dental healthcare - pharmaceutical press · dental anatomy and physiology 65 figure 3.1 section...

It is now reasonable to expect a set of permanentteeth to last a lifetime. This contrasts starkly withthe situation only a generation ago, when it waswidely accepted that teeth would have to beextracted and replaced by dentures well beforeold age.

Loss of teeth, other than by accident, is causedby two different pathological processes: dentalcaries and periodontal disease. Today, these arevery rarely life-threatening, although dentaltreatment may produce adverse effects in suscep-tible individuals. Certain pre-existing medicalconditions dramatically increase the risks oftreatment. For example, haemophiliacs are at riskof severe haemorrhage after dental procedures.Subacute bacterial endocarditis may occur inindividuals with a history of rheumatic fever orvalvular heart disease, as a result of a bacteraemiafollowing extractions, calculus removal (scaling),or other invasive dental procedures. Dentalhealthcare in susceptible individuals is, therefore,extremely important. However, for most people,dental disease is more of a social embarrassmentand inconvenience than a serious health risk; atworst, it may reduce the quality of life if manyteeth are lost.

In terms of the effects of dental disease on thecommunity, its treatment is costly and results inloss of time from school or work. Unfortunately,most expenditure is on the treatment of estab-lished disease rather than disease prevention. Inthe UK, millions of teeth are extracted every year.Some extractions are unavoidable (e.g. to reduceovercrowding), but the overwhelming majorityare a direct result of dental disease. An evengreater number of teeth undergo some form ofrestorative treatment. A dedicated commitment

to prevention by the individual is of far greaterbenefit than treatment.

The link between dental caries and diet haslong been recognised. The incidence of dentalcaries increased significantly after the seven-teenth century with the greater consumption ofrefined carbohydrates, particularly sugars. Theprevalence in developing countries has untilrecently been low compared with westernnations, but is now increasing as western-stylediets are adopted. Conversely, the high preva-lence in western nations reached a peak in the1960s, but is now declining as a result ofimproved dental health education and the use offluoride, especially in fluoride-containing tooth-pastes (see Anatomy and morphology below).

Surveys were conducted in the UK in 1973,1983 and 1993 to assess the dental health of chil-dren. The results show that over 20 years, thetotal decay experience of children has fallen dramatically (Downer, 1994):

• by 55% at five years of age• by 82% at eight years of age• by 75% at 12 years of age• by 74% at 14 years of age.

In 1973, just 7% of children of 12 years of age had no experience of permanent tooth decay; by 1993 this figure had risen to 50%. However,marked regional inequalities remain, with muchhigher caries rates in Northern Ireland and Scot-land than in England. It also appears that the rateof decline has levelled out in children of five yearsof age, so there is still room for improvement.

Periodontal disease is responsible for the lossof more teeth than dental caries. Although gener-ally considered a disease of adults, it also occurs

3Dental healthcare

Derrick Garwood

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Sample chapter from Handbook of Pharmacy Health Education, 2nd edition

in children. Surveys of the dental health of adultsin the UK have shown that the majority of peopleaged over 35 with some natural teeth exhibit evi-dence of periodontal disease. As the incidence ofcaries decreases, and the number of teeth that areretained consequently increases, periodontaldisease will assume even more importance as acause of tooth loss. In the past, periodontaldisease was thought to be a normal process ofageing, but this is not the case; it is totally pre-ventable.

Dental healthcare is not new; people haveattempted to clean their teeth with various abrasive substances throughout history. AncientEgyptians used mixtures of burnt egg shells,myrrh, ox hoof ashes and pumice; ancient Greeksused granulated alabaster stone, coral powder,emery, pumice, rust and talcum; and the Romansused bones, hooves, horns, shells and myrrh.Mouthwashes have also been used throughouthistory, and ancient Chinese writings advocatethe use of urine to treat periodontal disease.Toothbrushes or toothpicks in a variety of formshave been employed for thousands of years.

Modern dental healthcare products haveevolved as understanding of the mechanism andprevention of dental disease has increased. Theseproducts have traditionally been sold throughcommunity pharmacies, so the pharmacist canmake a significant contribution to dental healtheducation. However, a sound knowledge of theproperties, actions and uses of the products isessential, together with a basic understanding ofdental anatomy and the aetiology of dentaldisease and its prevention. These subjects and thepharmacist’s role are discussed below.

This chapter is concerned only with diseasesthat affect the teeth and gums. For diseases ofother tissues in the oral cavity, the reader isreferred to Disorders of the ear, nose, andoropharynx in Harman (1990).

Dental anatomy and physiology

The oral cavity is the area between the cheeks,lips, hard and soft palates, and the pharynx; thefloor of the oral cavity is formed by the tongueand its associated muscles. The structures

surrounding the oral cavity have important rolesin:

• masticating food• initiating digestion by salivary enzymes• swallowing food, fluid and saliva• respiration• speech.

Gingivae

The gingivae (gums) cover the alveolar ridges:bony horseshoe-shaped projections of the maxil-lae (upper jaw bone) and mandible (lower jawbone). The gingival epithelium is continuous withthe mucous membrane of the inner surface of thelips and cheeks, and with the epithelium of thehard palate and the floor of the oral cavity.Healthy gingivae are coral pink with a stippledsurface, whereas the oral mucous membrane isred. Folds of soft tissue (called fraena) run betweenthe alveolar ridges and the lips and cheeks. Gingi-val connective tissue forms a collar around eachtooth, and is attached to the tooth surface byjunctional epithelium. There is a shallow trough(the gingival crevice, Figure 3.1) between the crestof gingival tissue and the tooth, which in healthis between 0.5 and 1 mm in depth.

Teeth

The teeth are supported on the upper and loweralveolar ridges, and are important structuresrequired for mastication. They also profoundlyaffect speech, and facial appearance and expres-sion.

Anatomy and morphology

Each tooth consists of the crown, which projectsthrough the gingivae into the oral cavity, and oneor more roots, which anchor the tooth in itssocket (see Figure 3.1). The different types of teeth(Figure 3.2) reflect their varied functions:

• incisors are chisel-shaped and used for cuttinginto food

• canines have a pointed surface (the cusp) fortearing and shredding food

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• premolars (bicuspids) have two cusps forchewing food

• molars have four cusps for crushing and grind-ing.

The cusps of premolars and molars are separatedby fissures, and the whole biting surface of theseteeth is called the occlusal surface. Other surfacesinclude:

• the palatal surface – the surface of upper teethnearest the palate

• the lingual surface – the surface of lower teethfacing the tongue

• the labial surface – the surface of incisors andcanines facing the lips

• the buccal surface – the surface of premolarsand molars facing the cheeks.

The surfaces facing adjacent teeth are alsoimportant because of their association withdental caries and early periodontal disease (seeDental disease below). For effective mastication,each tooth should meet its opposing tooth in theother jaw; if one of the pair is missing, theremaining tooth is less effective because it hasnothing to work against.

Incisors, canines and premolars have only oneroot, with the exception of the upper first pre-molar, which usually has two. Lower molarsusually have two roots and the upper molarsthree, except the third molars, which may haveone, two or three.

The principal component of a tooth isdentine. In the crown, this is covered withenamel; in the root, it is covered with cementum.

Dental anatomy and physiology 65

Figure 3.1 Section through a molar to show the anatomy of a typical tooth.

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Dentine surrounds a cavity containing pulp; inthe crown, the cavity is termed the pulp chamber;in the root, it becomes the root canal.

DentineDentine is a hard yellowish substance consistingof calcium hydroxyapatite, water and an organicmatrix of collagen and mucopolysaccharides. It issensitive to touch and extremes of temperature,although the exact reason for this is not known.Dentine is deposited continuously throughoutlife, gradually reducing the size of the pulp cavity.This normal physiological process proceeds at arelatively slow rate compared with the secondarydeposition of dentine following loss of tooth sub-stance (e.g. as a result of dental caries, excessivewear or cavity preparation).

EnamelEnamel is the hardest substance in the animalkingdom, and consists mainly of calciumhydroxyapatite; the remainder is water and anorganic matrix similar to keratin. The primaryfunction of enamel is to protect teeth from theforces of mastication, which would otherwise

eventually wear them away. Enamel also insu-lates teeth from heat, cold and other pain-producing stimuli. However, it is brittle andrequires the support of dentine; if this support islost (e.g. as a result of caries) it readily fractures.Enamel is thinnest where it approaches the root,but at the cusps (or edges of incisors) it may be upto 2.5 mm thick. Its colour is governed by itsthickness, and it appears lightest and almosttranslucent at the tooth tip. Where the enamellayer is thin, the tooth appears yellow because the dentine beneath shows through. Colour,however, does not indicate the strength of teeth,which tend to darken with age.

CementumCementum is softer than dentine. It is a bone-likesubstance consisting of calcium hydroxyapatiteand an organic matrix of collagen andmucopolysaccharides. It is laid down continu-ously, and the thickness may treble throughoutlife; some cementum is resorbed, but these areasare repaired by further deposition. Cementumattaches the tooth to the socket by means of theperiodontal ligament (see below).


Figure 3.2 Morphology of teeth: (a) Primary dentition (b) Permanent dentition (see Table 3.1 for key to identification ofteeth).

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PulpPulp is composed of loose areolar connective tissuerichly supplied with blood vessels, lymphaticvessels and nerves, which reach it via the apicalforamen. The nerve supply consists of sympatheticnerves and sensory nerves, but as the only sensoryreceptors are pain receptors, all stimuli are per-ceived as pain. Pulp becomes more fibrous and lessvascular with age, and is reduced in overall size asdentine is laid down (see above). These changesreduce the sensitivity of teeth with age.

Periodontal ligamentA tooth is suspended firmly in its socket by the periodontal ligament, which connects thecementum to the underlying bone. Its function isto support the tooth, and protect both tooth andbone from excessive pressures during chewingand biting. The periodontal ligament is com-posed of collagenous fibrous connective tissue,with a rich vascular supply to provide essentialnutrients to the cementum. Its nerve supplyincludes both touch and pain receptors, whichare important in controlling mastication.Cementoblasts and osteoblasts are also present,and are responsible for laying down new cemen-tum and bone, respectively, throughout life.

Dentition

The term dentition refers to the natural teeth andtheir position in the alveolar ridges. In humans,there are two dentitions: the primary dentition(deciduous teeth, baby teeth or milk teeth) andthe permanent dentition. There are 20 primaryand 32 permanent teeth (Table 3.1).

Dental notationTwo different systems are used to identify theteeth in their positions in the alveolar ridges. Inboth systems, the two dental arches are dividedinto four quadrants: the upper left and right, andthe lower left and right (Figure 3.3).

Traditionally, a tooth has been identified byspecifying the quadrant in which it is situated andthe number or letter of the tooth itself; for example,the upper right six or the lower left D. Note,however, that it is always assumed that the observeris facing the patient, causing lateral inversion – as


Table 3.1 The dentitions

(a) Primary dentition (b) Permanent dentition

Figure 3.3 Permanent dentition: (a) Upper jaw (b) Lowerjaw (see Table 3.1 for key to identification of teeth).

A (1) central incisor 1 central incisorB (2) lateral incisor 2 lateral incisorC (3) canine 3 canineD (4) first molar 4 first premolarE (5) second molar 5 second premolar

6 first molar7 second molar8 third molar (wisdom tooth)

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in a mirror. Thus the upper left six is written as6 and the upper right C as C (Figure 3.4).

Today, the International Tooth NumberingSystem is becoming accepted all over the world asthe standard system of tooth identification. Inthis system, each quadrant is assigned a number(Table 3.2).

A tooth is denoted by specifying its quadrantnumber and then its individual number. In thissystem, the deciduous teeth are given thenumbers 1 to 5, not the letters A to E. Thus, theupper left six now becomes 26, and the upperright C becomes 53 (Figure 3.5). In speech, theseare referred to as ‘two-six’ and ‘five-three’, not‘twenty-six’ and ‘fifty-three’.

Tooth developmentTeeth usually start erupting at about six monthsof age with the emergence of the central incisors,followed at about eight months of age by thelateral incisors. The first molars appear at about12 months of age, the canines at about 18months of age, and the second molars at about 24months of age, although there is wide individualvariation. As a general rule, lower teeth tend toerupt before the corresponding upper teeth.

Contrary to popular belief, there is little evidence to suggest that the eruption of teeth inchildren causes systemic illness. As teeth begin toerupt, the shape of the jaw bone changes. Prema-ture loss of primary teeth may adversely affect thesubsequent spacing of the permanent teeth andthe shape of the jaws.

Teeth are mineralised before eruption, so theyare hard enough to withstand the rigours of mastication immediately. Secondary maturationtakes place after eruption; this is an importantprocess in increasing their resistance to dentalcaries (see Dental disease below). Fluoride is par-ticularly important in this process (see Preventionof dental disease below).

Teeth may become stained during develop-ment as a result of:

• systemic administration of some drugs (e.g.tetracyclines)

• ingestion of high levels of fluoride (see Pre-vention of dental disease below)

• systemic illness (e.g. chickenpox or measles).


E D C B A

E D C B A

A B C D E

A B C D E

8 7 6 5 4 3 2 1 1 2 3 4 5 6 7 8

8 7 6 5 4 3 2 1 1 2 3 4 5 6 7 8

UPPER RIGHTQUADRANT

LOWER RIGHTQUADRANT

UPPER LEFTQUADRANT

LOWER LEFTQUADRANT

(a) Primary dentition

(b) Permanent dentition

UPPER RIGHTQUADRANT

LOWER RIGHTQUADRANT

UPPER LEFTQUADRANT

LOWER LEFTQUADRANT

Figure 3.4 Traditional notation system.

1 upper right quadrant, permanent dentition2 upper left quadrant, permanent dentition3 lower left quadrant, permanent dentition4 lower right quadrant, permanent dentition5 upper right quadrant, deciduous dentition6 upper left quadrant, deciduous dentition7 lower left quadrant, deciduous dentition8 lower right quadrant, deciduous dentition

Table 3.2 Quadrants in the International ToothNumbering System

55 54 53 52 51

85 84 83 82 81

61 62 63 64 65

71 72 73 74 75

18 17 16 15 14 13 12 11 21 22 23 24 25 26 27 28

48 47 46 45 44 43 42 41 31 32 33 34 35 36 37 38

QUADRANT 5

QUADRANT 8

QUADRANT 6

QUADRANT 7

(a) Primary dentition

(b) Permanent dentition

QUADRANT 1

QUADRANT 4

QUADRANT 2

QUADRANT 3

Figure 3.5 The International Tooth Numbering System.

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These are intrinsic stains and cannot be removedfrom the tooth substance. Pathological lesions(e.g. dental caries or pulp necrosis, see Dentaldisease below) may cause intrinsic stains in devel-oped teeth.

The entire set of primary teeth is lost betweensix and 12 years of age, and replaced by the per-manent dentition. This permanent set is not,however, completed until adulthood. The first per-manent teeth to erupt are the first molars at aboutsix years of age, followed by the central incisors atabout seven years of age. The lateral incisorsappear at about eight years of age, and the canines,first premolars and second premolars betweennine and 11 years of age. The second molars eruptat about 12 years of age, and the third molars(wisdom teeth) between about 17 and 21 years ofage. Human evolution has resulted in a jaw thatmay be too small to accommodate the full denti-tion. In many cases, the third molars do not eruptfully but remain impacted; if they cause pain andinfection, they must be surgically removed. Insome cases, third molars fail to develop at all.

Saliva

Approximately 0.5 to 1.5 litres of saliva is secretedeach day. There are three pairs of salivary glands:the sublingual and submandibular glands in thefloor of the oral cavity, and the parotid glands (thelargest) below each external auditory meatus. Sali-vary flow is affected by various factors (e.g. age,sex, nutritional and emotional state, time of dayand season of the year). Over 50% of unstimulatedsaliva (resting saliva) is secreted from the sub-mandibular glands, whereas more than 50% ofstimulated saliva comes from the parotid glands.

Saliva is formed from serum and composed ofwater (99.5%) containing dissolved proteins andinorganic ions. The proteins include glycopro-teins (mucin), albumins, globulins and enzymes.One major protein component is the enzymeamylase, which initiates digestion of starch in the oral cavity. Antibacterial enzymes are alsopresent. The watery and mucinous character ofsaliva is important in:

• lubricating the mucous membranes of the oralcavity

• facilitating chewing and swallowing• assisting speech.

The inorganic component includes bicarbonate,calcium, chloride, magnesium, phosphate, pot-assium, sodium and sulphate.

The proportions of the different componentsvary with the source of the saliva and also withthe flow rate. This has the effect of changing thepH of submandibular saliva from 6.47 (flow rateof 0.26 mL/minute) to 7.62 (flow rate of3.0 mL/minute), and of parotid saliva from 5.8(flow rate of 0.1 mL/minute) to 7.8 (flow rate of3.0 mL/minute).

Saliva helps maintain oral hygiene andprevent dental disease in several ways:

• the bicarbonate and phosphate content acts asa buffer in acidic environments

• antibacterial enzymes (e.g. lysozyme and lactoperoxidase) control oral bacteria

• inorganic components help re-mineralisetooth enamel and prevent dental caries

• water and mucin assist the tongue in clearingfood debris and bacteria from the gingivae andteeth.

Saliva is continuously secreted to keep themucous membranes moist, but the flow increasesdramatically in response to stimulation by food.Heavy secretion of saliva continues after food hasbeen swallowed, to clean the mouth and bufferany acidic components.

Reduced secretion of saliva causes a dry mouth(xerostomia). This may result from certainmedical conditions (e.g. anaemia or diabetes mel-litus) or as a side-effect of some drugs (e.g. adren-ergic neurone blocking drugs, antidepressants,antihistamines, antimuscarinics, anxiolytics,diuretics, hypnotics or lithium). Sympatheticstimulation in response to fear or anxiety causesthe glands to stop secreting, giving a character-istic lack of saliva. Radiotherapy to the head andneck can also reduce salivary flow, although itusually returns to normal after a period ofmonths.

Dry mouth may be relieved by administeringArtificial Saliva DPF, an inert, slightly viscous,aqueous liquid containing sodium chloride,hypromellose ‘4500’, benzalkonium chloride, saccharin sodium, thymol, peppermint oil,


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spearmint oil and amaranth solution. Alternativeformulations may be used, and several commer-cial preparations are available. Frequent sips ofcool drinks and sucking pieces of ice or sugar-freepastilles may also be of value.

Dental disease

Two distinct dental diseases may ultimately resultin loss of teeth: dental caries and periodontaldisease. Both diseases can occur at any age, butdental caries is generally more prevalent in children, and periodontal disease in adults. Theaetiology of each disease is different, but thecommon factor is the presence of bacteria indental plaque.

Plaque

Plaque is a film of soft material that forms on theteeth, gingivae, restorations and orthodonticappliances. It is composed predominantly ofmicro-organisms, but other constituents include:

• dietary carbohydrates• organic acids formed by the bacterial metabol-

ism of carbohydrates• glucans (dextrans) resulting from the metabol-

ism of dietary carbohydrates by streptococci• proteins (including enzymes) from saliva• leucocytes• toxins from Gram-negative bacteria.

The first stage of plaque formation is the develop-ment of the salivary pellicle, a thin layer of muco-proteins derived from the glycoproteins of saliva.Mucoproteins are unstable in solution andadsorb to hydroxyapatite in tooth enamel. Pelli-cle formation begins immediately after cleaningthe teeth, and the whole of the crown, exceptareas exposed to friction, becomes covered. Thepellicle readily takes up extrinsic stains (seebelow). These are not necessarily harmful to theteeth, but are unattractive and generally con-sidered socially unacceptable. The pellicle is veryquickly colonised by commensal bacteria to formplaque.

Streptococcus spp. are usually the first bacteria

to form colonies on the salivary pellicle, afterabout three to eight hours. Streptococcus mutansis of particular importance. Actinomyces spp.may also be found at this stage. After 24 hours,other species, including Gram-negative anaer-obes, are attracted and start to multiply. Thebacterial composition continues to becomemore complex, and the earlier species ofcolonising microorganisms assume less import-ance. Plaque reaches its mature state after aboutseven days. Micro-organisms make up about70%, although the exact composition variesfrom one area of the oral cavity to another,depending upon the micro-environment andaccessibility for cleaning. Mature plaque has adifferent role from new plaque in the aetiologyof dental disease.

Food is not essential for plaque formation, butthe presence of dietary sugars, especially sucrose,increases its rate of formation and thickness. Bac-teria utilise sugars as an energy substrate, produc-ing extracellular mucilaginous polysaccharides(glucans), which provide the plaque matrix andfacilitate the firm adhesion of plaque to the toothsurface.

Plaque is highly tenacious and can only beremoved from the teeth by mechanical means(see Prevention of dental disease below). It formsrapidly over all tooth surfaces after cleaning,and is virtually always present in areas that aredifficult to clean. Plaque can only be detectedduring the initial stages of formation by usingdisclosing agents (see Prevention of dentaldisease below). However, if deposits are allowedto build up, it becomes clearly visible. In theearly stages of development, plaque is thoughtto be cariogenic; mature plaque, however, ismore likely to influence the development ofperiodontal disease.

Staining of the salivary pellicle or plaque mayoccur. Such extrinsic stains can be removed andshould not be confused with permanent intrin-sic stains that are part of the tooth substance (seeAnatomy and morphology above). The com-monest extrinsic stain is tar from tobacco,usually found on the lingual surfaces of thelower teeth and ranging in colour from lightbrown to black. The degree of staining generallyreflects the standard of oral hygiene rather thanthe amount of tobacco smoked. Brown-black


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stains may occur following use of chlorhexidinemouthwashes, and plaque may become staineda dull yellow by food dyes. Children sometimeshave black or green stains; these are thought tobe derived from chromogenic bacteria.

Calculus

Dental calculus (tartar or scale) is mineralisedplaque, which may occur in any area of themouth. Prevalence is high in most populationsand increases over 30 years of age. Calculus iscomposed of inorganic salts (70%) plus organicmaterial and micro-organisms (30%). Composi-tion varies with location and the age of the cal-culus. The organic constituents are similar tothose of plaque, and the micro-organisms com-parable to those in mature plaque.

Plaque acts as an organic matrix for calculusformation, although the exact mechanism isunknown; it is possible that a plaque com-ponent acts as a seeding agent. Calculus pro-vides a hard, rough surface for the formation ofmore plaque, which is difficult to remove andmay itself become calcified; in this way, incre-mental layers of calculus are built up. Calculusformation usually begins between two and 14days after the start of plaque development, butmay be as early as four to eight hours in someindividuals, and does not appear to be depen-dent on diet.

Calculus above the gingival margin (supragin-gival calculus) is formed from the minerals insaliva. It is especially prevalent opposite the ductsof the principal salivary glands (i.e. on the lingualsurface of lower front teeth and the buccal surfaceof upper molars). Supragingival calculus is mod-erately hard and usually white or pale yellow,although it may become stained by tar fromtobacco or pigments from food.

Subgingival calculus occurs below the gingi-val crest. It contains fewer micro-organisms thansupragingival calculus, is difficult to remove,very hard, and stained a dark colour by thebreakdown products of blood. Previouslythought to cause periodontal disease, subgingi-val calculus is now considered to be merely anindicator of its presence. However, calculus does influence the development of periodontal

disease by virtue of the plaque deposits presenton its surface.

Dental caries

Definition and aetiology Dental cariesdestroys the mineralised portion of the tooth,and is one of the most common diseases inwestern society; prevalence in the UK is particu-larly high. Once established, the disease processis irreversible; unless treated, it leads inexorablyto destruction of the tooth.

Dental caries is a disease of the modern world.Numerous studies have demonstrated that a highsugar diet is implicated in its aetiology, althoughthe exact mechanism remains unclear. However,it is known that sugars alone do not cause dentalcaries; it is the combination of sugars in the oralcavity and plaque on the teeth. Dietary sugarsdissolved in saliva readily diffuse into plaque,where bacteria (particularly streptococci in earlyplaque) ferment them to produce organic acids(e.g. lactic acid). These acids demineralise toothenamel and dentine. Bacteria then invade,causing infection and inflammation. The infec-tion progressively destroys the dentine until thepulp is reached. If unchecked, this eventuallyresults in pulp death. Infection then spreadsthrough the apical foramen to the apical part ofthe periodontal ligament and an abscess mayresult.

The frequency of sugar consumption has agreater influence than the quantity consumed(National Dairy Council, 1995). However, thequantity consumed is important in increasingplaque thickness and the rate of formation (seePlaque above). The incidence of caries is higher inchildren and adolescents than in adults becausesecondary maturation of dental enamel graduallyincreases its resistance to acid attack. Fluoridealso increases the resistance of enamel.

Several host factors may influence the initialdevelopment of caries or the rate of decay. Thestructure of teeth varies between individuals, andthe presence of deep fissures and pits predisposesto caries formation. The chemical composition ofenamel also varies, and some people have teeththat are more resistant to acid attack than others.Crowded or badly aligned teeth render good

Dental disease 71

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plaque control difficult; the resultant stagnationareas are more susceptible to caries.

Although dental caries may attack any surfaceof the tooth, more than 50% of lesions affect theocclusal surfaces of back teeth, with marginallymore occurring in the upper arch than the lower.First molars appear to be more susceptible thanother teeth, whilst the lowest prevalence is inlower incisors and canines. There are three typesof caries:

• Pit and fissure cariesLesions that occur in pits and fissures are themost common type of caries. The initial breakin the enamel is seen as a small black pit,which may extend into dentine. The under-lying dentine is destroyed more quickly thanenamel, and eventually a bluish-white areaappears around the initial pit. The enamel col-lapses as more of the underlying dentine isdestroyed, and the later stages are marked byan open cavity.

• Smooth surface cariesSmooth surface caries is the least common. Itcan occur on any smooth surface, but particu-larly on the proximal surfaces between teeth.Lingual surfaces are affected less frequentlythan buccal or labial surfaces. The lesion initi-ally appears chalky-white, becoming graduallyrougher as the enamel starts to break down.The subsequent stages are the same as in pitand fissure caries.

• Cervical cariesCervical caries is more common in olderpeople. It attacks exposed dentine at the neckof the tooth, where the crown meets the root.As there is no enamel at this point, an opencavity is formed from the beginning. The sub-sequent stages are as described above under pitand fissure caries.

On average, it takes about two years for a cavityto be clinically visible in permanent teeth,although there is wide individual variation. Thetime span may be as short as three months inprimary teeth.

Rampant caries (‘dummy’ caries or ‘bottle’caries) occurs in infants allowed to suck com-forters (dummies) coated with sugary substances(e.g. honey, jam or undiluted fruit syrups). Drink-ing concentrated sweetened liquids from feeding

bottles produces the same effect. Such practicesallow prolonged contact between the teeth andsugar, resulting in severe and extensive cariesaffecting several teeth, particularly the upperincisors.

The properties of saliva (e.g. mineral composi-tion, viscosity and rate of production) varybetween individuals, affecting their susceptibilityto caries. Saliva is the body’s natural means ofcleaning and buffering the oral cavity. It is alsoinvolved in the re-mineralisation of enamel,which can reverse early dental caries (see below).Xerostomia, caused by a reduction in salivarysecretion (see Anatomy and morphology above), isassociated with an increased incidence of caries.

Symptoms The initial stages of dental cariesare asymptomatic. Pain is first felt when dentineis exposed during the open-cavity stage, althoughthere is wide variation in the degree of painexperienced. Short-term pain on exposure toheat, cold or sweet substances during the earlystages of decay indicates that prompt treatmentmay save the pulp from irreversible damage.

Inflammation of the pulp (pulpitis) producesswelling of the pulp tissue in an enclosed area.This sometimes results in a throbbing pain thatis exacerbated by heat and relieved by cold.Pain lasting for some time (e.g. up to 20minutes) indicates that damage to the pulp isirreversible. Severe pain that is unconnectedwith any stimuli or disturbs sleep signifiesextensive decay. If untreated, the pain eventu-ally subsides once pulp necrosis occurs, becauseof degeneration of the nerve supply. However,the infection may spread through the apex andcause inflammation of adjacent tissues. A peri-apical abscess may then occur, which can beextremely painful during the acute phase aspressure builds up in the enclosed space aroundthe apical foramen. The pain is exacerbated bypressure on the tooth and subsides once the pushas discharged.

Treatment Early dental caries is reversiblebecause minerals present in saliva allow re-mineralisation of the enamel to take place. Theorganic matrix is still intact at this stage, whichallows the deposition of further crystals. Once the matrix collapses, this is impossible.


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Re-mineralisation is more likely to be successful iffurther acid attack is kept to a minimum by strictplaque and dietary sugar control. Fluoride ishighly beneficial in re-mineralisation (see Preven-tion of dental disease below), as it converts theinorganic hydroxyapatite in enamel to the moreresistant fluorapatite.

Irreversible caries may require a variety oftreatments, including:

• restorations (fillings)• root canal treatment (endodontics)• crowns or bridges• extraction.

Analgesics may be given for pain relief untildental treatment is available, but controlling thepain does not in any way control the disease, anddental referral should not be delayed longer thannecessary. For measures to prevent dental caries,see Prevention of dental disease below.

Periodontal disease

Definition and aetiology Periodontal diseaseencompasses several inflammatory disorderswhich affect the supporting structures of theteeth. It is one of the most common conditionsin the world, affecting the vast majority of peopleat some stage in their lives. Chronic periodontaldisease is slow, insidious and usually painless, butthe eventual result may be destruction of theunderlying bone. It causes the loss of more teeththan dental caries because the supporting struc-tures cannot be repaired as effectively as teeth canbe restored.

Like dental caries, periodontal disease iscaused by plaque bacteria. However, diet is notthought to be an important factor in its develop-ment, and dental caries is not a cause; completelyundecayed teeth can be affected. Plaque depositsaround the gingival margin and within the gin-gival crevice are most important in the aetiologyof periodontal disease.

Where inflammation is confined to the gingi-vae, the condition is called gingivitis. Spread ofinflammation to the periodontal ligament andalveolar bone is termed periodontitis. Chronicgingivitis precedes chronic periodontitis, butdoes not always lead to it. The reason why somecases progress and others do not is not known.

Prevention of chronic gingivitis therefore pre-vents chronic periodontitis. Gingivitis may alsobe an acute condition, but, unlike chronic gin-givitis, this is always painful.

Chronic gingivitis

Definition and aetiology Chronic gingivitis isthe result of inflammatory changes produced inthe gingivae by endotoxins and enzymes fromplaque bacteria. Undisturbed plaque depositsmay cause the initial inflammatory reactionwithin two to four days.

Some medical conditions (e.g. diabetes melli-tus, leukaemias and scurvy) may increase the riskof chronic gingivitis. The precise mechanism forthis is unknown, but it may be a result of alteredhost response to bacterial products (e.g. toxinsand enzymes). Administration of some drugs (e.g.cyclosporin, nifedipine, oral contraceptives orphenytoin) may also predispose to gingivitis. Insome cases, these may cause severe gingivalhyperplasia in which the gingivae cover most ofthe crown of the tooth. Any disorder or drugwhich reduces salivary secretion increases thesusceptibility to chronic gingivitis (see also Dentalcaries above).

People who habitually keep their lips apart,particularly when asleep, show a greater inci-dence of inflammation of the anterior gingivae,most likely as a result of excessive drying of thetissues. Smokers are also more susceptible; it isnot certain whether this is caused by tobaccosmoke or poor oral hygiene, which has beenshown to be greater in smokers than non-smokers.

Pregnant women are more susceptible to gingivitis (‘pregnancy gingivitis’) as a result ofhormonal changes affecting connective tissues,including those of the gingivae. Some pregnantwomen may even complain of loose teeth.Scrupulous oral hygiene will prevent pregnancygingivitis, and the tissues revert to normal afterparturition. Puberty is also commonly associatedwith an increased incidence of gingivitis; again itis not clear whether this is associated with hor-monal changes or poor standards of oral hygiene.

Symptoms Inflammation results in oedema,causing the gingival crevice to deepen and

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pockets to develop between the gingivae and theteeth. At this stage, these are called ‘false pockets’;they should not be confused with the true peri-odontal pockets of chronic periodontitis (seebelow). The epithelium of the crevice becomesulcerated. Subgingival plaque accumulates in the deepened crevices, and bacterial productsproduce further inflammation. A vicious cycle isset up, which causes the crevices to enlargefurther.

In the presence of gingivitis, gingival crevicularfluid exudes through the junctional epitheliuminto the gingival crevice. This cannot be detectedby the patient, but can be measured using crevicu-lar strips (small filter paper strips), and is an indi-cator of the extent of inflammation. Crevicularfluid contains immunoglobulins (IgA, IgG andIgM) and neutrophils (polymorphonuclear leuco-cytes), which may exert a protective effect.

The outward symptoms of chronic gingivitisare mild, so many sufferers do not realise theyhave the condition. Established chronic gingivi-tis is marked by changes in appearance: the gin-givae become reddened, glossy, soft and swollen.Halitosis may also be present. Pain is usuallyabsent, although abrasive food or vigorous tooth-brushing may produce discomfort. The mainsymptom, bleeding gums, is all too often attrib-uted to toothbrushing trauma and ignored.

Treatment Mild chronic gingivitis can betreated by good plaque control (see Prevention ofdental disease below). The only dental treatmentrequired may be oral hygiene instruction, but it iswise to refer patients to their dentist. In manycases, scaling is necessary. This involves theremoval of plaque and calculus from the crownand exposed root surfaces. The surfaces are thenpolished to remove any rough areas that mayattract plaque accumulations. For measures toprevent chronic gingivitis, see Prevention ofdental disease below.

Chronic periodontitis

Definition and aetiology Chronic periodonti-tis, which is always preceded by chronic gingi-vitis, results in irreversible damage to theperiodontal ligament and alveolar bone. It is rarein children under 13 years of age, but becomes

more common from the late teens onwards. It isthe most common cause of loss of teeth inpatients over 30 years of age.

Symptoms Inflammation spreads through thegingival crevice and eventually destroys the peri-odontal ligament, with the junctional epitheliummoving downwards onto the root. A true peri-odontal pocket is formed and gingival recessionmay occur, exposing the coronal portion of theroot. As periodontal pockets deepen, plaque anddebris can collect within them, exacerbating theinflammatory process. The depth of the pocketsmay be measured using a dental probe and indicates the progression of the disease. Furtherspread of inflammation to the supporting bonecauses resorption, which eventually loosens theteeth.

Many symptoms of chronic gingivitis arepresent. As the periodontal pockets deepen,however, the swelling and reddening of the gin-givae may subside, leading to the mistaken beliefby the patient that the gingivitis has resolved. Infact, inflammation is still present, but is nowmuch deeper in the tissues. Chronic periodonti-tis eventually causes extensive damage that islargely irreversible, and patients should seektreatment at the earliest opportunity (Figure 3.6).

Treatment Treatment of chronic periodontitisis similar to that of chronic gingivitis (see above).It involves thorough scaling and polishing,usually over several appointments. Root planingto clean the roots and remove infected cemen-tum is usually necessary. In severe cases, whereperiodontal pockets are very deep, surgery may


initial lesion

early lesion

established lesion

advanced lesion

gingivitis(reversible)

periodontitis(irreversible)

years

�Figure 3.6 The chronological progression of gingivitis toperiodontitis.

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be required to reshape the gums and facilitateroutine plaque removal by the patient. In the lastfew years, it has become possible to replace lostalveolar bone by sophisticated techniques (e.g.periodontal bone grafting and guided tissueregeneration), but these are highly specialisedand not widely available.

Chlorhexidine mouthwash or gel may beuseful to control plaque deposition, but is no sub-stitute for toothbrushing. It is not recommendedfor long-term use, may stain the teeth, andshould be restricted to the treatment phase.

Treatment of chronic periodontitis may be along process, and is heavily dependent onimproved home dental care by the patient. Oralhygiene measures alone will not arrest chronicperiodontitis, but serve as a valuable adjunct toperiodontal treatment and are essential toprevent further disease. Corrective measures (e.g.restorations or orthodontic procedures) in areasprone to plaque accumulation may also be beneficial. For measures to prevent chronic peri-odontitis, see Prevention of dental disease below.

Periodontal abscess

Definition and aetiology A periodontalabscess may develop from a periodontal pocketwhich becomes blocked with exudate or a foreignbody (a lateral periodontal abscess). Alterna-tively, infection of the pulp may spread throughthe apical foramen (periapical periodontalabscess).

Symptoms Both types of periodontal abscesspresent with a throbbing pain, exacerbated bypressure on the tooth involved. Gingivae in thearea of the abscess become red and swollen; thismay spread to surrounding tissues (e.g. thecheeks or lips). Once pus has discharged, theacute phase subsides and, if untreated, often leadsto a painless chronic abscess which may continueto exude pus. Abscesses cause further resorptionof the surrounding bone.

Treatment Treatment of periodontal abscessesmay involve drainage, mouthwashes andadministration of antibiotics. Root canal therapy,extraction or periodontal surgery may sub-sequently be required.

Juvenile periodontitis

Definition and aetiology Juvenile periodonti-tis (periodontosis) is a chronic periodontaldisease occurring in adolescents and youngadults. Its development appears to be indepen-dent of the level of oral hygiene. The cause of thissevere chronic periodontal disease is not known,although it has been suggested that the bacterialflora in the mouths of sufferers may be exces-sively virulent.

Symptoms The features of juvenile periodonti-tis appear similar to chronic periodontitis, but itsearly onset and associated bone loss make it amore serious condition. Pain is usually absentunless a lateral periodontal abscess develops. Themost common presenting features are drifting ofteeth and localised periodontal pockets. These areusually only apparent during dental examin-ation; radiographs may also show severe boneloss. The disease often progresses relentlesslydespite dental intervention, and the prognosisfor affected teeth is not good.

Treatment Treatment is similar to that forchronic periodontitis, but more follow-upexaminations are required to monitor progress ofthe disease. Periodontal surgery is not always successful. Treatment may have to rely on strictplaque control measures plus frequent scaling,root planing and polishing. Chlorhexidine solu-tion is only of value if it can penetrate the peri-odontal pockets, which in juvenile periodontitisare very deep; use of a syringe with a suitablenozzle may be required.

Primary herpetic gingivostomatitis

Definition and aetiology Primary herpeticgingivostomatitis is an acute gingivitis occurringmainly in children between six months and fiveyears of age. It is caused by a primary infectionwith herpes simplex virus type 1 (HSV 1). Onrecovery, the virus lies dormant in the ganglia ofthe trigeminal nerve and produces latent herpeslabialis (cold sores) in response to various stimuli(e.g. emotional disturbance, fever, menstruation,sunlight or local trauma).

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Symptoms Symptoms include fever, malaise,gingivitis, pharyngitis and generalised adenopa-thy. Vesicles appear all over the oral cavity and onthe lips, rupturing to form excessively painfululcers. Accompanying symptoms may includeprofuse salivation and halitosis. The childappears unwell, irritable, unable to eat, and has ahigh temperature.

Treatment The condition is self-limiting, anduntreated ulcers heal without scarring within 14to 21 days. Treatment is not generally given forprimary HSV 1 infection, but measures that maybe taken to relieve the discomfort include para-cetamol for pain, bland mouthwashes and softfood. Chlorhexidine mouthwash or gel may be ofvalue as an alternative to toothbrushing until thepain subsides. Where secondary infection occurs,systemic antibiotics may be necessary.

Acute ulcerative gingivitis

Definition and aetiology Acute ulcerative gin-givitis (acute necrotising ulcerative gingivitis,trench mouth or Vincent’s disease) is an acute,destructive, ulcerative condition affecting thegingivae. It occurs most commonly between 14and 30 years of age. The micro-organisms mostoften present are fusiform bacilli and spiro-chaetes, but the evidence suggests that these arenot the causative agents. Predisposing factors arestress, worry, and fatigue. After an initial attackthere is a strong tendency for recurrence.

Symptoms Acute ulcerative gingivitis is ofsudden onset, usually begins in the gingival papil-lae, and may extend throughout the gingivae. It ischaracterised by general malaise, marked gingivalbleeding, inflammation and swelling. Fever isgenerally absent, but the pain may be so severe asto render eating and talking impossible. Halitosisand excessive salivation are also common.Characteristic ‘punched-out’ grey ulcers, whichbleed readily, often develop at the crest of the gin-gival papillae. These ulcers develop a pseudomem-brane composed of a necrotic grey slough.

Treatment Treatment comprises the adminis-tration of metronidazole or nimorazole in conjunction with local debridement of necrotic

and infected tissue. Hydrogen peroxide mouth-washes may be used between dental appoint-ments, and the patient should be fully instructedin good oral hygiene procedures. All patientsshould be followed up regularly as tissue destruc-tion may make subsequent plaque removal diffi-cult in some areas.

Tooth wear

Definition and aetiology Recent evidence sug-gests that tooth wear is now a significant problemin both children and adults (Smith, Bartlett andRobb, 1997). It is rarely possible to differentiatebetween the different aetiological factors, but thedental profession is particularly concerned aboutdental erosion. This may be defined as the pro-gressive loss of hard dental tissues caused by theaction of acids on the teeth, without the involve-ment of bacteria.

Erosion may result from occupational exposureto acid fumes or chronic contact with gastric acidas a result of frequent vomiting or oesophagealreflux. However, the frequent ingestion of dietaryacids, in the form of carbonated drinks and fruitjuices, is now considered to be of major import-ance, particularly in children. The extent of theproblem was measured by the 1993 Child DentalHealth Survey. 52% of children of five and sixyears of age had erosion of the deciduous incisors,and the permanent teeth of more than 30% ofthose of 14 years of age were affected (Office ofPopulation Censuses and Surveys, 1994).

Prevention and treatment Prevention consistsof reducing the frequency of contact with thecausative agent, where this can be identified.Teeth that are severely worn may require exten-sive restoration work.

Gingival recession

Definition and aetiology Gingival recessionmay occur in healthy mouths, even in theyoung. Recession can take place around teeththat have a thin bone covering, teeth that are subject to excessive biting forces or wherethere are bony defects. Trauma produced by


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over-zealous toothbrushing may exacerbate thisprocess.

Symptoms The gingivae are pushed back andthe underlying cementum is worn away toexpose dentine. This may cause increased sensi-tivity and pain, particularly on exposure to heat,cold or sweet substances. Gingival recession canincrease the risk of developing root caries.

Treatment The primary cause of recessionshould be eliminated where possible. Forexample, selective grinding by the dentist is aneffective way of equalising biting forces andreducing excessive loading on an individualtooth. Desensitising toothpastes (see Preventionof dental disease below) may be used to reduce thesensitivity of the dentine. Topical application ofsuch a toothpaste directly to the sensitive areamay also be beneficial. Fluoride varnishes may beapplied by the dental surgeon to promote re-mineralisation of the exposed dentine. Thepatient should be encouraged to adopt a less vigorous toothbrushing technique to preventfurther recession.

Halitosis

Definition and aetiology Halitosis (badbreath) is characterised by an offensive breathodour. It is highly prevalent and is a source ofsocial embarrassment to many.

Halitosis is often a symptom of periodontaldisease. However, abnormal breath odours areproduced by elimination of certain substances viathe lungs, and may be a symptom of systemicdisease (e.g. ketones in uncontrolled diabetesmellitus or ammoniacal compounds in uraemia).However, in the majority of cases, halitosis resultsfrom anaerobic bacterial putrefaction in the oralcavity and is not caused by systemic disease. Mal-odorous breath may also arise following smoking,alcohol consumption or ingestion of certainfoods (e.g. garlic).

Treatment Halitosis may be controlled byminimising the oral bacterial population. Allmeasures advocated to reduce the level of gumdisease and hence bleeding (see Prevention of

dental disease below) will also improve breathodour.

Mouthwashes (see Prevention of dental diseasebelow) are often used to freshen the breath,although their value in treating halitosis is ques-tionable.

Prevention of dental disease

Dental disease may not be life-threatening, but itcan severely affect the quality of life. Loss ofmany or all the permanent teeth necessitates theuse of dentures, which can create a different setof problems. For the young, the social stigma ofwearing dentures is now much greater than in the past, when the wholesale loss of teeth wascommon.

Lost teeth which are not replaced by denturescreate problems for the remaining teeth, and mayeven alter the shape of the jaw. Adjacent teeth tendto tilt or drift into the gaps, which may alter thebiting pattern. Loss of one tooth from a comple-mentary pair may limit chewing movementsbecause the remaining tooth has nothing to biteagainst, and it often over-erupts. There is also thepsychological aspect of altered appearance,because gaps in the permanent dentition are notgenerally considered attractive. Premature loss ofprimary teeth may affect the spacing of the sub-sequent permanent teeth and influence jawdevelopment.

Decayed teeth may be restored if treated intime, but scrupulous dental healthcare is essen-tial to save them from further damage. Secondarycaries may form around the margins or under-neath a filling if bacteria and sugar can gainaccess. Should this occur, the tooth must be refilled. Subsequent fillings are larger, andeventually the tooth may need to be crowned oreven extracted.

It is absolutely essential that the gingivae arein peak condition before advanced dentistry iscarried out, because the position of the gingivalmargins is used as a reference point. Inflamedgingivae may be swollen and cover more of thecrowns of the teeth than normal. If the inflammation subsequently subsides followingimprovements in dental healthcare, the margins

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may recede to a more normal position and, for example, expose the edges of crowns andbridges.

Almost all dental disease is completely pre-ventable, but this requires a high degree of moti-vation on the part of the individual. The onlypassive measure available is water fluoridation,which reduces the incidence of dental caries butnot periodontal disease. Both caries and chronicperiodontal disease are painless conditions untilthe later stages, by which time irreversibledamage has already occurred. Many people areunable to appreciate that a problem exists if thereare no outward signs and symptoms. Conse-quently, they cannot easily be convinced of theneed to take preventive measures. This representsone of the greatest barriers to be overcome indental health education.

Plaque control

Plaque control is the basis of prevention of dentaldisease. Plaque bacteria, particularly those ofmature plaque, are responsible for the vast major-ity of periodontal disease; therefore, preventionis aimed at keeping the level of plaque to anabsolute minimum. The role of plaque in dentalcaries is more complex because it is the combi-nation of sugar and plaque that results in toothdecay (see Dental disease above). Theoretically, ifplaque were removed from the teeth immediatelybefore consuming sugar, dental caries would notdevelop. However, for most people this is totallyimpractical. It is also unlikely that the teeth areever completely plaque-free, because plaqueforms extremely rapidly after cleaning, and someareas are inaccessible. Prevention of caries must,therefore, combine both good plaque control andsugar control.

The most effective means of removing plaquefrom teeth is with a toothbrush; invariably,toothpaste is used as well. Regular toothbrushingis begun by many people when young and continued throughout life. However, in manycases, the brushing regimen is inadequate forcomplete plaque control. Some areas of the den-tition cannot be reached by a toothbrush, andadditional methods (e.g. dental floss or inter-proximal brushes) must also be employed.

Disclosing agents

Plaque cannot readily be seen on teeth, making itdifficult to convince an unwilling or scepticalperson of its presence. A disclosing agent thatstains plaque should be recommended. Variousproprietary disclosing tablets and fluids are avail-able. Some can distinguish between new andmature plaque, staining each a different colour.Re-application after brushing serves to illustratethe effectiveness of brushing technique and high-light areas where improvements may be required.Patients should be advised to smear white softparaffin on their lips, to prevent discoloration bythe dye contained in the disclosing agent.

Toothbrushing

Toothbrush designSelecting a toothbrush can be daunting whenfaced with the vast array of designs available,backed up by impressive claims from manu-facturers. In reality, there is no general consensusof opinion on the best design for a toothbrush,and the ultimate selection is based on personalpreference. However, certain factors may helpwhen making a choice.

Nylon bristles are preferable to natural bristlesbecause they do not absorb fluids or harbourmicro-organisms as readily, and the control ofbristle quality during manufacture is easier.Natural bristle toothbrushes also have the dis-advantage that they become soft (and thereforeless effective) when wet. Multi-tufted, small bristles are better than fewer, larger bristles.Rounded ends to the filaments generally offer nomajor advantage over cut ends, although theymay prevent soft tissue injury by over-enthusi-astic toothbrushers.

Soft-texture brushes are less efficient in remov-ing plaque than medium brushes, but may be ofvalue for those with sensitive teeth, painful gumdis-orders or gingival recession. Hard brushesshould be avoided because they may cause gingi-val trauma or recession. The brush-head should besmall enough to reach awkward areas, but not sosmall that effective plaque removal requires pro-longed brushing. A medium-sized brush-headwith multi-tufted nylon bristles of mediumtexture is probably the best choice for most adults.


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Interproximal brushes or brushes shaped likeminiature bottle brushes may be required forextremely awkward areas (e.g. badly aligned teethor bridges) or large interdental spaces.

Electric brushes can be particularly valuablefor people with mental or physical disabilities.When used by the able-bodied, there is no evidence that they are intrinsically superior tomanual toothbrushes, but they can achieve effec-tive plaque removal much more quickly. Manypeople, especially children, find them pleasant touse, and are therefore more likely to maintain asatisfactory oral hygiene regime. Rechargeableelectric toothbrushes are considered preferable to battery-operated brushes, which lose torquequickly.

Toothbrushes should be renewed relativelyfrequently. A worn toothbrush cannot effectivelyremove plaque, but there is no simple means ofdetecting when a toothbrush is past its prime. Ithas been estimated that the lifespan of a tooth-brush being used correctly is probably only a fewweeks.

Toothbrushing techniqueThe aim of toothbrushing is to remove plaqueand food debris; it can also deliver the topical flu-oride in toothpastes to the teeth. Toothbrushingtechnique has been the subject of much argu-ment and many suggestions have been putforward. However, different dentitions mayrequire different techniques; any technique thatresults in good plaque control without causingdamage to the teeth or soft tissues can beregarded as satisfactory.

Two of the most frequently recommendedtechniques are the Bass and Charters methods. Inthe Bass method, the head of the brush is appliedat an angle of 45º to the long axis of the teeth andpressed in an apical direction against the gingivalmargin (Figure 3.7). It is then moved antero-posteriorly with short vibratory strokes. In orderto gain adequate access to the lingual surfaces ofthe anterior teeth, the brush must be turned intoa vertical position. This method effectivelyremoves soft deposits located above and belowthe gingival margin.

In the Charters method, the head of the brushis applied to the teeth at an angle of 45º to theocclusal plane (Figure 3.8), and jiggled back and

forth in a circular motion. It is particularly usefulif the interdental papillae have receded, leavingthe proximal surfaces of the teeth accessible tothe toothbrush.

Whichever technique is used, the mostimportant factor in toothbrushing is that everyaccessible surface of every tooth should bethoroughly cleaned during each session. Manypeople concentrate on the buccal and labial sur-faces, but forget the lingual and occlusal surfaces.It is helpful to divide the dentition into sectionsand concentrate on one section at a time.Patients who are concerned about their tooth-brushing technique should be referred to theirdental surgeon for evaluation.

Toothbrushing frequencyThe most widely accepted routine is once in themorning and once at bedtime. Some authoritiesalso advocate brushing the teeth after lunch, butthis is probably not practical for many people.The thoroughness of plaque removal is moreimportant than the frequency; nothing is gainedby several cursory attempts at toothbrushingthroughout the day.

Toothbrushing before bed is important to


45°

Figure 3.7 The Bass method.

Figure 3.8 The Charters method.

45°

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prevent the reduced salivary flow during sleepallowing the build-up of thick plaque deposits.Therefore, removing as much plaque and debrisas possible before sleeping considerably reducesovernight plaque levels. Theoretically, the besttime to brush teeth would be before eating,because sugar is only cariogenic in the presenceof plaque. In practice, plaque is unlikely to becompletely removed, so it is probably best to rec-ommend toothbrushing after meals, to removeplaque and sugars together.

However, toothbrushing should be avoidedimmediately after consuming acidic foods ordrinks, and after vomiting. This is because at thispoint the enamel is particularly delicate, being inthe first stages of acid attack. After approximately30 minutes, the enamel is stabilised as a result ofre-mineralisation.

Toothpaste

A toothpaste (dentifrice) is applied with a tooth-brush to clean the teeth, but the action of thetoothbrush is far more important than the tooth-paste. It has even been suggested that toothpasteis not necessary for plaque removal. However,toothbrushing with water alone is of little benefitin stain removal. Toothpastes also polish thetooth surfaces, and plaque forms less readily onsmooth surfaces than rough surfaces. Manypeople like the freshening effect toothpaste has inthe mouth, particularly first thing in the morning.

Toothpastes are composed of the followingingredients:

• humectants, which prevent the toothpastedrying out, control microbial growth andprovide a vehicle for the other ingredients

• abrasives, which polish the tooth surface andremove debris, plaque and stains

• surface-active agents, which loosen debris andfacilitate its removal

• binders and thickeners, which prevent separ-ation of the aqueous and non-aqueous con-stituents and thicken the formulation

• flavourings, which improve consumer accept-ability, thereby increasing the likelihood ofpatients maintaining good plaque control

• colourings, used to improve appearance andconsumer acceptability.

Toothpastes may act as vehicles for active ingredi-ents. About 95% of all toothpastes sold in the UKcontain fluoride (see below) in the form of sodiumfluoride or sodium monofluorophosphate (MFP).The fluoride content of toothpaste is usuallyabout 0.1%. Fluoride-containing toothpastesdeliver fluoride to the enamel surface, which isextremely important in preventing dental decay.Desensitising toothpastes contain various com-pounds to block the perception of painful stimuliby dentine. Chlorhexidine (see below) inhibitsplaque formation on the teeth and is included intoothpaste indicated for the control of gingivitis.

Most people cover the entire brush head withtoothpaste, which is far in excess of the quantityneeded. All that is required is an amount the sizeof a pea. Too much toothpaste generates a lot offoam and induces a premature desire to spit andrinse. For many people, this signals the end oftoothbrushing. Ingestion of too much fluoridetoothpaste by children, who swallow much morethan adults, could possibly result in fluorosis, par-ticularly if fluoride supplements are also beingadministered.

Dental floss and interdental woodsticks

Dental floss and interdental woodsticks are usedto remove plaque from the areas between theteeth (embrasures) where a toothbrush cannotreach. These areas should be cleaned regularly,but not every time the teeth are brushed; once aday should be sufficient.

Dental flossDental floss is available in waxed or unwaxedforms; the choice is one of personal preference.Unwaxed floss splays out in contact with thetooth surface and may be more efficient atremoving plaque. It may also be easier to passthrough tight interdental spaces. However, theloose threads may tear against the margins of fill-ings, in which case waxed floss may be preferable.Dental tape, which is wider than dental floss, isalso available, and special types of floss are manu-factured for cleaning bridges. Correct use of flossmay remove some subgingival plaque.

A long piece of floss (approximately 30 cm)should be wound around the first two fingers ofeach hand, leaving approximately 10 cm in


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between. The floss is held taut and carefullyinserted into the space between two teeth. It isthen held firmly against one of the teeth andcarefully moved vertically up and down toremove the plaque. This is repeated for the toothon the other side of the space. On no accountshould the floss be moved horizontally betweenthe teeth; this can severely damage the gingivae.The procedure is repeated until all the teeth havebeen thoroughly cleaned.

An alternative method of using dental flossinvolves tying a length of floss (approximately15 cm) into a loop. The lower teeth are cleanedby holding the floss between both index fingers.The left thumb and right index finger are used to clean the upper left quadrant, and the rightthumb and left index finger to clean the upperright quadrant.

Interdental woodsticksInterdental woodsticks should not be usedwithout proper instruction from a dentist as theycan cause tissue damage. They are less effectivethan floss and do not remove subgingival plaque;they should not be used where teeth are closelypositioned.

Interdental spaces can be cleaned by insertingand manipulating the woodstick, taking care tofollow the normal contour of the interdentalpapillae (Figure 3.9). The mouth must be cleanand the gingivae healthy; rubbing inflamed gin-givae over subgingival calculus will exacerbateperiodontal disease. Regular use of woodstickscan improve the shape of the interdental papillaeand reduce food stagnation.

Water irrigation

Water irrigation units direct jets of water at andbetween the teeth, and are promoted for plaqueremoval. However, plaque is an extremely sticky,tenacious substance and is unlikely to beremoved by water alone. Water irrigation unitsare ineffective in removing stains from tooth sur-faces. It is also possible that the water jet couldforce bacteria into the crevicular epithelium andthe underlying connective tissue. Any resultantbacteraemia would pose a serious risk for patientssusceptible to bacterial endocarditis (e.g. thosewith a history of rheumatic fever).

Mouthwashes

Mouthwashes are liquid preparations containingmany of the same constituents as toothpastes (seeabove). Essential differences are the exclusion ofabrasives and thickening agents. They may, inaddition, contain antibacterial agents, astringents,demulcents or ethanol. Antibacterial mouth-washes may help control gingivitis, but not peri-odontitis; however, the evidence is not conclusive,except for chlorhexidine. Mouthwashes do assistin the removal of debris, tenacious mucus andpurulent secretions, and in the cleansing of trau-matised areas (e.g. aphthous ulcers).

Patients using mouthwashes to treat orallesions should be referred to their doctor or dentalsurgeon if the condition persists for more thanseven days; severe cases should be referredimmediately. Anti-plaque mouthwashes intendedto loosen plaque before toothbrushing have beendeveloped, although the evidence for their effec-tiveness is inconclusive.

ChlorhexidineChlorhexidine is a cationic antibacterial agentavailable in a mouthwash or dental gel. Chlorhex-idine gluconate has proven activity against plaque


Figure 3.9 The woodstick should follow the gingivalcontour.

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bacteria and prevents the build up of plaquedeposits. However, it is not an effective substitutefor toothbrushing, except for short-term use inpainful oral conditions (see Dental disease above).In some cases, chlorhexidine stains the teeth ablackish colour along the gingival margins.

Hydrogen peroxideThe antimicrobial action of hydrogen peroxide isnegligible.

Sodium chlorideA sodium chloride mouthwash can be preparedby dissolving half a teaspoon of salt in a tumbler-ful of warm water, or by diluting CompoundSodium Chloride Mouthwash BP in an equalvolume of warm water. It is particularly useful inpromoting healing (e.g. of extraction sockets andaphthous ulcers) and establishing the drainage ofpus.

Sodium bicarbonateSodium bicarbonate may be used as a 2% solutionto rinse the mouth. Its alkalinity makes it aneffective mucolytic agent, but it does not haveany antibacterial action.

Prevention of dental caries

Dietary management

Dental caries is unlikely to be prevented byplaque control alone; a reduction in sugar consumption is also important. Soft, sticky foodsrelease sugars over a long period of time by cling-ing to tooth surfaces. Also, different sugars affectpH to varying degrees: lactose and galactose causea smaller fall in pH than glucose, maltose, sucroseor fructose. There is no difference in cariogenicpotential between refined and unrefined sugars,or some ‘natural’ (e.g. honey) and processedproducts. All should be avoided as far as possible.Fruits and vegetables are a preferred alternative tocakes, biscuits, puddings, confectionery and anyother foods with a high sugar content.

Animal studies suggest that complex carbo-hydrates may be cariogenic, although to whatextent is not known. However, suggesting thatthese should also be avoided would contradictthe advice given to prevent other disorders. A

compromise must be made so that the health ofthe body as a whole is considered. Thus, it is rec-ommended that the frequency of carbohydrateconsumption, rather than the amount, should bereduced. If snacks are eaten between meals, theyshould consist of non-sticky savoury rather thansticky sweet foods, but it must be borne in mindthat sugar is also present in many processedsavoury foods.

Non-cariogenic sugar substitutes may be used,although it is probably wiser to attempt to dowithout sweet foods and drinks. Sugar alcohols(e.g. sorbitol, mannitol and xylitol) are available;they are not as cariogenic as sugars becauseplaque bacteria are less able to utilise them as sub-strates to produce energy. However, large quanti-ties cause osmotic diarrhoea, and the daily intakeshould not exceed 50 to 80 g. Hydrogenatedglucose syrups are licensed for use in the UK, andavailable evidence suggests that they are less cariogenic than sucrose.

Fluoride

In the early 1900s, it was noted that the inhabi-tants of certain areas of America had mottledteeth. This was eventually found to be caused byincreased levels of fluoride in the local drinkingwater; the condition was therefore called fluoro-sis. These people had a lower prevalence of dentalcaries than the population as a whole. Similarobservations were made in the UK and elsewhere;children living in areas supplied with water con-taining a high level of natural fluoride hadhealthier teeth than those in areas whose waterhad a low fluoride content. The role of fluoride inthe prevention of dental caries was investigated;worldwide epidemiological studies confirmedthat caries is reduced in areas where the watersupply contains at least 1 mg/L (1 ppm) of fluo-ride. However, concentrations of fluoride above1 mg/L may cause fluorosis. Fluoride is alsopresent in many foodstuffs, but significantamounts are found only in tea and the bones ofsea-fish.

There is a strong anti-fluoridation lobby in theUK, which objects to fluoridation of water sup-plies on the grounds that it is dangerous, unnec-essary, uneconomic and of negligible benefit.Careful and controlled studies have refuted all


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these claims, and fluoridated water has beenshown to be safe and effective. However, most ofthe UK population does not benefit from fluori-dated water supplies. This contrasts starkly withother nations (e.g. Russia and the USA) where fluoridation is widespread; it is mandatory in theRepublic of Ireland.

Fluoride is effective both topically and sys-temically (Duckworth, 1993). The topical effect isnow considered more important as the greatestconcentrations of fluoride are found at the toothsurface. There are several theories to explain themode of action of fluoride. The most popular isthat the calcium hydroxyapatite in enamel isreplaced by calcium fluorapatite. This has a lowercritical pH and therefore increases the resistanceof enamel to acid attack. Fluoride is also import-ant in re-mineralisation and the reversal of earlycaries, especially smooth surface caries. Fluoridecan block the enzymes of plaque bacteria andmay inhibit the metabolic conversion of sugars toacids. Application of topical fluoride can re-mineralise enamel and completely reverse thedevelopment of early carious lesions; it may alsoarrest, or slow down, the progress of later lesions.There is some evidence that the presence of sys-temic fluoride during tooth development resultsin a smoother, less fissured morphology that isless susceptible to caries.

Oral fluoride supplements containing sodiumfluoride may be given to children living in areaswhere the level of fluoride in the water is less than1 ppm. Pharmacists should check the level withthe water authority, and issue the followingguidelines when selling fluoride supplements.Doses are expressed as the amount of fluoride ionto be taken daily. These guidelines are for tem-perate climates; the dose may be less in tropicalclimates where more water is consumed.

• Fluoride level less than 300 µg/L (0.3 ppm)six months to two years of age – 250 µgtwo to four years of age – 500 µgmore than four years of age – 1000 µg

• Fluoride level of 300 to 700 µg/L (0.3 to0.7 ppm)less than two years of age – no supplementa-tion requiredtwo to four years of age – 250 µgmore than four years of age – 500 µg

• Fluoride level above 700 µg/L (0.7 ppm)no supplementation required.

These doses take into account the small amountof fluoride ingested during toothbrushing. Twodivided doses should be administered each day toavoid the plasma concentration peaking at avalue that could cause fluorosis. However, thisrequires a high degree of motivation, and oncedaily administration (preferably in the evening)is an effective compromise; forgotten dosesshould not be doubled the following day. Fluo-ride tablets should be sucked or dissolved in themouth rather than swallowed whole, to allow atopical as well as a systemic effect. In the UK, fluoride supplementation is now consideredunnecessary for infants under six months of age,irrespective of local water concentrations.

Additional protection may be provided forthose at increased risk of caries by the use of fluoride rinses or the application of fluoride gels.Rinses may be used daily or weekly. A concen-tration of 0.05% sodium fluoride may be used fordaily rinsing, and of 0.2% for weekly or fort-nightly rinsing. The mouth should be rinsed forone minute; the rinse should not be swallowed,and eating and drinking should be avoided for 15 minutes after use. Gels must be applied by adental surgeon, usually twice a year; extremecaution is necessary to prevent any excess frombeing swallowed. Less concentrated gels haverecently become available for home use. Fluoridevarnishes may also be applied by the dentalsurgeon; they are particularly valuable for youngor disabled children as the varnish adheres to theteeth and sets in the presence of moisture.

It should be borne in mind that fluoride doesnot confer complete protection, and minimalsugar consumption, together with good plaquecontrol, is still essential to prevent dental decay.

Dental intervention

It cannot be emphasised too strongly that themost important preventive measures are thoseroutinely undertaken by the individual at home.However, regular visits to the dental surgeon arenecessary to identify early caries, some of whichmay be reversed. For lesions that cannot be


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reversed, restorative treatment limits the amountof tooth tissue lost. X-ray examination is essentialto detect some cavities, especially those betweenteeth, and will also show early periodontal bonedestruction.

Some individuals are more susceptible tocaries than others. Some of the factors respons-ible may be outside their control (e.g. those thatare genetically inherited or occur during toothdevelopment, see Dental disease above). The risksmay be minimised by strict attention to oralhygiene and use of fluoride products. However,dental intervention may be necessary to ensureeffective plaque control (e.g. orthodontic pro-cedures, which involve moving teeth into morefavourable positions under mild pressure, orextractions to reduce overcrowding). Orthodon-tic appliances provide a surface for plaque build-up and can irritate the gingivae. They mayincrease susceptibility to dental disease, and mustbe kept scrupulously clean.

Fissures on the occlusal surfaces of molars andpremolars are most prone to dental caries. Here,fluoride is less effective in preventing caries thanin other areas of the tooth (see above). Deep fis-sures may be treated with proprietary sealants.This involves filling the fissures and pits with aplastic substance. If applied properly, no decayshould occur as long as the sealant remains inplace. Sealants should be applied as soon as poss-ible after eruption. The method is painless buttime-consuming, and may be difficult if a child isunco-operative.

Regular dental check-ups are also importantfor adults. The dental surgeon is able to offeradvice and training in good plaque control tech-niques. It is generally recommended that routinecheck-ups should take place every six months,although some young children may benefit fromvisits every four months. Adults with goodplaque control may only need an annual check-up. It must be stressed that regular dental check-ups are not a substitute for good oral hygiene.

Prevention of dental disease in children

In children, caries is more of a problem than periodontal disease, so dental healthcare

measures should be directed towards reducingtooth decay. However, the practices and habitsadopted during childhood will also combat peri-odontal disease if continued into adulthood.

Instilling good dietary habits (see above) isabsolutely essential in the early years, togetherwith fluoride supplementation (see above), ifnecessary. Parents should not add sugar tofeeding bottles or coat dummies with sweet sub-stances. Children should be discouraged fromadding sugar to foods or drinks (e.g. cereals, fruit,tea or coffee). A taste for savoury foods should be encouraged because, once attained, a ‘sweettooth’ is very difficult to eliminate.

Toothbrushing should be started as soon as thefirst tooth erupts, and the child encouraged totake an active part as soon as possible. Reasons forcleaning the teeth should be explained, and thepresence of plaque demonstrated using a disclos-ing agent. Children’s toothbrushes with smallheads and short handles should be employed.Use of dental floss is not usually necessary in chil-dren, and would be difficult because of lack ofmanual dexterity. However, flossing should bestarted as soon as possible in adolescence.Thumbsucking should be actively discouraged,because it may alter the alignment and spacing ofthe front teeth.

Children should be introduced to the dentalsurgeon at an early age, certainly by the time allthe primary teeth have erupted. Good oralhygiene practices reduce the necessity for treat-ment and ensure that a child builds a goodrelationship with the dental surgeon right fromthe start.

Care of dentures

Anyone who wears a complete set of denturesmay assume that it is too late to worry aboutdental healthcare. However, plaque accumulateson dentures in exactly the same way as onnatural teeth, and must be removed regularly toavoid mucosal inflammation. Removal ofplaque and food debris also reduces the likeli-hood of bacterial putrefaction and the resultantoffensive mouth odours. Plaque on dentures issubject to the same risks of staining (e.g. from


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coffee, tea, tobacco or red wine) as natural teeth.Regular cleaning will maintain an attractiveappearance. Partial dentures must be keptscrupulously clean in order to preserve theremaining natural teeth. Dentures shouldalways be cleaned out of the mouth, once ortwice a day. They are not usually worn at night,when they should be placed in water to preventthem drying out and distorting.

Dentures are generally made of acrylic materi-als that are softer than enamel, so equipment andproducts designed for natural teeth should neverbe used. Some partial dentures are metal: chrome-cobalt alloy is most commonly used. Denturebrushes resemble nail brushes on long handles.There is very often a thick tuft of bristles on theopposite side of the head, which can be used toclean awkward areas. Toothpastes specificallydesigned for dentures should be used and highlyabrasive cleansers avoided, because of the risks ofscratching; household bleach, disinfectants orantiseptics should never be used. Alternatively,brushing with soap and water can be just as effec-tive. Disclosing solutions may be used to detectplaque on dentures and assess the thoroughnessof cleansing routines in exactly the same way asfor natural teeth.

Tablets or powders that release oxygen whendissolved in water may be used to soak the den-tures to remove plaque; a stronger acidic cleansermay be required for stubborn stains. Soaking,however, is no substitute for brushing and canlead to ‘crazing’ of the acrylic surface; minutecracks develop which make the denture appeardull and render it much more susceptible to stain-ing. Metal components may corrode in certainsolutions, and the manufacturer’s instructionsshould always be consulted before soaking. Somedentures have soft linings; the dental surgeonshould be consulted about the safest way to cleanthese.

Dentures must be handled with great care;they should be cleaned over a bowl of water or asoft surface in case they are dropped. Denturerepair kits are available to carry out emergencyrepairs, but should only be used as a very lastresort; the slightest misalignment or excess ofrepair material can make a denture unwearable.Household adhesives should never be used; the

dentures should be taken to a dental surgeon ordental technician for professional repair as soonas possible.

Once a tooth has been lost, the surroundingalveolar bone gradually resorbs, the rate varyingdramatically between individuals. Dentures reston the alveolar ridge and extensive bone lossresults in a poor fit. Loose dentures affect eatingand speaking; the effects may be severe enough tomake the wearer withdraw socially. Eating mayalso be painful, because uneven contact meansthat the soft gingivae are excessively loaded insome areas. The hard palate provides a widesurface over which biting forces are distributed,whereas lower dentures can only cover the alveo-lar ridge, because the floor of the oral cavity istaken up by the tongue and its associatedmuscles. Consequently, lower dentures tend to be more difficult to wear than upper dentures.Denture fixatives, usually containing karaya gumor tragacanth, are used by many people toincrease retention. However, anyone havingproblems should be referred to their dentalsurgeon.

The risk of developing oral lesions is increasedin some systemic disorders. Pharmacists shouldalways enquire about any underlying conditionwhen a patient presents with denture problems(e.g. there is an increased incidence of oral can-didiasis in diabetics). A dry mouth may also makewearing dentures difficult and uncomfortable, sopharmacists should be aware of the conditionsand drugs that reduce salivary secretion (seeDental diseases above). Patients may need to bereferred to their doctor as well as their dentalsurgeon.

New dentures may take getting used to, especi-ally if the patient has not worn dentures before.They may produce gum discomfort and evensores or ulcers. Unless the symptoms areextremely mild, patients should be referred totheir dental surgeon as the dentures may requireadjustment. In the meantime, an oral prep-aration containing a local anaesthetic may beapplied to the affected area.

The fit of dentures is rarely satisfactory formore than five years, and they must be renewedperiodically. Denture wearers should visit theirdental surgeon every one to three years (every six


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months if they have partial dentures) to havetheir dentures checked and the fit re-evaluated.

The role of the pharmacist

Pharmacists have traditionally been involved inselling dental products to the public, and aretherefore ideally positioned to reinforce healtheducation messages from the dental professionand other dental healthcare authorities. Inaddition, pharmacists can recognise disorders of the oral cavity and refer patients to generalpractitioners or dental surgeons as appropriate.Dental healthcare is essential for a healthy life-style, and should be placed equally among otherforms of lifestyle modification. Pharmacistsshould not take over the role of dental healtheducation from dental surgeons, but ratheraugment it. Much can be achieved by dental sur-geons and pharmacists liaising. This also ensuresthat pharmacists endorse the dental healthcareadvice given by the dental profession.

In most cases, the sale of dental healthcareproducts is a passive process. It would not bepractical to become actively involved in everysale, but pharmacists may perceive that aproblem exists (e.g. by noticing repeat purchasesof mouthwashes or a customer’s difficulty inselecting a toothbrush or toothpaste). Dentalhealthcare products should be positioned so thatpharmacists can observe customers, and there-fore offer help when necessary. In large pharma-cies, locating the dental healthcare section closeto the dispensary serves to raise the status ofdental products in the eyes of the public frommere toiletries to essential healthcare items.

Pharmacists should be aware of the importanceof sugar control in the prevention of dental caries,and therefore only counter-prescribe non-cariogenic liquid medicines, particularly for chil-dren. Mouth and throat lozenges may containcariogenic sugars, and this should be pointed outto patients. Pharmacists have little control overmedicines supplied on prescription unless genericitems are requested. However, a discussion withlocal doctors to make them aware of any sugar-free alternatives may be valuable. Pharmacistsshould also check the manufacturer’s information

to see if alternative diluents to syrup may be usedwhen dispensing reduced-strength preparations.

Whenever the opportunity arises, pharmacistsshould stress:

• the insidious and painless nature of dentaldisease

• prevention is better than cure• complete prevention is totally feasible• regular dental check-ups are essential at any

age.

It should also be emphasised that periodontaldisease is not a normal ageing process, but a patho-logical disease that can be prevented by good oralhygiene. Children should be encouraged to adoptgood habits from as early an age as possible.

Pharmacists should be familiar with diseasesand drugs that may increase the susceptibility todental caries or periodontal disease (see Dentaldiseases above), and offer counselling on preven-tive measures where appropriate. It is imperative,however, that pharmacists do not compromisepatients’ confidence in prescribed medicines, orincrease their anxiety over a disease state. The dis-cussion needs to be handled with tact and sensi-tivity, maintaining a positive attitude throughoutand emphasising there is nothing difficult aboutgood dental heathcare. Sometimes, there is noalternative to a prescribed medicine, and thepatient’s medical health may seem more import-ant than their dental health. Neither should becompromised at the expense of the other and, inmost cases, dental health can be maintained withgood plaque and sugar control. If a patient isover-anxious, pharmacists should discuss thematter with the patient’s doctor and dentalsurgeon in an attempt to resolve the difficulty.Pregnant women are prone to gingivitis andshould be counselled that good plaque controlwill minimise problems. It is also essential thatpregnant women and children do not take tetra-cyclines, as these may cause intrinsic discol-oration of children’s permanent teeth during thedevelopmental stages.

There may be occasions when patients consultpharmacists about dental problems. Anyone withdental pain should always be referred to a dentist,because it may be difficult to establish the cause,and usually only a dentist will be able to carry outthe treatment necessary to alleviate the patient’s


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discomfort. If patients are unable to obtain emer-gency treatment from their own dental surgeon,pharmacists should supply the address and tele-phone number of the nearest emergency dentalservice. Analgesics may be administered in themeantime, but it must be stressed that theproblem does not disappear with the pain, anddental treatment must be sought at the earliestavailable opportunity. The belief that placing anaspirin tablet against the offending tooth willrelieve toothache should be firmly discouraged,because of the risk of extensive mucosal ulcera-tion; aspirin is of greater benefit in pain relief iftaken systemically.

Some patients may have been given the all-clear by their dentist, or told that their problemis due to gingival recession and exposure of theroot surface. In this case, pharmacists can recom-mend one of the proprietary brands of desensi-tising toothpaste, preferably one containingfluoride. It should be explained that two or threeweeks’ conscientious brushing is required beforethese toothpastes exert their maximum effect.

Most people have mouth ulcers occasionally.Aphthous ulcers are the ordinary mouth ulcersthat appear singly or in small numbers, often attimes of stress. Various proprietary remedies areon the market, some of which contain a localanaesthetic to render the ulcers less painful. Pharmacists should recommend an appropriateproduct, as well frequent hot salty mouthwashes,which often have a beneficial effect.

A patient with mouth ulcers need only bereferred to a dental surgeon if the ulcers are:

• particularly large• last more than ten days or so• repeatedly occur in the same place, which

implies that they could be traumatic in origin(e.g. caused by a sharp tooth or rough filling)

• widespread or in large clusters, especially inyoung children, which could indicate infec-tion with herpes simplex virus

• associated with an objectionable taste or halitosis

• caused by dentures.

A number of emergency kits are available forpatients to insert their own temporary fillingsand temporarily cement crowns that havebecome detached. These are a good interim

measure, but often require a high degree ofmanual dexterity on the part of the patient. At allcosts, patients should be dissuaded from usinghousehold glues to re-cement a crown. The resultcan be painful and cause difficult and expensivedental problems.

Teeth which have been knocked out in an acci-dent may be successfully re-implanted; however,they may not survive a lifetime, or may discolourand require crowning. Such teeth should beplaced in a clean container of milk and immedi-ately taken by the patient to the dental surgeon.On no account should the teeth be washed,rinsed or cleaned in any way. It is vital that thereis the minimum delay possible in seeking treat-ment. If the tooth has fallen onto a dirty surface,the patient may require immunisation againsttetanus.

People who visit a dental surgeon have beensufficiently motivated to make an appointment.However, many people never see a dentalsurgeon, but buy dental healthcare products.Others may not follow any sort of oral hygieneregimen, but still visit a pharmacy for otherreasons. Pharmacists, therefore, can interact withsignificantly more people than dental surgeons,and should take advantage of this situation when-ever possible. The impact of any educationalmaterial (e.g. books, leaflets or posters) in a phar-macy is potentially greater than in a dentalsurgery, and pharmacists would do well to includedental health information among their displays.

References

Downer M C (1994). The 1993 national survey of chil-dren’s dental health: a commentary on the prelimi-nary report. Br Dent J 176: 209–214.

Duckworth R M (1993). The science behind caries pre-vention. Int Dent J 43: 529–539.

Harman R J, ed. (1990). Disorders of the ear, nose, andoropharynx. In: Handbook of Pharmacy Health-care:Diseases and Patient Advice. London: PharmaceuticalPress, 239–248.

National Dairy Council (1995). Diet and Dental Health.London: NDC.

Office of Population Censuses and Surveys (1994).

The role of the pharmacist 87

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Dental disease among children in the UnitedKingdom. OPCS Monitor. London: OPCS.

Smith B G N, Bartlett D W, Robb N D (1997). The preva-lence, aetiology and management of tooth wear inthe United Kingdom. J Prosthet Dent 78: 367–372.

Further reading

Centre for Pharmacy Postgraduate Education (1995). Adistance learning course for community pharma-cists. Oral Health, Volumes I & II. London: HMSO.

Ekstrand J, Fejerskov O, Silverstone L M, eds (1988). Flu-oride in Dentistry. Copenhagen: Munksgaard.

Embery G, Rolla G, eds (1992). Clinical and BiologicalAspects of Dentifrices. Oxford: Oxford UniversityPress.

Levine R, ed. (1996). The Scientific Basis of Dental HealthEducation. London: Health Education Authority.

Löe H, Kleinman D V, eds (1986). Dental Plaque ControlMeasures and Oral Hygiene Practices. Oxford: IRLPress.

Mehta D, ed. (1998). Dental Practitioner’s Formulary1998–2000. London: British Medical Associationand Royal Pharmaceutical Society of Great Britain.

O’Brien M (1993). Children’s Dental Health in the UnitedKingdom. London: HMSO.

Rugg-Gunn A J (1993). Nutrition and Dental Health.Oxford: Oxford University Press.

Tay W M, ed. (1990). General Dental Treatment. Edin-burgh: Churchill Livingstone.

WHO (1985). Prevention methods and programmes fororal diseases: report of a WHO expert committee.WHO Tech Rep Ser 713.


Useful addresses

British Dental Association (BDA)64 Wimpole StreetLondon W1M 8ALTel: 020 7935 0875

British Fluoridation SocietySandlebrookMill LaneAlderley EdgeCheshire SK9 7TYTel: 01565 873936

British Society for Disability and Oral HealthDepartment of Sedation and Special Care DentistryFloor 26, Guy’s TowerLondon SE1 9RTTel: 020 7955 5000 Ext. 3047

General Dental Council37 Wimpole StreetLondon W1M 8DQTel: 020 7887 3800

The Oral and Dental Research TrustKeats’ House36 St. Thomas StreetLondon SE1 9RNTel: 020 7955 4699

FDI World Dental Federation7 Carlisle StreetLondon W1V 5RGTel: 020 7935 7852

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