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Aciclovir is used for treating chickenpox (varicella) or shingles (herpes zoster) and treating or suppressing genital herpes infections.

Active Ingredient:

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Other articles

Zoral diseases

What is the burden of oral disease? Oral disease burdens and common risk factors

Despite great achievements in oral health of populations globally, problems still remain in many communities all over the world - particularly among under-privileged groups in developed and developing countries. Dental caries and periodontal diseases have historically been considered the most important global oral health burdens. At present, the distribution and severity of oral diseases vary among different parts of the world and within the same country or region. The significant role of socio-behavioural and environmental factors in oral disease and health is evidenced in an extensive number of epidemiological surveys.

Dental caries is still a major oral health problem in most industrialized countries, while it appears to be less common and less severe in most African countries.

Dental caries is still a major oral health problem in most industrialized countries, affecting 60-90% of schoolchildren and the vast majority of adults. It is also a most prevalent oral disease in several Asian and Latin-American countries, while it appears to be less common and less severe in most African countries. Figure 1 highlights the dental caries experience among 12-year-old children in the six WHO regions in the year 2000, based on the DMFT (Decayed, Missing and Filled Teeth) Index, an index that measures the lifetime experience of dental caries in permanent dentition. Currently, the disease level is high in the Americas but relatively low in Africa. In light of changing living conditions, however, it is expected that the incidence of dental caries will increase in many developing countries in Africa, due particularly due to a growing consumption of sugars and inadequate exposure to fluorides.


In many developing countries, access to oral health services is limited and teeth are often left untreated or are extracted because of pain or discomfort. Throughout the world, losing teeth is still seen as a natural consequence of ageing. While in some industrialized countries there has been a positive trend of reduction in tooth loss among adults in recent years, the proportion of edentulous adults aged 65 years and older are still high in some countries (Table 1).

  • Prevalence of edentulousness
    pdf, 22kb

Globally, most children have signs of gingivitis and, among adults, the initial stages of periodontal diseases are prevalent. Figure 2 illustrates the periodontal health status of 35-44-year-olds by WHO region, using the so-called Community Periodontal Index. Severe periodontitis, which may result in tooth loss, is found in 5-15% of most populations. Juvenile or early-onset aggressive periodontitis, a severe periodontal condition affecting individuals during puberty that leads to premature tooth loss, affects about 2% of youth.

  • Mean percentages of 35-44-year-olds by maximum Community Periodontal Index scores according to WHO region
    pdf, 58kb

In industrialized countries, studies show that smoking is a major risk factor for adult periodontal disease, responsible for more than half of the periodontitis cases among this age group. Risk decreases when smokers quit and the prevalence of periodontal disease has decreased in countries experiencing reductions in tobacco use.

  • Comparison of the most common cancers in more and less developed countries in 2000
    pdf, 58kb

While oral and pharyngeal cancers are both preventable, they remain a major challenge to oral health programmes. The prevalence of oral cancer is particularly high among men, the eighth most common cancer of the world (Figure 3). Incidence rates for oral cancer vary in men from 1-10 cases per 100,000 inhabitants in many countries. In South Central Asia, cancer of the oral cavity ranks amongst the three most common types of cancer. However, sharp increases in incidence rates of oral/pharyngeal cancers have been reported for several countries such as Germany, Denmark, Scotland, Central and Eastern Europe and, to a lesser extent, Japan, Australia, New Zealand and USA.

In Asia, the age standardized incidence rate per 100,000 population ranges from 0.7 in China to 4.6 in Thailand and 12.6 in India. The high incidence rates relate directly to risk behaviours such as smoking, use of smokeless tobacco (e.g. betel nut or miang chewing) and alcohol consumption. In Thailand, for example, the prevalence of smoking is about 60%, betel nut chewing 15% while alcohol consumption is 35%.

  • Cases of Noma reported in regions of the world
    pdf, 45kb

Qat is a leafy narcotic substance that is popular in several countries in East Africa and the Arab Peninsula. Qat can be consumed as a liquid in the form of tea or smoked like tobacco. However, the most common mode of ingestion is by chewing the fresh leaves. Consumption of Qat can lead to adverse oral effects including oral mucosal lesions, dryness of the mouth, discoloration of teeth, poor oral hygiene and periodontal disease.

There are variations in oral health profiles across regions. In some developing countries, oral diseases are increasing and countries in Africa and Asia must urgently address a number of very serious oral conditions including Noma (Cancrum Oris), ANUG (Acute Necrotizing Ulcerative Gingivitis), oral pre-cancer and cancer. Cases of Noma are reported for young children aged 3-5 years in Africa, Latin America and Asia (Figure 4); with 90% of them dying without having received any care. Also, Africa and Asia have the highest prevalence of HIV/AIDS, oral manifestations of which are widespread.

In contrast to dental caries and periodontal disease, reliable data on the frequency and severity of oro-dental trauma are still lacking in most countries, particularly in developing countries. Some countries in Latin America report dental trauma for about 15% of schoolchildren whereas prevalence rates of 5-12% are found in children aged 6-12 years in the Middle East. However, recent studies from certain industrialized countries revealed that the prevalence of dental traumatic injuries is on the increase, ranging from 16-40% and 4-33% among 6-year-old and 12-14-year-old children respectively. A significant proportion of dental trauma relates to sports, unsafe playgrounds or schools, road accidents or violence. In industrialized countries, the costs of immediate and follow-up care for dental trauma patients are high.

Estimates of the frequency of different traits of malocclusion are available from a number of countries, primarily from Northern Europe and North America. For example, prevalence rates of dento-facial anomalies are reported at 10%, according to the Dental Aesthetic Index. Malocclusion is not a disease but rather a set of dental deviations which in some cases can influence quality of life. There is insufficient evidence that orthodontic treatment enhances dental health and function. Treatment is often justified by the potential enhancement of social and psychological wellbeing through improvements in appearance.

Given the extent of the problem, oral diseases are major public health problems. Their impact on individuals and communities, as a result of pain and suffering, impairment of function and reduced quality of life, is considerable. Moreover, traditional treatment of oral disease is extremely costly, the fourth most expensive disease to treat in most industrialized countries. In low-income countries, if treatment were available, the costs of dental caries alone in children would exceed the total health care budget for children.

A core group of modifiable risk factors are common to many chronic diseases and injuries. The four most prominent noncommunicable diseases (NCDs) - cardiovascular diseases, diabetes, cancer and chronic obstructive pulmonary diseases - share common risk factors with oral diseases, preventable risk factors that are related to lifestyle. For example, dietary habits are significant to the development of NCDs and influence the development of dental caries. Tobacco use has been estimated to account for over 90% of cancers in the oral cavity, and is associated with aggravated periodontal breakdown, poorer standards of oral hygiene and thus premature tooth loss.

The greatest burden of all diseases is on the disadvantaged and socially marginalized. A major benefit of the common risk factor approach is the focus on improving health conditions for the whole population as well as for high risk groups; thereby reducing inequities. The solutions to the chronic disease problems are to be found through shared approaches. The WHO Global Strategy for the prevention and control of noncommunicable diseases is a new approach to managing the prevention and control of oral diseases. Continuing surveillance of levels and patterns of risk factors is of fundamental importance to planning and evaluating community preventive activities and oral health promotion.

Oral health - European Commission

European Commission
Public health
Oral health Introduction

The information in the oral health field can be affected by the inadequate quality of data available for data planning, implementation, service management and evaluation. The profusion of internationally recommended indicators may complicate the national selection of indicators and may lead to unnecessary and costly monitoring efforts. The Commission works to change this situation by funding projects on oral health indicators or by collecting data on the self perceived oral health status of Europeans in a representative and comparable way.

Eurobarometer on oral health

This survey (fieldwork in 2009, publication in 2010) is based on a questionnaire designed by the EU project EGOHID (European Global Oral Health Indicators Development) developed under the Public Health Programme. The results provide key data on the state of the oral health of Europeans and their preventative or risk behaviour. A minority of Europeans still have all their natural teeth: 41% state that they have all their natural teeth while a third of them say that they still have 20 natural teeth or more. Among those who do not have all their natural teeth, almost a third (31%) wear a removable denture; with small differences from one country to another. 29% of Europeans who have a denture have worn it for at least ten years.

EU funded projects

In 2003, the European Commission launched the EU Project European Global Oral Health Indicators coordinated by the Université Claude Bernard de Lyon, to support European Member States in their efforts to reduce the toll of morbidity, disability related to oral health diseases. The project aimed at identifying indicators of oral health. Main outcomes of this project were:

Report of the Consensus Workshop, University of Granada (Spain), 7-8 May 2004.

The EGOHID final report was the basis for a second phase of the project based on common approaches for oral health on health interview surveys and national health clinical surveys. The European project EGOHID II published in 2008 the final catalogue Oral Health Interviews and Clinical Surveys: Guidelines.

See also DG Research funded projects:

Information on oral health by WHO

The objective of CAPP - the WHO Oral Health Country/Area Profile Programme - is to present global information on dental diseases and oral health services. The "CAPP" was established at the WHO Collaborating Centre for Education, Training and Research at the Faculty of Odontology, Malmö, Sweden, in 1995.

The World Oral Health Report 2003 presents oral diseases as a major public health problem owing to their high prevalence and incidence in all regions of the world, and as for all diseases, the greatest burden of oral diseases is on disadvantaged and socially marginalized populations. The severe impact in terms of pain and suffering, impairment of function and effect on quality of life must also be considered. Traditional treatment of oral diseases is extremely costly in several industrialized countries, and not feasible in most low-income and middle-income countries. The WHO Global Strategy for Prevention and Control of Non communicable Diseases, added to the common risk factor approach a new strategy for managing prevention and control of oral diseases.

Other useful oral health information

In the ECHI data tool, see data on

In the Eurobase (Eurostat), see data on

See oral health chapters in the EU funded reports

Zoral Drug Information, Indications - Other Medicaments on

Zoral Drug Information Zoral forms, composition and dosages: Indications, usages and classification codes:
  • D06BB03 - Aciclovir
  • J05AB01 - Acyclovir

There is an additional general information about this medication active ingredient acyclovir:

Pharmacological action

Antiviral agent. Thymidine kinase of virus-infected cells actively converts acyclovir through a series of sequential reactions in the mono-, di- and triphosphate of acyclovir. The latter interacts with the viral DNA polymerase, and embedded in DNA, which is synthesized for new viruses. Thus it is formed a "defective" viral DNA which leads to suppression of replication of new generations of viruses.
This mediciine acyclovir is active against Herpes Simplex virus types 1 and 2, Varicella Zoster virus, Epstein-Barr virus and cytomegalovirus.


For oral administration bioavailability is 15-30%. Widely distributed in tissues and body fluids. Plasma protein binding is 9-33%. Metabolised in liver. T1/2 for oral administration - 3.3 h, intravenous - 2.5 hours; acyclovir excreted in the urine, also in small quantities - with feces.

Why is Zoral by Drug Houses of Australia prescribed?

For systemic use (oral and IV): infections caused by Herpes Simplex virus types 1 and 2 and Varicella Zoster; prevention of infections caused by viruses Herpes Simplex and Varicella Zoster (including in patients with low immunity); in combined therapy with the pronounced immunodeficiency (including in the clinical picture of HIV infection) and in patients undergoing marrow transplantation, prevention of cytomegalovirus infection after marrow transplantation.
For topical use in ophthalmology: keratitis and other eye damage caused by Herpes Simplex virus.
For external use: infections of the skin caused by Herpes Simplex virus and Varicella Zoster like Herpes Simplex of the skin and mucous membranes, genital herpes (primary and recurrent) localized zoster (support therapy).

Dosage and administration

For oral usage for adults and children older than 2 years - 200-400 mg of 3-5 times / day, if necessary - to 20 mg / kg (up to 800 mg per dose) 4 times / day. For children under 2 years are used in doses equal to half the adult dose. Duration of treatment - 5-10 days. In renal insufficiency is recommended correction dosing regimen.
IV in adults and children over 12 years - 5-10 mg / kg, the interval between infusions - 8 hours. Children under the age of 3 months to 12 years - 250-500 mg / m2 body surface, the interval between infusions - 8 hours, for infants dose is 10 mg / kg, the interval between infusions - 8 hours.
In renal insufficiency must be corrected dosing regimen.
Locally and externally applied 5 times / 24 h. Dose and duration of treatment depends on the testimony and the use of dosage form.
Maximum dose for adults for IV usage is 30 mg / kg / 24 h.

Zoral by Drug Houses of Australia side effects

For oral usage: nausea, vomiting, diarrhea, abdominal pain, skin rash, headache, dizziness, fatigue, reduced concentration, hallucinations, drowsiness or insomnia, fever, rarely - hair loss, a transient increase in blood concentrations of bilirubin, urea, creatinine, liver enzymes, lymphocytopenia, eritropeniya, leukopenia.
For IV usage: acute renal failure, crystalluria, encephalopathy (confusion, hallucinations, agitation, tremors, convulsions, psychosis, drowsiness, coma), phlebitis, or inflammation at the injection site, nausea, vomiting.
For topically usage: a burning sensation in the application area, superficial punctate keratitis, blepharitis, conjunctivitis.
For external usage: in the application area may be a burning sensation, skin rash, itching, peeling, erythema, dry skin in contact with mucous membranes - inflammation.


Hypersensitivity to acyclovir and valaciclovir; for IV usage - lactation (breast feeding).

Using during pregnancy and breastfeeding

Pregnancy. Perhaps, if the expected effect of the therapy outweighs the potential risk to the fetus (adequate and strictly controlled studies of safety in pregnant women is not conducted); acyclovir passes through the placenta. Data on the outcome of pregnancy in women taking acyclovir systemic action in the I trimester of pregnancy showed no increase in birth defects compared with the total population. Since the observation was included a small number of women, reliable and definitive conclusions about the safety of acyclovir in pregnancy can be done.
Breastfeeding. acyclovir penetrates into breast milk. After taking acyclovir by mouth, it was determined in breast milk in concentrations, the ratio of which, with concentrations in blood plasma was 0,6-1,4. At these concentrations in breast milk, children who are breastfed can receive acyclovir at a dose of 0.3 mg / kg / day. Given this, should appoint acyclovir lactating women with caution, only if necessary.

Special instructions

Do not use with severely impaired renal function.
Note that the application of acyclovir may develop acute renal failure due to precipitate formation of crystals of acyclovir, which is especially likely during rapid IV introduction, the simultaneous use of nephrotoxic drugs in patients with impaired renal function and lack of water stress.
When applying aciclovir should monitor renal function (determination of the level in the blood urea nitrogen and creatinine in blood plasma).
Treatment of elderly patients should be conducted with a sufficient increase in water load and under the supervision of a physician, because among these patients increased half-life of acyclovir.
In the treatment of genital herpes should avoid sex or use condoms, because use of acyclovir does not prevent transmission to partners.
This medication acyclovir in the form of dosage forms for topical use should not be applied to mucous membranes of the mouth, eyes, vagina.

Zoral by Drug Houses of Australia drug interactions

With simultaneous use of probenecid decreases the tubular secretion of acyclovir, and thereby increases the concentration in blood plasma and the half-life of acyclovir.
With simultaneous use of acyclovir with other nephrotoxic drugs increases the risk of nephrotoxicity (especially in patients with impaired renal function).
Enhancing effect of acyclovir is noted while appointing immunostimulators.
When mixed solutions should be considered an alkaline reaction to acyclovir for IV introduction (pH 11).

Zoral by Drug Houses of Australia in case of emergency / overdose

Symptoms: headache, neurological disorders, shortness of breath, nausea, vomiting, diarrhea, renal failure, lethargy, convulsions, coma.
Treatment: symptomatic therapy, the maintenance of vital functions, adequate hydration, hemodialysis (especially in acute renal failure and anuria). There is no data for overdose when applied topically.


Be sure to consult your doctor before taking any medication!

Drugs and medications - Zoral 200

Acyclovir USP 200 mg/400 mg per tablet

200 mg: Light blue, hexagonal and convex tablet, 10mm diameter with score-line and "DHA" logo.
400 mg: Light pink, round and convex tablet, 12mm diameter with cross score-line and without logo.

Acyclovir is active against herpes simplex virus types 1 and 2 (HSV-1 & 2) and against varicella zoster virus. This activity is due to intracellular conversion of acyclovir by viral thymidine kinase to monophosphate with subsequent conversion to diphosphate and to the active tiphosphate. This active trlphosphate is a potent inhibitor of HSV-1 & 2 DNA polymerase enzyme and
a DNA chain terminator. This process is highly selective for infected cells.

Acyclovir is only partially absorbed from the gut. Mean steady state peak plasma concentrations following doses of 200mg administered 4 hourly were 3.1µmol and equivalent trough plasma levels were 1.8µmol. Corresponding levels following doses of 400 and 800mg administered 4-hourly were 5.3µmol and 8µmol, respectively, and equivalent levels were 2.7µmol and 4µmol.

Plasma Acyclovir levels dropped approximately 60% during dialysis.

Herpes simplex infections of the skin and mucous membranes. Treatment of herpes zoster (shingles) and varicella (chicken-pox) infections.

Adults: Herpes simplex: Treatment: 200 mg, 5 times daily for 5 days. Treatment may be extended in severe cases. Prophylaxis: 200 mg, 4 times daily. Herpes zoster and varicella: Treatment: 800 mg, 5 times daily for 7 days. Doses to be taken with or without food.

Immune-compromised patients: Suppression of herpes simplex: 200 mg 4 times daily at approximately 6-hourly intervals or 400 mg twice daily at approximately 12-hourly, intervals. Dosage may be titrated down to 200 mg twice or 3 times daily. Therapy should
be interrupted periodically at intervals of 6-12 months in order to observe possible changes in natural history of the disease.

Prophylaxis of herpes simplex infections: 200 mg 4 times daily at approximately 6-hourly intervals. Dosage may be doubled in severely immune-compromised patients (e.g. after marrow transplant) or in patients with impaired absorption from the gut.

Treatment of varicella and herpes zoster infections: 800 mg 5 times daily at approximately 4-hourly intervals, omitting the night-time dose. Treatment should continue for 7 days.

Children: For treatment of herpes simplex infections and for prophylaxis of herpes simplex infections in the immune compromised, children above 2 years should be given adult dosages and children below 2 years should be given half of the adult dose.

For treatment of varicella infections: Children above 6 years: 800 mg 4 times daily; 2-6 years: 400 mg 4 times daily; Below 2 years: 200 mg 4 times daily; Dosing may be calculated as 20 mg Zoral/kg body weight (not to exceed 800 mg) 4 times daily. Treatment should continue for 5 days.

Elderly: Adequate hydration of elderly patients taking high oral doses of Zoral should be maintained.

Renal Impairment
For patients with renal impairment the following dosing regimen should be followed:

Creatinine clearance (mL/min)

Epidemiology of oral diseases

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Oral Diseases: Recognizing and Preventing

Oral Diseases: Recognizing and Preventing

Beware though, because neglecting your teeth can lead to serious problems, including gum disease, diseases of the teeth and even other serious health problems not specifically related to your teeth.

Causes of Gum Disease

Gum disease occurs when plaque that forms on the surface of your teeth and around your gum line isn’t properly removed, but there are other ways for gum disease to occur.

  • Smoking or chewing tobacco
  • A family history of gum disease
  • Diseases that suppress your immune system:
    • AIDS
    • diabetes
    • leukemia
  • Malnutrition can also cause gum disease

Improper oral hygiene – not brushing and flossing your teeth regularly or properly – is the most common cause of gum disease.

Gingivitis is a mild form of gum disease, and many people have a mild case of it at one time or another in their lives.

While there are a few different reasons gingivitis can develop, the most common reasons are simply not brushing and flossing regularly or for as long as needed.

Gingivitis only affects the gums, though some people with gingivitis may think that they have a toothache if pain is present.

In many cases, gingivitis is undetected since it rarely causes serious pain.

Symptoms of Gingivitis

The most common symptoms of gingivitis are red, swollen gums.

In some cases your gums may bleed when you brush your teeth, though this does not always occur with gingivitis.

Typically, gingivitis can be remedied through regular brushing and flossing.

Some people find that mouthwash made specifically to fight gingivitis can be helpful, especially if they don’t have the ability to brush their teeth after each meal.
Mouthwash should not be a replacement for brushing and flossing however.

Periodontitis is a more severe form of gum disease.

Unlike gingivitis, which only affects the tissue surrounding the teeth – the visible part of your gum line – periodontitis can actually make your gums pull away from your teeth, leaving areas where bacteria from plaque can cause damage to the tooth and bone structure that holds your teeth in your jaw.

In some cases, periodontitis can cause loose teeth, tooth loss or require extraction due to infection.

Symptoms of Periodontitis

The same symptoms that show signs of gingivitis can apply to periodontitis, though more severe, noticeable symptoms may be present as well.

Severe bleeding of the gums, persistent bad breath, which is often related to an infection, clear or yellow pus coming through the teeth or gums and hard buildups of plaque and tartar that you can feel with your fingernails, sometimes referred to as catches, are the most common signs of periodontitis.

Other Types of Periodontitis

Periodontitis can come in a few other forms.

Aggressive periodontitis is not particularly common, mostly because it only happens in people with an otherwise healthy body.

Aggressive periodontitis often involves rapid tooth loss and loss of bone.

Necrotizing periodontal disease is another type, and while it can show up in generally healthy adults with severe dental problems, it is most common among people with systemic conditions like AIDS,

HIV or other immune disorders.

Tooth decay is what causes cavities, and while a very small amount of decay is normal for most people, too much can lead to serious problems.

The most common cause of tooth decay is a buildup of plaque on your teeth – that sticky stuff dentist scrapes off.

When too much plaque builds up it starts to eat away at the hard enamel that protects the soft dentin of your teeth – the real body of the tooth.

When plaque breaks through the enamel, it starts to eat little holes in your tooth, also known as a cavity.

Signs of Tooth Decay

The most common signs of tooth decay are

  • pain when chewing or biting into food
  • tooth sensitivity
  • pus around your tooth
  • visible holes in the tooth
  • general toothache

Tooth decay isn’t always visible when a cavity first starts to form, which is when it needs to be dealt with by a dentist so it doesn’t cause a more serious problem like tooth erosion.

Tooth erosion occurs after plaque from the gums eats through the enamel, past the layer of dentin and into the pulp of the tooth, which is the innermost layer.

When this happens, a severe toothache is usually present.

The signs of tooth erosion are much like those of general tooth decay, but they are often more severe.

Tooth erosion can damage the bone structure holding the teeth in place if an infection and abscess occurs because of the damage.

Oral cancer, sometimes referred to as mouth cancer, can develop in the lips, gums, tongue and on the roof of your mouth.

While gum disease and tooth damage doesn’t result in oral cancer, the most common early complications of oral cancer are gum disease and tooth decay in many people.

Causes of Oral Cancer

The most common cause of oral cancer is tobacco use

  • Smoking
  • Chewing
  • Using tobacco in any form

Alcohol abuse and years of sun exposure are also known causes.

The number of cases or oral cancer related to tobacco use far outweigh all others because of the carcinogenic effects of tobacco.

Symptoms of Oral Cancer

Initially, oral cancer may be somewhat hard to detect.

  • Loose teeth
  • Gum pain
  • White or off-white spots on the gums
  • Tongue pain
  • Thickening of the skin within the mouth

These are all symptoms that could imply oral cancer.

In addition to these symptoms, some people that have oral cancer may notice a general feeling that something is caught in their throat, jaw pain or painful swallowing.

The Importance of Oral Hygiene

Good oral hygiene is necessary to avoid gum disease and tooth damage, but in recent years, poor oral hygiene has been linked to heart disease, clogged arteries and endocarditis.

According to the American Academy of Periodontology, people that suffer from periodontal disease and other serious gum and tooth problems are almost twice as likely to have heart problems, and can even suffer strokes.

Good oral hygiene also reduces inflammation in the body, which can help your body fight off infection in other areas.

The most important part of preventing gum disease, tooth decay and oral cancer are regular checkups and screenings provided by your dentist.

Most people need to visit their dentist every 6 to 8 months. People with conditions and diseases that can make it hard for the body to fight infection like diabetes or HIV will need to visit the dentist more often.

Dentists also advise that you brush your teeth when you wake up, after each time you eat, and don’t forget to floss.

Good oral hygiene at home doesn’t mean you don’t have to visit the dentist, but it is a major part of the battle against gum disease and tooth problems.

Marcela De Vivo is free lance writer in Los Angeles covering health and wellness. She works as an independent consultant for Northwest, a Canadian pharmacy.

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11 Oral Disease

11 Oral Disease Oral Disease

Key learning points

A working knowledge of

  • the causes and risk factors involved in dental caries
  • the process of cavity formation, and its progress ultimately to an alveolar abscess
  • non-carious tooth surface loss
  • the causes and risk factors involved in periodontal disease
  • the onset of gingivitis and its progress to periodontitis
  • the non-surgical treatment of periodontal disease

A factual awareness of

  • other periodontal conditions
  • the risk factors associated with oral cancer

The two main oral diseases of concern to the dental team are dental caries and chronic periodontal disease, and the prevalence of both throughout the human race provides the vast majority of the day-to-day work of dental team members. Other periodontal conditions that may be seen from time to time are also mentioned.

Dental caries and chronic periodontal disease are discussed in detail within this chapter, while full details of oral health assessment and diagnosis techniques, and oral disease prevention are covered elsewhere.

Although oral cancer was discussed in Chapter 7, it is included again here as a worryingly increasing disease condition that may be seen from time to time in the dental workplace, and the importance of the dental team in its early diagnosis and prevention cannot be overestimated.

Dental caries

Dental caries (tooth decay) is a bacterial disease of the mineralised tissues of the tooth, where the strong crystal structure found in both enamel and dentine is demineralised (dissolved) by the action of acids. This allows the softer organic component of the tooth structure to be broken down to form cavities.

The acids involved are created as a waste product by oral bacteria, as they digest the foods we eat for their own nutrition. Although the acids are relatively weak organic ones, such as lactic acid or citric acid. they are strong enough to attack enamel and dentine. Not all the bacteria found in the oral cavity are associated with the production of these acids – the usual ones are:

  • Streptococcus mutans (initial stages of cavity formation)
  • Streptococcus sanguis
  • Some lactobacilli (later stages of cavity formation).

Not all the foods that we eat can be broken down into acids either, but those foods that can easily be formed into these damaging organic acids contain carbohydrates. Foods that consist of protein or fats are not relevant to the onset of dental caries. So in summary, the relevant factors in the development of dental caries are:

  • the presence of certain types of bacteria
  • carbohydrate foods
  • the production of weak organic acids by these bacteria
  • adequate time or frequency for the acids to attack the tooth.

The bacteria need to become attached to the tooth surface to be able to digest food debris and initiate dental caries, and they do this by forming themselves into a sticky layer called bacterial plaque .

Bacterial plaque

Millions of bacteria live in our mouths, flourishing on the food that we eat. Some of this food sticks to our teeth and attracts colonies of bacteria to the tooth surfaces. This combination of bacteria and food debris on a tooth surface forms a thin, transparent, protein-containing, soft and sticky film called plaque. It tends to form and stick most readily in areas where it cannot be easily ­dislodged, such as at the gingival margins of the teeth, in the fissures of teeth, and around the edges of dental restorations. These are called stagnation areas .

The build-up of plaque at the gingival margins of the teeth is directly associated with the onset of gingivitis and periodontal disease .

The plaque that sticks to the tooth surfaces allows the bacteria living within it to turn sugar into weak acids, which in turn dissolve enamel to produce dental caries .

The main micro-organism which initiates the process of caries is Streptococcus mutans. Large numbers of lactobacilli are then able to thrive in the acid environment, and the presence of these two micro-organisms is put to practical use as a test for caries activity. By periodically counting the number of streptococci or lactobacilli in a patient’s saliva, the level of caries activity and the effect of preventive measures can be monitored.


As referred to in Chapter 5, all types of food are classified into three distinct groups.

  • Protein – such as meats, fish and various dairy products and pulses.
  • Fat – such as animal fats and vegetable oils.
  • Carbohydrate – natural sugars and starches from fruit and vegetables, and artificial sugars from processed foods.

Of these, only carbohydrates can be turned into acid by bacteria and thereby cause caries – so they are described as cariogenic foods because they are capable of causing caries. The most acid-­producing carbohydrates are those which are artificially added during food preparation, and which therefore tend to be based on non-milk extrinsic sugars (NMEs).

As their name suggests, these types of sugar are not derived from milk and have been added artificially during the manufacturing process, rather than being found naturally in the food product itself. The most damaging ones of all are the refined sugars sucrose and glucose (also called dextrose).

Naturally occurring sugars that produce so little organic acid that they are considered harmless to teeth include the following.

  • Intrinsic sugars – found naturally in foods, such as fructose in fruits.
  • Milk extrinsic sugars – especially lactose.

Refined sugars can be instantaneously turned into acid by the bacteria concerned and available types include table sugar, sugar used in cooking, and sugar added to anything else taken by mouth, whether liquid or solid. Any food containing added sugar can cause caries and some obvious ones are:

  • cake, biscuits, jam and sweets
  • breakfast cereals
  • pastry, desserts, canned fruit, syrups and ice cream
  • soft drinks
  • hot beverages sweetened with sugar.

Sugar is widely added to many savoury foods too, in order to flavour or preserve them but without making its taste apparent. Such foods can include soups, sauces, canned vegetables and breakfast cereals which are accordingly sources of hidden sugar. Medicines may also contain hidden sugar and can be a significant cause of caries in chronically sick children.

Sugar occurring naturally in milk, fruit and vegetables is not a significant cause of caries. Naturally starchy and fibrous vegetables such as potatoes, carrots, peas and beans are rich in carbohydrate but may be regarded as insignificant causes of caries as long as no sugar is added by producers or during cooking. The prime cause of dental caries is refined sugar (sucrose), processed from sugar beet and sugar cane, and commercial glucose, which together constitute such a large proportion of the manufactured and sweetened food in our diet. Unfortunately, foods containing these NMEs tend to be cheap and readily available in most First World countries, along with acidic drinks such as carbonated fizzy ′pops’.

Acid formation

As soon as the carbohydrate source is eaten, the oral bacteria take the sugar component into the plaque structure and begin to digest it themselves. Within just a minute or two, it is turned into acid by the plaque bacteria and then attacks the enamel surface beneath the plaque. Enough acid is produced to last for about 20 min and in this initial acid attack, a microscopic layer of enamel is dissolved away. This phase is called demineralisation .

At the end of the meal or snack, when the intake of sugar is over, the acid persists for a period of time ranging from 20 min to 2 h before it is neutralised by the buffering action of saliva.

Saliva is the fluid bathing the oral cavity that is secreted from the salivary glands (see Chapter 10). Amongst its many roles, it maintains the mouth at a neutral level. being neither acidic nor alkaline. The measure of acidity/alkalinity of a solution is called its pH level and the neutral level maintained by saliva is pH 7. When the weak organic acids are produced by the oral bacteria, the pH level starts to fall and once it passes the critical pH 5.5, the environment is acidic enough to attack the enamel and dentine of teeth, and produce cavities.

Once neutralisation has occurred, no further demineralisation can take place until such time as more sugar is consumed. In this phase where no more sugar is present in the plaque, some natural healing takes place; mineral constituents naturally present in saliva enter demineralised enamel and restore the part lost by the initial acid attack. This healing phase is called remineralisation .

What happens next is entirely dependent on the frequency of sugar intake. If it is confined to mealtimes only, for example, at breakfast, midday and early evening, there can only be three acid attacks a day on the teeth. The amount of time available for remineralisation will greatly exceed that of demineralisation and the initial phase of caries will be arrested. But if a series of snacks is eaten between meals throughout the day, the reverse will occur. Most processed snacks contain some added sugar and the result is a rapid succession of acid attacks, with insufficient respite between them for saliva to neutralise the acid and allow the healing process of remineralisation to become dominant. Caries can then spread rapidly through affected teeth, as described later.

The longer the sugar stays on the teeth, the longer the duration of acid production. Thus sweet fluids, such as tea or coffee with sugar, which are rapidly washed off the teeth by saliva, are not normally a major cause of caries unless many drinks are taken throughout the day, whereas the much more frequent consumption of very sweet soft drinks by children is far more serious. But, overall, the most dangerous sources of sugar are those which have a sticky consistency when chewed, as it is far more difficult for the natural saliva flow to wash them away. The adherent nature of such foods allows them to cling to the teeth for a very long time, throughout which they are supplying plaque bacteria with the raw materials for prolonged acid formation and demineralisation.

Foremost among these sticky forms of sugar which cause caries are:

  • toffee and other sweets
  • cakes, biscuits, white bread and jam
  • puddings with syrup or treacle.

With our modern diet, added sugar is consumed nearly every time something is eaten, and the teeth are attacked by acid on each of these occasions. If snacks containing such sugar are ­frequently taken between meals, there will be a corresponding increase in the number of acid attacks on the teeth. The delicate balance between the forces of destruction (demineralisation) and those of repair (remineralisation) will then be completely upset in favour of tooth destruction and irreversible damage will occur.

Thus it is evident that the prime cause of caries is the frequent and unrestricted consumption of sweet snacks between meals. It is not the amount of sugar eaten but the frequency with which it is eaten that is all-important. This fundamental fact forms the basis of personal caries prevention and good dental health education.

Sites of caries

The parts of a tooth most prone to caries are those where food tends to collect and plaque bacteria can flourish. Such sites are known as stagnation areas. Occlusal fissures and the spaces between the mesial and distal surfaces of adjoining teeth (the interproximal areas, or contact points) are the most common stagnation areas. That is why caries occurs most often on occlusal and proximal surfaces. However, anywhere food debris can accumulate is a stagnation area where plaque will proliferate and caries is likely to occur. Such food traps are the necks of teeth covered by ill-fitting partial dentures, irregular teeth and unopposed teeth.

Minimal harm is caused by partial dentures which fit perfectly, but those which do not are a menace to dental health. They leave spaces between the necks of the teeth and the acrylic plate, or between any metal clasps and the teeth, which are dangerous stagnation areas.

During mastication, the movement of saliva and the food bolus over the tooth surfaces as it is chewed actually helps to clean teeth which are in good occlusion. This does not prevent plaque formation, but does reduce the amount of retained food debris which is responsible for the harmful effects of plaque. Teeth which are not in good occlusion, such as irregularly positioned and unopposed teeth, are not so exposed to this beneficial cleansing effect. Consequently food collects around these instanding or outstanding irregular teeth. It also covers the crown of any tooth which has lost its opposite number, and remains unopposed because the space has not been replaced artificially. To make the situation even worse, the sticky sweet food most likely to produce caries needs the minimum amount of mastication anyway, and therefore has a negligible cleansing effect – even on teeth in good occlusion.

Caries and cavity formation

Unrestricted consumption of carbohydrates and their sugar content produces an abundance of acid-forming bacteria in the plaque which collects in stagnation areas. The resultant series of continual acid attacks prevents remineralisation and allows acid to eat through the enamel until it reaches dentine, whereupon the caries spreads more rapidly through the more open structure of this inner tooth layer (Figure 11.1 ).

Microscopically, the process of cavity formation is as follows.

  • Very early acid attacks will show as ‘white spot lesions’ on the enamel surface.
  • Continued and frequent acid attacks will follow the prism structure of the enamel, and eat into any exposed cementum on the tooth root.
  • Demineralisation occurs, followed by episodes of remineralisation if the acid attacks are not too frequent – these areas of repair often appear as brown lesions on the teeth, especially at contact points (Figure 11.2 ).
  • With frequent or prolonged acid attacks, the mineral structure of the enamel is eventually destroyed and caries enters the tooth.
  • Caries extends deep into the enamel and eventually reaches the amelodentinal junction (ADJ).
  • Up to this point, the patient will feel no pain as enamel contains no nerve tissue.
  • Once past the ADJ, the caries enters dentine and can spread more rapidly because of the hollow structure of this tooth layer and its lower mineral content compared to enamel.
  • This undermines the overlying enamel, and normal occlusal forces are able to fracture off pieces of the tooth surface, leaving a hole in the tooth structure – this is called a cavity (Figure 11.3 ).
  • Odontoblast cells at the ADJ react to the bacterial attack by laying down secondary dentine in an attempt to protect the underlying pulp tissue.
  • The nerve fibrils lying within the dentine tubules will be stimulated as the caries progresses, and the patient will begin to feel sensitivity to temperature changes and to sweet foods.
  • The pulp tissue will also become irritated and inflamed – this is called pulpitis.
  • At this point, the caries can be removed by the dentist and the cavity restored with a filling ­(see Chapter 15), the inflamed pulp will settle and the tooth will be restored to its normal function – the inflammation is better described then as reversible pulpitis.
  • Otherwise, the cavity will continue to enlarge and the caries will progress towards the pulp chamber, as the production of secondary dentine is overrun by the speed of the bacterial attack.
  • The patient will be experiencing more severe pain of longer duration, and will eventually be unable to bite with the affected tooth.
  • When the carious attack reaches the immediate surroundings of the pulp chamber, the level of inflammation is too great to be resolved simply by removing the caries – this is called irreversible pulpitis.
  • The pain will become constant and throbbing in nature, often disturbing the patient’s sleep.
  • Once the pulp chamber itself is breached by the caries, a carious exposure of the contents occurs and the pulp will eventually die.
  • The tooth can now only be treated by undergoing an endodontic procedure (see Chapter 15) or by extraction (see Chapter 17).

Irreversible pulpitis

Pulpitis occurs when caries extends through the dentine to reach the pulp. The pulp is then said to be cariously exposed and the sequence of events described under inflammation (see Chapter 7) follows.

  • There is an increased blood flow through the apical foramen into the pulp.
  • Swelling cannot occur, however, as the pulp is confined within the rigid walls of the root canal and pulp chamber.
  • Pressure therefore builds up instead and causes intense pain.
  • A much more important result of this pressure, however, is the compression of blood vessels passing through the tiny apical foramen – this cuts off the blood supply and causes death of the pulp.
  • When the pulp dies, its nerves die too, and the severe toothache stops abruptly.
  • The respite is short, however, as pulp death leads to another very painful condition called alveolar abscess .

Pulpitis may be acute or chronic. It has many causes, apart from caries, but almost always ends in pulp death. Other causes of pulpitis are covered in Chapter 15.

Alveolar abscess

When pulpitis occurs, the pulp eventually dies as its blood supply is cut off by inflammatory pressure. The dead pulp decomposes and infected material passes out of the tooth through the apical foramen and into the alveolar bone at the apex of the tooth. These irritant products give rise to another inflammatory reaction in the tissues surrounding the apex. Pus formation occurs and an acute alveolar abscess develops.

  • This is an extremely painful condition.
  • The affected tooth becomes loose and very tender to the slightest pressure.
  • There is a continual throbbing pain and the surrounding gum is red and swollen.
  • Frequently the whole side of the face is involved in inflammatory swelling and the patient may have a raised temperature.
  • Looseness is caused by swelling of the periodontal ligament.
  • Pain is caused by the increased pressure of blood within the rigid confines of the periodontal ligament and alveolar bone. The tooth is so tender that it cannot be used for eating.
  • Thus an acute alveolar abscess may show all the cardinal signs of acute inflammation:
    • pain
    • swelling
    • redness
    • heat
    • loss of function
    • raised body temperature.

Pulp death is sometimes followed by the development of a chronic alveolar abscess instead of an acute one. This usually gives rise to very little pain and most patients are quite unaware of its presence. It may often be detected by the presence of a small hole in the gum called a sinus. which is a track leading from the abscess cavity in the alveolar bone to the surface of the gum. Pus drains from the abscess through the sinus into the mouth. This outlet prevents a build-up of pressure inside the bone and explains the lack of pain. Patients often refer to this lesion as a ‘gum boil’.

If an acute abscess is not treated, it eventually turns into a chronic abscess by the drainage of pus through a sinus (see Figure 7.3 ). This relieves the pain and the features of acute inflammation largely disappear. The relative freedom from pain does not last indefinitely, however, as a chronic alveolar abscess is liable to revert into an acute abscess at any time.

It should now be clear that pulpitis is followed by pulp death, and this eventually leads to an acute alveolar abscess, either directly or via a chronic abscess.

It was formerly taught that all carious dentine should be removed, but this is now considered unnecessary. Adequate preparation, filling and sealing of a cavity cuts it off from further plaque and acid formation, and allows a vital pulp to remineralise the deeper underlying dentine. Removal of carious dentine should therefore stop short of exposing the pulp when possible.

Role of saliva in oral health

The oral soft tissues in health are constantly bathed in saliva, the watery secretion from the three pairs of major salivary glands as well as from the numerous minor salivary glands present in the cheeks and lips (see Chapter 10).

Saliva contains the following components.

  • Water. as a transport agent for all the other constituents.
  • Inorganic ions and minerals. such as calcium ions and phosphate.
  • Ptyalin. a digestive enzyme which acts on carbohydrates (also called salivary amylase ).
  • Antibodies. as part of the defensive immune system, and known as immunoglobulins.
  • Leucocytes or white blood cells, also part of the body’s defence system.

These constituents all have important functions in the maintenance of a healthy oral environment.

  • The inorganic ions and minerals are released as required to act as buffering agents to help control the pH of the oral environment, by neutralising the organic acids produced by bacteria.
  • A high inorganic ion/mineral content produces thick, stringy saliva which gives the teeth good protection against caries, but allows dental calculus (tartar) to form easily and in large amounts.
  • A low inorganic ion/mineral content produces watery saliva, which offers little protection against caries to the teeth, but prevents large amounts of calculus from forming.
  • Calculus formation is associated with periodontal disease.
  • Water forms the carrying agent for the other salivary constituents, and allows self-cleansing of the oral environment to occur by dislodging food debris from the teeth before being swallowed.
  • The water also moistens the food bolus and the soft tissues, allowing swallowing (deglutition) and speech to occur.
  • It also dissolves food particles, so that the sensation of taste is produced – the taste buds on the tongue can only detect the taste of food when it is in solution.
  • Both antibodies and leucocytes help to protect and defend the oral environment from infection by micro-organisms.
Reduced salivary flow

The condition of reduced salivary flow is called xerostomia or dry mouth. There are many reasons why a patient can suffer from this, apart from it being the result of normal age-related changes of the salivary glands themselves.

  • Normal age-related changes to the salivary glands and their ability to function.
  • Low fluid intake over a period of time, or even dehydration.
  • Some autoimmune disorders, especially Sjögren’s syndrome which specifically affects the salivary glands and the lacrimal glands of the eyes, which produce tears.
  • Several routinely prescribed drugs, including diuretics (prescribed to alleviate water retention in patients with heart failure), some antidepressants (prescribed to alleviate anxiety), and beta-blockers (prescribed to slow down the heart rate, especially in angina sufferers).

Reduced salivary flow has several important consequences for the patient and for the oral health team.

  • Reduced self-cleansing allows more food debris to accumulate around the teeth, increasing plaque production and the likelihood of caries and periodontal disease developing.
  • It will also allow food debris to stagnate in the mouth, causing halitosis (bad breath).
  • Reduced buffering of the oral environment allows longer and more frequent acid attacks, increasing the likelihood of caries developing.
  • Poor lubrication of the oral soft tissues makes speech and swallowing more difficult.
  • Reduced amounts of water in the saliva affects the sensation of taste.
  • Reduced flow and amounts of saliva in the mouth will make the retention of dentures more difficult.

The opposite condition to xerostomia, that of excessive saliva production, is called ptyalism. which is often seen in patients with periodontal disease. It can also occur in Parkinson’s disease and in pregnancy.

Diagnosis of caries

Before caries is treated, it must first be detected. Early diagnosis is very important in controlling the extent of the damage done, as well as the level of discomfort experienced by the patient. The earlier a cavity is detected, the better the chance of saving the tooth. This is why regular dental examinations are recommended, and the frequency of attendance should be determined by the caries experience of the patient – those with a high caries incidence need to be examined more frequently than others. Unfortunately, these are often the very patients who do not attend regularly for dental examination, for whatever reason.

Large cavities are obvious to the naked eye but it is easier to treat caries before cavities reach such a size. The dentist has various methods available for detecting smaller carious les/>

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Jan 8, 2015 | Posted by mrzezo in Dental Nursing and Assisting | Comments Off on 11 Oral Disease

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