Dental caries – the bacterial infection of the mineralised tissues of the tooth
Gingivitis – the inflammation of the gingival tissues at the neck of the tooth
Periodontitis – the inflammation of the supporting structures of the tooth
Dental caries
A bacterial disease of the mineralised tissues of the tooth, where the strong crystal
structure found in both enamel and dentine is demineralised by the action of acids.
This allows the softer organic component to be broken down to form cavities.
The acids involved are produced as a waste product by oral bacteria and although relatively
weak, they are strong enough to attack enamel and dentine.
Bacteria associated with the oral cavity:
Streptococcus mutans (initial stages of cavity formation)
Streptococcus sanguis
Some lactobacilli (later stages of cavity formation)
The foods that are broken down into acids can be formed into damaging organic acids that
contain carbohydrates. Foods that contain protein or fats are not relevant to the onset of
caries.
Summary:
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
Bacterial plaque
Food sticks to teeth and attracts colonies of bacteria to the surface of the tooth.
This combination of food and bacteria forms a thin, transparent, protein-containing,
soft and sticky film called plaque.
Usually found in gingival margins, fissures and around the edge of restorations –
stagnation areas.
Build-up of plaque at gingival margins is associated with the onset of gingivitis and
periodontal disease.
Plaque that sticks to surfaces allows bacteria to turn sugar into weak acids which
dissolve enamel to produce dental caries.
The main microorganism is Streptococcus mutans.
Large numbers of lactobacilli can then thrive in the acid environment
Carbohydrates and sugars
Proteins – meats, fish, various dairy products and pulses
Fat – animal fats and vegetable oils
Carbohydrates – natural sugars and starches from fruit and veg and artificial sugars
from processed foods
, Only carbohydrates can be broken down into acids by bacteria – so are described as
cariogenic foods.
The most acid-producing carbohydrates are those artificially added during food
preparation and tend to be based on non-milk extrinsic sugars (NMES)
The most damaging are the refined sugars sucrose and glucose (dextrose)
Naturally occurring sugars are harmless and include
o Intrinsic sugars – found naturally in foods like fructose in fruit
o Milk extrinsic sugars – especially lactose
Refined sugar can be instantly turned into acid by the bacteria – prime cause of
caries
Hidden sugars are those which are added to savoury foods in order to flavour or
preserve them, along with some medicines
Sugar occurring naturally in milk, fruit and veg isn’t a significant cause of caries
Acid formation
As soon as carbohydrate food is eaten the oral bacteria take the sugar component
into the plaque component and digest themselves.
Turned into acid by plaque bacteria which attacks enamel surface
Demineralisation – where a microscopic layer of enamel is dissolved away.
After eating, acid persists for 20mins to 2 hours before being neutralised by saliva.
Saliva pH level is 7
When weak organic acids are produced the pH level falls and the environment
becomes acidic enough to attack enamel and dentine.
Once neutralisation has happened, no further demineralisation can take place.
Remineralisation – natural healing due to lack of sugar in plaque
More episodes of demineralisation than remineralisation will happen with regular
snacking due to less time available for remineralisation.
The longer sugar stays on teeth, the longer the duration of acid production.
Irreversible damage is done when the balance between demineralisation and
remineralisation.
Prime cause of caries is the frequent and unrestricted consumption of sweet snacks
between meals.
Site of caries
Caries are more likely in areas where food collects during normal chewing
movements and plaque bacteria can thrive – stagnation areas.
Occlusal fissures and spaces between teeth are common stagnation areas.
Other stagnation areas include the necks of teeth covered by ill-fitting partial
dentures, irregular teeth in the arch line, and unopposed teeth in either jaw.
During mastication, the movement of saliva and food bolus over tooth surface as its
chewed helps to clean teeth which doesn’t prevent plaque formation but does
reduce the amount of retained food debris.
Teeth that aren’t in good occlusion collect food as they aren’t exposed to beneficial
cleansing effects of mastication.
Caries and cavity formation
, Unrestricted consumption of carbohydrates produces lots of acid-forming bacteria in
plaque which collects in stagnation areas.
Lots of acid attack stops remineralisation from occurring as allows acid to eat through
enamel until it reaches dentine, where caries can spread more rapidly.
Process of cavity formation:
o White spot lesions on enamel surface
o Acid attacks will follow prism structure and eat into cementum on root
o Demineralisation occurs, followed by remineralisation – brown lesions
o Mineral structure of enamel is destroyed, and caries enter tooth
o Caries extend deep into enamel and reached amelodentinal junction – the point
where enamel and dentine layers meet
o Patient feels no pain, as enamel contains no nerve tissue
o Once past the ADJ, caries enters dentine and spread more rapidly due to hollow
structure and lower mineral content
o Normal occlusal forces are able to fracture off pieces of tooth surface, leaving a
hole in the tooth – cavity
o Odontoblast cells at the ADJ react to bacterial attack by laying down secondary
dentine to protect underlying pulp tissue
o Nerve fibrils within dentine tubules are stimulated as caries progresses and the
patient will feel sensitivity to temperature changes
o The pulp tissue will become irritated and inflamed – pulpitis
o The caries can be removed by dentist and cavity restored with filling – inflamed
pulp will settle (reversible pulpitis)
o If not treated, cavity will enlarge, and caries will progress towards pulp chamber
o Patient will have severe pain and will be unable to bite
o When carious attack reaches surroundings of the pulp chamber, the level of
inflammation is too great to be resolved by removing caries – irreversible
pulpitis
o Once the pulp chamber is breached by caries, a carious exposure of the contents
occurs, and pulp will die
o The tooth can only be treated by an endodontic procedure or extraction
Irreversible pulpitis
Pulpitis occurs when caries extends through dentine to reach the pulp which is
then cariously exposed
o Increased blood flow through apical foramen into pulp
o Swelling cannot occur as pulp is confined within rigid walls of root canal
and pulp chamber
o Pressure builds up causing pain
o Pressure results in compression of blood vessels passing through the tiny
apical foramen – cuts off blood supply to tooth pulp dies
o When the pulp dies the nerve dies too and toothache stops
o The respite is short as pulp death leads to alveolar abscesses
Pulpitis can be acute or chronic and has many causes
Almost always ends in pulp death
Alveolar abscess
, When pulpitis occurs, the pulp dies and its blood supply is cut off by
inflammatory pressure.
Dead pulp decomposes and infected material passes through the apical foramen
and into alveolar bone surrounding apex
These irritant products create another inflammatory response in the tissues
Pus formation occurs and an acute alveolar abscess develops:
o Extremely painful
o Affected tooth becomes loose and tender
o Continual throbbing pain with redness and swelling in the area
o Inflammatory dwelling involves the side of face and patient may have a
raised temperature
o Looseness is caused by swelling of the periodontal ligament
o Pain Is caused by increased pressure of blood within confines of PDL and
alveolar bone.
o The tooth is so tender it cannot be used for eating
o Acute alveolar abscess may show all cardinal signed of acute
inflammation
Pain
Swelling
Redness
Heat
Loss of function
Raised body temperature
Pulp death can be followed by a chronic alveolar abscess instead of an acute one
Gives rise to little pain and most patients are unaware its there
Can be detected by dentist as 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 abscess through the sinus into the mouth which prevent built up
pressure and pain
If acute abscess is not treated, it will turn into a chronic abscess by the drainage
of pus which relieves pain and features disappear
Role of saliva in oral health
The saliva is a watery secretion from the three pairs of salivary glands as well as from
the minor salivary glands in the cheeks and lips
Saliva contains the following:
o Water – as a transport agent for other constituents
o Inorganic ions and minerals – such as calcium ions and phosphate
o Ptyalin – a digestive enzyme that acts on carbohydrates (salivary amylase)
o Antibodies – as part of defensive immune system, known as
immunoglobulins
o Leucocytes – white blood cells are part of body’s defence system
These parts have important functions in the maintenance of a healthy oral
environment as described:
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