogen peroxide naturally occurs in the body, even in the eyes, in low concentrations. It is manu­factured and regulated by the body, and often involved in wound healing. In higher concentrations, it is bacteriostatic, and in very high concentrations is mutagenic, possibly by disrupting the DNA strand. However, the body has mechanisms for immediate repair of natural damage, low concentrations of hydrogen peroxide do not cause serious problems,the carcinogenic capabilities of hydrogen peroxide are more often caused by other peroxide derivatives, and the body uses the peroxidisesand other mecha­nisms for regulating hydrogen peroxide. Also, other conditions are often required to allow action by hydro­gen peroxide on cells. Because hydrogen peroxide occurs extensively within the body, and because it has been used topically for many years, it has been studied extensively. The understanding of the role of hydrogen peroxide offers clues to understanding many of the body's actions at the cellular level and to under­standing the naturally occurring inflammation and healing processes.

The mechanism of action of hydrogen peroxide in tooth bleaching is considered to be oxidation, although the process is not well understood. It is felt that the oxidizers remove some unattached organic matter from the tooth without disolving the enamel matrix, but also may change the discolored portion to a color­less state. There is some concern that continued long‑term treatment will result in dissolution of the enamel matrix, but reports to date on nightguard vital bleaching techniques have not supported this theory. Tetracycline stains are more resistant to oxidation because the molecule is tightly bound to the mineral in the enamel prism matrix during formation and hence is less accessible to immediate action (Cren­shaw M: Personal communication). Teeth stained with tetracycline therefore require prolonged treatment times before any results are demonstrated and often are unresponsive to the procedure.

Generally, bleaching is considered an elective process, although there are other indications that may make bleaching a necessity.

Safety over time

The first area to consider when evaluating safety is how long the technique has been used, and the obser­vations that have been made over that time. Esthetic dentistry was a popular topic in the late 1800s, including such present‑day concepts as recontouring of teeth; the portion proposed to be removed was shaded with indict ink for patient approval. Recontouring and bleaching were recommended procedures, along with gold inlays and porcelain inlays, to avoid the waste of sound tooth structure by the casual crowning of the tooth. Dentistry was in an era of affluence, and esthetics was a prime consideration. Dentists were concerned that too many teeth were being crowned, about the inappropriate use of base metal in restora­tions, about proper uses of better pins in teeth, and about the need for better use of the rubber dam.

From the middle 1800s until early 1900, the reputable dental journals contained 40 to 60 articles a year on tooth bleaching. The chemistry seemingly was well understood, the eminent leaders of the profession con­ducted experiments showing the safety of bleaching to the tooth, and the plea for conservative dentistry and preservation of tooth structure was ever the standard. Prominent dental leaders and editors of major textbooks gave lectures supporting bleaching, and chapters or sections in operative dentistry textbooks were devoted to this treatment. The discussions concerned whether or not bleaching worked, the appropriate indications, how long it lasted, and the relative safety of the various procedures.

Practitioners speaking against bleaching argued that it took too long to occur and was too technique sensi­tive to perform. They argued that because the teeth often reverted back to their original color, bleaching was not worth the effort, and they would rather crown the tooth. Those practitioners in favor of bleaching demonstrated the scientific approach to the application of the different bleaching techniques to avoid failure and minimize relapses, reported longevity averaging 6 to 25 years, and stated that professional dentists gave the needed time to get the best, most conservative treatment for their patients.

As early as 1848, nonvital tooth bleaching with chloride of lime was practiced. Truman is often cred­ited with introducing, well before 1864, the most effective technique for bleaching nonvital teeth, which used chlorine from a solution of calcium hydrochlo­rite and acetic acid. The commercial derivative of this, later known as Labarraque's solution, was a liquid chloride of soda. Numerous other bleaching agents were also successfully employed on nonvital teeth in the late 1800s, including aluminum chloride,oxalic acid, pyrozone (ether‑peroxide), hydrogen dioxide (hydrogen peroxide or perhydrol), sodium peroxide, sulphorus acid, sodium hypophosphate, chloride of lime, and cyanide of potassium. All these substances were considered either direct or indirect oxidizers, which acted on the organic portion of the tooth, except for sulphorus acid, which was a reducing agent. It later came to be recognized that the most effective direct oxidizers were Pyrozone (Mc Kesson & Robbins), Superoxol (Merk), and sodium dioxide, while the indirect oxidizer of choice was a chlorine derivative.

The bleaching agents were categorized according to which stains they were most effective in removing. Iron stains were removed with oxalic acid, silver and copper stains with chlorine, and iodine stains with ammonia. The stains of metallic salts from metallic restorations such as amalgam were considered the most resistant to bleaching. Although cyanide of potassium would easily remove such metallic stains, its use was not recommended because of its being a very active poison. It was recognized that restorations were not affected by bleaching, but the bleaching would remove the stains around margins and under esthetic restorations that were leaking, giving them a longer esthetic life. Earlier concerns of the profession about the potential dissolution of teeth from the caustic nature of some of the materials had been disproved by laboratory experiments and clinical observation.

Techniques that allowed the practitioner to perform the procedures in-office or place the medicament and change it at subsequent appointments were de­scribed. Sodium peroxide and hydrogen dioxide were used independently or together to bleach teeth; sodium peroxide actually had the advantage of giving the most natural translucency to the nonvital teeth. It had long been recognized that some stains were more resistant to treatment than others, and great care was taken during endodontic therapy to avoid allowing the pulpal tissues to bleed into the chamber, since this caused the tooth to discolor.

Although most of the early dental literature focused on bleaching nonvital teeth, vital teeth were also treated, as early as 1868, with oxalic acid, and later hydrogen peroxide or Pyrozone. By 1910, these vital bleaching techniques generally included the use of hydrogen peroxide with a heating instrument or a light source. The steps to ensure patient comfort, including the covering of the eyes, the number of appointments, four or five, and the minimum of 3‑day intervals between appointments, as well as the favorable prognosis, were well documented and recognized by the profession.

As early as 1893, it was common knowledge that a 3% solution of Pyrozone (ether‑peroxide), the aqueous solution of hydrogen dioxide, could be used freely as a mouthwash by both children and adults and that, in children with pitted teeth, it had the beneficial side effect of reducing caries and bleaching the teeth. It was reported that the 5% solution could be used in a like manner to bleach teeth, but that the 25% solution, the most effective bleaching agent, should be used carefully, to prevent contact with the soft tissue, because of its caustic nature.

Since there were few manufacturing companies in the 1800s, most dentists were excellent chemists, and mixed a variety of solutions in their offices. When the manufacturing industry began to develop in the 1900s, this versatility was lost to the profession, and the choices of materials to the profession were limited to those offered by the manufacturing companies. Super­oxol was introduced by a manufacturing company early in the 1900s, and later became the chemical used by the majority of dentists because of its safety, although it was recognized that hydrogen peroxide bleaching sometimes left a yellow or brown tinge in some teeth, which the other, previously used materials had not, and that Pyrozone (ether‑peroxide) was the more effi­cient bleaching material.

From about 1913 until 1940, which included the time of World War I, the Depression, and World War II, very little was written about bleaching. However, articles began to appear in the 1940s and 1950s as the United States began to recover economically, as com­munications improved nationally, and as the profession began treating fluorosis, tetracycline‑stained teeth, and discolored teeth saved by endodontic therapy rather than lost to extraction. In the 1940s, hydrogen peroxide and ether were again used on vital teeth.

Pyrozone continued to be used effectively for nonvital teeth in the late 1950s and early 1960s,52 as was sodium perborate. In the late 1960s, Nutting and Poeelected to use Superoxol instead of Pyrozone, for safety, and combined it with sodium perborate to achieve a synergistic effect. They recommended use of Amosan (Knox Mfg Co), a sodium peroxyborate mono­hydrate, because it released more oxygen than did sodium perborate. They also advised that the gutta­percha be sealed before the procedure was initiated.

Also in the late 1960s, a successful technique for home bleaching using a 10% carbamide peroxide, delivered in a custom‑fitting mouth tray, was discov­ered by Klusmier. Although he presented several table clinics at the Arkansas State Dental Society and the Southwestern Orthodontic Society (Klusmier B: Personal communication), this technique went rela­tively unnoticed until Haywood and Heymann de­scribed the technique in March 1989 and a similar product was introduced by a manufacturing company that same month. For the first time, this technique offered the possibility of whiter vital teeth to a wider section of the general patient population at a lower cost, with much less danger and fewer side effects, than any of the previous options. Since that time, numerous other products and techniques making claims for bleaching teeth have been introduced. These options include variations on the dentist‑pre­scribed/home‑applied techniques, as well as "bleaching kits" sold directly to consumers in stores for unsuper­vised home use. The nightguard vital bleaching techniques and the OTC bleaching kits have kindled a resurgence of interest in tooth bleaching and have reopened the questions asked 100 years ago: Does it work, is it safe, what are the indications, and how long does it last?

Current safety

Nonvital bleaching

The walking bleaching technique is probably the most popular option for bleaching nonvital teeth, and no major problems of safety were initially observed other than those associated with the handling of the material and the potential for burns from the high concentration of hydrogen peroxide. This technique involves sealing a mixture of 30% hydrogen peroxide and sodium per­borate in the pulp chamber and changing the solution every 2 to 7 days.

The in‑office alternative treatment for bleaching non­vital teeth usually involves a single appointment in which 30% hydrogen peroxide is activated by a heating instrument, which is more efficient. However, later in the 1970s, external resorption was noted in the cervical areas of nonvital bleached teeth. Early reports linked this to overzealous use of heating instruments or to previous trauma to the tooth. Onset was 1 to 7 years posttreatment, and the tooth was often lost.

Although the etiology of the resorption is still un­known, later reports have questioned the heat and trauma theories and proposed that the resorption may result from exiting of the peroxide through the tooth where the enamel and cementum do not join. Approx­imately 10% of teeth do not have an intact cemento­enamel junction (CEJ). This theory, along with the observation that pressure in the chamber often causes transient pain, reaffirm that a base material should be placed, before the peroxide is inserted, over the exposed root canal filler and over areas that might communicate with the CEJ. However, placement of this base often means that a portion of the tooth that is discolored will have to be masked with the base material and possibly will not lighten.

A significant drop in pH has been observed in the cervical area of the tooth from passage of the peroxide through the tooth and its exit at the CEJ. Later ob­servations have indicated that the resorption is not ac­tually at the CEJ, but is more apical. This observation, along with experience gained using calcium hydroxide in the treatment of resorption and incomplete root for­mation, have led to the practice of filling the pulp chamber with calcium hydroxide powder after the completion of the bleaching to alter the pH and halt the potential osteoclastic activity. More recent re­ports have recognized the greater potential for cervical resorption from the combination of heat and 30% hydrogen peroxide over either treatment alone. For these reasons, the safer nonvital bleaching technique appears to be the walking bleaching technique, rather than the in‑office technique using a heating instrument.

Another approach to treatment involves using sodium perborate alone, rather than in conjunction with hydrogen peroxide, as the primary bleaching agent. Although this may be a slower process, it is potentially less destructive to the tooth and hence safer.

It is unclear why these resorption problems should appear so late in the history of nonvital bleaching, but their recent appearance raises the possibility that changes in materials for root canal fillers, sealers, or bleaching, or a wide variation by practitioners in ad­ministration of the technique, may be the cause. At this time, the walking bleaching technique seems reasonably safe, with only a slight chance of cervical resorption. The benefit of treatment is relatively great (considering the cost of a crown or veneer, the preser­vation of remaining tooth structure, the potential for an esthetic outcome, the avoidance of a subsequent weakening of the tooth, and the finite life of the other restorative possibilities), and the risk is small. Precau­tions include sealing the root‑filled portion preopera­tively with a material such as polycarboxylate cement, placing calcium hydroxide powder in the chamber postoperatively for 14 days, and following the patient for a number of years with frequent recall radiographs. If there is any evidence of resorption, it may be ar­rested with calcium hydroxide treatment, and the tooth can be crowned (with or without extrusion of the tooth to manage the defect).

Vital bleaching

For any vital bleaching procedure, patients are classi­fied by whether they have tetracycline‑stained teeth, or teeth stained from other reasons. Tetracycline­stained teeth are the least responsive to bleaching, depending on the severity of the stain. With external bleaching, tetracycline‑stained teeth generally get lighter, but not whiter. Some clinicians have recently advocated intentional endodontic therapy on those teeth, with the use of the walking bleach, to overcome this problem. While the esthetic result appears to be much better than that of external bleaching, this ap­proach raises questions about the success of the endo­dontic therapy over time, the longevity of the walking bleaching technique, and the potential of the treat­ment or retreatment to cause cervical resorption.

The most popular technique for the in‑office bleach­ing of vital teeth involves 35% hydrogen peroxide, etching the teeth with phosphoric acid to facilitate bleaching, and either a heating element or a light source to enhance the action of the peroxide. Be­cause this technique must be accomplished without anesthesia to allow the patient's pain threshold to determine the appropriate heat level, there have been numerous studies on the effects of both the heat and the concentrated hydrogen peroxide on the pulp. Although there is insult to the tissue, most of the research has shown that the pulp remains healthy, and the insult is reversible in approximately 2 months. The observations of many clinicians who have per­formed this procedure over many years attest to the fact that pulpal necrosis is not associated with vital bleaching. Research in this area has shown how easily the hydrogen peroxide, because of its low molecular weight, passes through the enamel and dentin to the pulp.

More current clinical studies have eliminated the etching with phosphoric acid, and the most recent products on the market advocate no use of heat or light for the reaction.

A number of studies have evaluated the effect of bleaching with this high concentration on dentin and enamel and have found some hints of structural changes in tetracycline‑stained teeth. However, the most important observation has been the decrease in bond strengths of composite resin to bleached, etched enamel immediately after the bleaching process. Later studies in this area have attributed the decrease to residual peroxide left immediately in the tooth or on the surface.

The main safety advantages of the in‑office vital bleaching technique are that, although it uses caustic chemicals, it is totally under the dentist's control, the soft tissue is generally protected from the process, and it has the potential for bleaching quickly in situations in which it is effective. Disadvantages are primarily the cost, the unpredictable nature of the result, and the unknown duration of the treatment. The unsafe features include the potential for soft tissue damage to patient and provider, the discomfort of rubber dam, the temperature on the pulp, and the resultant post­treatment sensitivity. Although early concerns about pulpal response were identified, subsequent research seems to have shown that although this high concen­tration of hydrogen peroxide causes changes, they are reversible. If etching is performed, polishing is required after each visit, with some enamel loss.

It is well accepted that this technique works, but the patient must be counseled that, although the result may be permanent, the process more likely will have a 1‑ to 3‑year duration, at which time the treatment will need to be redone. Also, it cannot be determined prior to treatment whether the teeth will respond, and treatment may take as many as four to six treatments. The labor‑intensive nature of the treatment, which in turn requires a higher fee, coupled with the discomfort to the patient and uncertainty of the outcome, keep this method of bleaching from being a treatment that is widely accepted, although it can be successful.

Recent innovations for in‑office bleaching include chairside‑mixed gels, some of which are activated by composite resin curing lights (Hi Lite Dual Activated Bleaching System, Shofu). According to the manufac­turer, this light‑activated material changes color when the bleaching process is completed, which should take only 3½  minutes. Chemical composition and effects on tooth structure of this technique are unknown at this date. Other gel forms do not use heat or light. Although they require approximately the same treat­ment time as the conventional Superoxol bleaching technique, the gels are much easier to manage clini­cally.

Nightguard vital bleaching or dentist‑prescribed/home­applied bleaching

The most recently introduced vital bleaching technique, originally called nightguard vital bleaching (NGVB), but also referred to as home bleaching or dentist‑monitored bleaching, has created a resurgence in the area of bleaching, primarily because of its relative ease of application, the safety of the materials used, the lower cost, its general availability to all socio­economic classes of patients, and the high percentage of successful treatments. It may be more appropriately termed a "dentist‑prescribed/home‑applied" tech­nique. Because the 10% carbamide solution is equiva­lent to a 3% hydrogen peroxide solution, this solution is approximately one tenth the concentration of the solutions used for "power," or in‑office, bleaching. Results are generally seen in 2 to 3 weeks, and the final outcome is complete in 5 to 6 weeks. However, treatment times vary extensively, and much depends on the amount of time per day that the patient chooses or is able to apply the technique. Later products have offered solutions of hydrogen peroxide that range from 1% to 10% and carbamide peroxide solutions that are either 10% or 15% concentration. The details of this technique have been reported in many articles.

Numerous articles have attested to the efficacy of the technique, which has been successful in clinical trials for approximately 91% of persons with mate­rially or genetically discolored teeth, and somewhat less successful in 91% of persons with tetracycline­discolored teeth. Tetracycline‑stained teeth generally get lighter, but not whiter. Nightguard vital bleaching generally has the same indications and prognosis as conventional, in‑office bleaching, but can be accom­plished at a much lower cost and with fewer side effects, such as tissue burns and sensitive teeth, in the general patient population. A recent survey of 7,617 dentists indicated a success rate of greater than 90% for the technique; ninety percent of the responding dentists use a 10% carbamide peroxide.

Specific questions as to the safety of NGVB were recently addressed in an article by Haywood and Hey­mann. The controversial element that the nightguard vital bleaching technique adds to conventional bleaching options is the potential for contact of the soft tissue during treatment and from ingestion of the material. This contact sometimes results in one of the two common side effects, an irritation of the gingival tissue. More than half the time, this irritation is related to an ill‑fitting prosthesis. Other times, it is the tissue's re­sponse to the peroxide.

There are numerous reports of the effects of hydrogen peroxide on tissue. However, those effects are gen­erated by conditions that exceed greatly the time and dosage of peroxide used in this bleaching technique. The previously mentioned survey confirmed that one third of patients bleaching their teeth in the home manner did not have side effects, while those that did experienced either transient tooth sensitivity or gingi­val irritation. The fit of the guard was a major cause of gingival irritation. Reports from industries that make hydrogen peroxide state, "It is improbable that humans will be exposed to high oral doses of H2O2 due to the acute toxicity of concentrated solutions and the corrosivity of H2O2 to mucous membranes. An in­dividual would theoretically have to drink daily 23 mL of 35% hydrogen peroxide for a lifetime to develop the lesions seen in mice." Hydrogen peroxide is approved as safe for use as human food additive with no residues.

More recent studies directly evaluating the effects of 10% carbamide peroxide on tissues and in animals systemically have indicated that the effects of 10% carbamide peroxide on tissue are less than or equal to those of many other accepted dental medicaments, such as eugenol, or other dental procedures. The most conclusive evidence to date has been the work of Woolverton et al establishing the nonmutagenic nature of 10% carbamide peroxide, the safe level of ingestion, and the minimal effects on cell lines. Even in tray designs that seek to avoid covering the attached gingiva, the interdental papillae are still exposed to the solution. Hence, the total avoidance of soft tissue con­tact is impossible as the technique currently stands. Conclusions from evaluations of the other studies indicate that toxicity and mutagenicity of hydrogen peroxide are dose related, and the concentrations used in the at‑home bleaching technique are not of sufficient strength to warrant concern about the soft tissue. In fact, although a high, sudden dose of hydro­gen peroxide is toxic to cells, a lower dose over a longer time allows cells to adjust and actually ultimately tolerate a higher dose than that which originally would have been toxic. Also the long history of clinical usage of the solutions with soft tissue contact ranging from 7 days to 3 years, in patients ranging from new­born infants to geriatric patients, has demonstrated no problems.

Various effects of carbamide peroxide on teeth have been studied. Generally, these reports find the effects to be nonexistent or to be no worse than those already found with in‑office bleaching. Although there have been varying reports concerning the effect on enamel, there does not seem to be a significant effect on the morphology of the enamel surface outside the normal variation of enamel. No published re­ports have demonstrated any change in hardness of enamel, nor have studies at the University of North Carolina shown any significant concerns. Studies that evaluate change in the surface must take into account the remineralization potential in the mouth, which may negate any potential changes. There has been one observation that toothbrush abrasion was more significant in the presence of bleaching agents, while yet another slightly different study showed brushing with the solutions had no effect. Another report has shown the at‑home bleaching procedure to be a controlled oxidation process in which the organic phase of the enamel is mobilized without producing grossly unacceptable enamel surface topography. Clinically, there is no apparent loss, and the tooth retains its glossy appearance. There have been reports of internal matrix changes from bleaching with 35% hydrogen peroxide after laboratory‑induced tetracycline staining, but there is no direct correlation between this study and the milder hydrogen peroxide, nor have these changes been demonstrated to have any clinical significance. Studies directly on dentin and enamel with 10% carbamide peroxide materials have demon­strated no structural loss.

The effects on the pulp were extensively evaluated in the previous generation of bleaching with 35% hydrogen peroxide, and the lower concentration of peroxide would not be expected to be as detrimental to the pulp. The effects on pulp have not been directly evaluated with the weaker peroxide solutions, but the research on 35% hydrogen peroxide has shown effects that are reversible over time, with no clinical conse­quence other than immediate, but transient, sensitivity. Clinical trials on nightguard vital bleaching techniques in progress at the University of North Carolina have found no predictors of sensitivity relative to patient age, pulpal size, presence of exposed dentin or cemen­tum, caries, or leaking restorations. The limitation for how young the child is able to be treated is related more to the available number of permanent teeth to retain the guard and the desire not to impede the erup­tion of permanent teeth as they attempt to rapidly enter the oral cavity than to pulpal sensitivity. The occasional mild tooth sensitivity associated with night­guard vital bleaching is attributed to the easy passage of the hydrogen peroxide and urea through the enamel and dentin to the pulp and the resulting mild irritation. This ceases on termination of treatment. Because the concentration of hydrogen peroxide is lower, certain patients that could not tolerate the in‑office bleaching because of discomfort have found the nightguard vital bleaching technique to be acceptable.

Effects on restorative materials have been limited primarily to composite resins, both with color change and surface integrity. Basically, there is no appreciable change in the color of any restorative material clinically. Although there have been conflicting reports recently in this area as to composite resins, the ability of the colorimeters to measure differences is limited, and this color difference has not yet been calibrated to clini­cally detectable changes. Clinicians must assume there will be no color change in any material (although the stains may be removed from the surface and margins of porous composite resins, etc), and patients should be advised of the potential need for replacement of any esthetic restorations if the shade of the composite resin is not clinically acceptable postbleaching. Reports of the dissolution of a portion of the matrix have also concluded that it may be clinically inconsequential. Since the composite resin may have to be replaced afterward, any loss may be of no significant concern. Whether this bleaching technique will have a significant effect on the long‑term wear of posterior composite resins is still unknown, because other reports have shown that composite resin hardens after exposure to bleaching solutions. Porcelain, amalgam, and gold have not responded with either color change or alter­ation of structure, so they are considered unchanged by the bleaching process.

Of current interest to the clinician is the effect of bleaching on bond strength of etched enamel to com­posite resin. Earlier reports had associated a decrease in bond strength of treated enamel to composite resin with bleaching using 35% hydrogen peroxide. This occurrence has also been confirmed with the 3% per­oxide, but has been related to the residual oxygen in the tooth, and the bond has been shown to increase, approaching the original strength over time. More recent studies of the 35% in‑office bleaching techniques have also attributed this loss to residual peroxide tempor­arily remaining in the tooth or to surface changes. Another study of home bleaching techniques demon­strated that roughening the surface slightly also elimi­nates this phenomenon. Generally, etching and bonding should be delayed at least 14 days after termi­nation of bleaching until further studies can determine a more precise waiting time.

Safety to the occlusion and the temporomandibular joint during the bleaching process must also be consi­dered. Typically, occlusal problems during NGVB may be mechanical or physiologic. Mechanically, the patient may occlude on only posterior teeth, rather than on all teeth simultaneously. Sequentially removing posterior teeth from the guard until all the teeth contact will rectify the problem, and avoid the potential for joint disturbances. If the patient exhibits bruxism, he or she usually will wear a hole in the appliance over time, and another will have to be made. There has been no success to date in fabricating an occlusal device for bruxism that can also serve as a well‑fitting guard for bleaching. Physiologically, if the patient has pain in the joint, the posterior teeth can be removed from the guard until only anterior guidance is remaining, and the patient's wear time should be reduced or limited to the day only.

Another area of concern with safety is how often the procedure will have to be administered. Current research at the University of North Carolina on longevity of the result indicates that, although the change may be permanent, the patient will probably need re‑treatment in 1 to 3 years. It has been noted that re‑treatment involves significantly less time than the original treatment.

Over‑the‑counter bleaching kits

The newest systems that claim to bleach teeth are bleaching kits sold directly to consumers. These kits are described as a three‑step process: a 15‑second pre­treatment acetic rinse, a 1‑ to 2‑minute application of a 6% hydrogen peroxide gel with a cotton swab on the facial surfaces of the teeth, and an application of a tooth‑whitening pigment.

Early concerns have been expressed as to whether the process actually works, especially as it is shown in television advertisements. Although results shown in advertisements seem dramatic, the manufacturers' literature reports that bleaching may take from 2 days to 2 weeks, and sometimes up to 60 applications, for successful lightening. No reports from dental studies have demonstrated any effectiveness. In a screening project for the US Federal Trade Commission at the University of North Carolina, administration of the OTC technique, on patients who had already success­fully bleached one arch with the dentist‑prescribed/ home‑applied technique in a clinical bleaching study, did not effect any change after one, two, 14, or 60 applications. One report has shown that there is no harm to composite resins from any of the bleaching agents, including this type of system.

A more disturbing concern relates to the safety of the material and technique. A recent report cites the dissolution of enamel in a young person using the technique. Although the person was also a heavy cola drinker, this result raises the question of the safety of unsupervised use of a treatment as well as the lack of baseline data. If the material is not effective as a bleaching treatment, this lack of success could further foster abusive use in an attempt to achieve results. In those patients who have other problems resulting in dissolution of enamel, this could be an additional in­sult.

It may be this lack of proof of efficacy and safety with some techniques that has prompted both the American Dental Association to advise caution and the US Food and Drug Administration to issue warning letters to manufacturers requesting data supporting their claims. Further determination of both efficacy and safety of these OTC bleaching kits and other variations of the conventional NGVB technique are certainly indicated. However, the ruling by the US

Food and Drug Administration is directed toward manufacturers, and does not restrict, limit, or affect bleaching treatments performed in a legitimate dentist­patient relationship (US Food and Drug Administra­tion: Personal communication).

Relative safety of the nightguard vital bleaching technique

Safety of nightguard vital bleaching must be assessed relative to that of the other bleaching techniques, but it also must be compared to the safety of other accepted dental practices. With teeth, as with any living tissue, there will always be a response to treatment. The ques­tions are the risk‑banefit of the treatment and what is known from observations and studies on other dental treatments. The question of safety is always a dose­over‑time relation, as has been noted in the questions of fluoride toxicity and the recent amalgam and mercury concerns. Other areas in dentistry are also currently being examined for their safety. These indude concerns about the nickel‑beryllium content of non­precious metals, the carcinogenicity of nickel, and the reported toxicity of Sargenti techniques.

As to the concern of the effect of materials on the pulp and other tissues, it has been shown that one in five teeth that receive a crown will need root canal therapy, 73% of the single pins placed in teeth cause a fracture in the dentin that communicates directly with the pulp, and heat on the pulp from restora­tions and direct provisional restorations has adverse effects. Dentists observe postoperative pain from the cementation of crowns or ceramic inlays with glass­ionomer or zinc phosphate cements, hypersen­sitivity reactions to polyether impressions, and aller­gic reactions to the poly(methyl methacrylate) acrylic resins. It has been shown that poly(methyl metha­crylate) is cytotoxic and produces non‑neoplastic lesions and that some glass‑ionomer cements exude cytotoxic substances even after a hardening period of 48 hours. In the more esthetic materials, it has been shown that all composite resin is cytotoxic in its unset form and when incompletely cured, and some com­posite resin is even cytotoxic if cured for less than 60 seconds. The cytotoxicity of orthodontic adhesives has been demonstrated even after 2 years, and the cytotoxicity of orthodontic solder joints to tissue has been shown. Recently, Gluma 3 (Miles Inc) has been identified as a mutagenic agent, the cytotoxicity of dentinal bonding agents has been demonstrated, and detrimental effects of dentinal bonding agents on the pulp have been cited. Although the relative thickness of remaining dentin determines the cytotoxic effects of composite resin and glass‑ionomer ce­ment on the pulpal tissues, it is impossible to know how much dentin is present in the mouth. There is also the danger of damage to the gingival tissues from in­discriminate use of the microabrasion technique, as well as with the conventional in‑office bleaching techniques.

As to effects of other dental treatments on the surface of teeth or restorations, 5 to 50 µm of enamel is re­moved during a prophylaxis and 5 to 50 µm of enamel is removed at banding and debanding of ortho­dontic appliances. Hence, even a possible effect on the surface of enamel from bleaching may be considered negligible compared to the 5‑ to 10‑µm loss of enamel from every rubber cup prophylaxis over the life of a patient, including the loss of the fluoride‑rich layer. Merely etching the enamel dissolves at least 10 µm in addition to the 25 to 50 µm that is etched. Treatment with microabrasion to remove stained enamel results in 12 µm of enamel loss with the first 5‑second applica­tion, and an average of 26 µm of loss for every succes­sive 5‑second application. Acidulated phosphate fluoride, which contains hydrofloric acid, is capable of etching porcelain in the mouth (Bayne S: Personal com­munication). It has also been shown that judicious use of the Cavitron can remove resin‑bonded fixed partial dentures or other cemented prostheses.

As to overall safety, it is reported that 8% of patients are allergic to latex gloves. Studies on the previous effects of eugenol in periodontal dressings on bone have resulted in a change in the formulation to non­eugenol‑containing periodontal dressings. However, no significant clinical problems from the use of the eugenol‑containing periodontal dressings on soft tissue has been identified in the literature. Detrimental ef­fects of hydrogen peroxide on the bone have been reported, but it is unlikely that the nightguard vital bleaching techniques would ever be used in patients with exposed bone. Recent reports have described the toxic effects of zinc oxide‑eugenol cement to the pulp, the dangers and toxicity of sodium hypo­chlorite, the toxicity of endodontic obturation materials, and allergic reactions to implants. This, in conjunction with the radiation from normal exposure of radiographs, the potential for an allergic reaction to local anesthetic, the hazards of eye damage from composite resin curing lights, and the hearing loss caused by the high‑speed handpiece, make dental treatment full of risk‑banefit judgments in the light of current knowledge. Even the choice between a direct pulp cap or endodontic therapy, between placement of another foundation or a casting, or to remove a questionable restoration, which takes more tooth structure and weakens the tooth, is subjective but significant in the long‑term safety and health of the tooth.

One concern often expressed about the nightguard vital bleaching technique is the potential danger of making bleaching materials available to patients at home, where abuse may occur. It is important to dis­tinguish between nightguard vital bleaching (dentist­prescribed/home‑applied), and OTC kits available directly to consumers. In the "prescribed" method, the materials are held in a custom‑fabricated guard, and approximately 1 to 2 oz is used in a 4‑ to 6‑week period. If the patient uses more than 2 oz during that time, the dentist should reevaluate the patient's appli­cation technique. The availability of the dentist for monitoring, the slowness of the treatment, and the contained environment reduce the potential for abuse. Clinical trials have also indicated there is a level of lightness beyond which the teeth do not pass. Hence the treatment is somewhat self‑limiting over time. Patients could continue for extended periods of time, but at this time there is no clinical evidence that this is occurring. There is always the potential for abuse by some persons, but there is the same potential danger of abuse from ingestion of fluoride‑containing tooth­paste or rinses, alcohol‑containing mouthwashes, and aspirin, even when these materials are correctly pre­scribed.

On the other hand, OTC kits place the consumer in a position of diagnosing the reason for discoloration of their teeth, as well as prescribing a treatment that has no professional evaluation of the baseline standard, the side effects, or the results. Unsupervised or exces­sive use of any material has potential for harm, espe­cially in certain persons in whom the physiologic status of the teeth and saliva or psychological status exaggerates otherwise reasonable treatment responses. These effects are seen in the case of toothbrush abrasion or the detrimental erosive effects of excess consumption of carbonated drinks and fresh citrus fruits on enamel and dentin. Most unknown about the OTC kits is the effect of the prerinse on enamel over time. Further research and unbiased reports are needed to establish the appropriateness of claims for both safety and effi­cacy. The safer option currently available is a system where there is some establishment of indications for treatment by a trained professional, baseline recording of data, fabrication and insertion of a custom‑fitted mouthguard, monitoring of treatment, availability for questions, evaluation of success or concerns, and in­struction in application.

Some concern also has been expressed about the safety of wearing the guard. However, the history of dentures, mouthguards for sports, Hawley or Frankle appliances, orthodontic positioners, bite splints, and other occlusal devices that have served dentistry so well over the years make this an unreasonable concern.

Indications and applications for nightguard vital bleaching

The primary indication for the nightguard vital bleach­ing technique has been for persons dissatisfied with the original color of their otherwise sound teeth (Figs 1 and 2). Special concerns are for staining related to ingestion of tetracycline as an antibiotic during tooth formation or as an acne treatment during the teenage years (Figs 3 and 4). Other persons interested in bleaching originally had lighter teeth, but now the teeth have been darkened by age, coffee, tea, smoking, or other staining habits (Figs 5 and 6). Brown fluorosis stains are generally responsive, but white spots are unaffected (Figs 7 and 8). Other motivations for treat­ment may warrant consideration. These may include bleaching to avoid any of the developmental personality changes in young persons who are ostracized by their peers for having discolored teeth; persons in public contact areas whose appearance greatly influences their success; or persons who are so dissatisfied with their present appearance that they are considering more invasive procedures, such as bonding, veneers, or crowns. In these instances, bleaching should be con­sidered as an alternative procedure, not as an elective procedure. Bleaching can also prolong the life of un­esthetic but otherwise acceptable dentistry.

Other indications include single teeth that have darkened from trauma, but are still vital or have a poor endodontic prognosis because of the absence of a radiographically visible canal. If all the other teeth are the appropriate color, the section of the guard cover­ing the adjacent teeth can be removed so that material is placed only on the darkened tooth (Figs 9 to 11). If all the teeth are slightly darkened, but one is still darker than the remaining teeth, then a conventional­style guard is constructed and all the teeth are bleached (Figs 12 and 13). Because it has been ob­served that teeth lighten to a certain point, then main­tain that color, the treatment is merely continued on the darker tooth until it approaches or matches the other lightened teeth.

Other options presented in the literature for treat­ing the single darkened tooth have included intentional endodontics or creating an artificial pulp chamber and bleaching the tooth with the walking bleaching technique. Because of the slight potential for cervi­cal resorption, the loss of tooth structure, and the less than 100% chance of success with endodontics, home bleaching should be considered the first choice for altering the color of these teeth.

Often the walking bleaching technique is desirable to ensure the removal of debris and discolored restora­tive materials from the pulp chamber. However, occa­sionally a tooth that has previously been bleached by the walking bleaching technique and sealed with a finished etched composite resin will discolor. In this instance, the first treatment considered should be bleaching the tooth externally with the nightguard vital bleaching technique, especially if the lingual access has since been covered by another restoration, such as an etched‑metal, resin‑bonded fixed partial denture retainer (Fig 14). External bleaching avoids unnecessary removal of an acceptable dental restora­tion, and the loss of tooth structure during the process, which weakens the tooth, and prevents additional insult to the cervical area from another 35% hydrogen peroxide treatment. Even after successful treatment with a walking bleach, often the bleached tooth is more yellow than the other teeth. Nightguard vital bleaching then can be used to harmonize the colors of the vital and nonvital teeth. Teeth that are endodontically treated, but have such a thin portion of remaining dentin at the cervical area that there is concern about potential cervical resorption from use of the 35% hy­drogen peroxide, are also amenable to the nightguard vital bleaching technique as the first choice of treat­ment.

The nightguard vital bleaching technique should be considered as the first choice of treatment for any dis­colored teeth, even those considered for the place­ment of porcelain or other esthetic veneers. Attempt­ing nightguard vital bleaching first may avoid the need for veneers. However, even if the technique is unsuc­cessful in achieving the desired shade, or if there are other indications for veneers other than the tooth color, bleaching may lighten the underlying tooth base and make the subsequent veneer more esthetic, as well as allow the patient to evaluate the results of the more conservative option first. Home bleaching can be used prior to placement of single porcelain‑fused to‑metal or ceramic crowns, fixed partial dentures, or removable partial dentures to offer a lighter, younger­looking shade, as well as to eliminate some of the dif­ficult crack lines or characterizations that are not eas­ily duplicated in ceramic restorations. Nightguard vital bleaching can minimize the discoloration of the stained incisal edges of mandibular teeth and minimize the effects of white‑spot lesions by lightening the tooth structure adjacent to the white‑spot lesion.

Not only is nightguard vital bleaching effective as a preoperative treatment, but it is also effective post­treatment to lighten natural teeth to match existing ceramic crowns, fixed partial dentures, or Dicor resto­rations (Dentsply International) (Figs 15 and 16). This lightening can be achieved to match crowns to adjacent teeth in one arch or to teeth in the opposing arch. Bleaching can also increase the longevity of three­quarters crown abutments, onlays, or resin‑bonded fixed partial denture abutments that have darkened more than their originally matched porcelain poetic (Figs 17 and 18). Bleaching has even been used successfully to increase the life of previous composite resin bonding by lightening the underlying tooth structure to com­pensate for the wear of the composite resin or to lighten the apparent color of veneers already cemented by light­ening the underlying tooth structure. This lightening effect is due to the ability of the carbamide peroxide to pass freely through enamel and dentin and to per­meate to all parts of the tooth, even those protected by restorations.

Although the success and acceptance of the night­guard vital bleaching technique has been phenomenal, it has not eliminated the in‑office bleaching. Some patients' lifestyles do not lend themselves to extended treatment times, or outside‑the‑office appliances. Also, they may not be willing to wait the time for home bleaching to be effective. They may not be con­cerned about the greater financial investment of in­office bleaching or may not be able to wear the guard and tolerate the taste of the solutions used in night­guard vital bleaching. In these situations, in‑office bleaching is indicated. It is also indicated if the patient does not respond well to the nightguard vital bleach­ing regimen. In clinical trials at the University of North Carolina, a single in‑office bleaching treatment, delivered after a lack of response to nightguard vital bleaching, followed by continuation of the nightguard vital bleaching treatment, has achieved results that neither technique showed independently. In those cases, the teeth were not etched, and neither heat nor light was employed. Other recommendations include beginning bleaching with the in‑office treatment, fol­lowed by the home treatment.

Other clinical pilot studies at the University of North Carolina have shown reduction in the buildup of chlorhexidine stains when a 10% carbamide peroxide is used in an alternating fashion with the mouthwash. Other preventive opportunities being explored have included using the nightguard vital bleaching system to attempt to reduce the incidence of root caries that is unresponsive to traditional fluoride and tray sys­tems. This caries is often related to xerostomia and is a sequelae to radiation therapy, chemotherapy, med­ical problems, or aging. There is hope to evaluate the nightguard vital bleaching application in nursing homes or hospitals, where attendants may be able to add this application technique to the oral hygiene reg­imen of patients with inability to perform adequate oral hygiene measures.

Conclusions

The profession should neither propose a sweeping con­demnation nor offer a sweeping endorsement of bleaching any more than it should any other treatment option or medicament used in dentistry. Bleaching techniques that have been shown to be reasonably and relatively safe and effective, both in current usage and over time, should be accepted as a reasonable treat­ment option, knowing the risks and benefits. Con­tinued research should be undertaken on these and all other dental treatments. These accepted techniques include the nonvital bleaching with 35% hydrogen peroxide and/or sodium perborate (but without heat), in‑office vital bleaching with 35% hydrogen peroxide (but without etching), and nightguard vital bleaching (dentist‑prescribed/home‑applied bleaching) with 10% carbamide peroxide materials or similar products. Conversely, claims that any use of hydrogen peroxide will bleach teeth and that all techniques are safe can­not be accepted blindly. Especially in question are the OTC bleaching kits and toothpastes containing car­bamide peroxide. Effectiveness and safety of the bleaching technique must evaluate not only the prod­uct but also the delivery method and treatment time.

Unbiased research is still the best avenue for sifting through the claims and reports to achieve a better un­derstanding of what is correct and what it incorrect. Over time, the understanding of temporomandibular joint function has changed radically, the correlation between occlusion and pain has altered, the change from pins to slots in amalgam restorations has occur­ red, the noncrowning of anterior, endodontically treated teeth has been advocated, and the nonposting of endodontically treated anterior teeth, unless the post is needed to retain the preparation form of the crown, has been reported. So must the dental profes­sion be ever vigilant for changes that provide the most conservative esthetic treatment options for patients. More importantly, the profession should continually examine these treatment options in the light of new evidence or techniques, always applying the same stand­ards of safety to all treatment options.