The most common disorder of teeth is dental caries

Dental caries

Dental caries is the result of damage to the enamel and dentine by acid formed within
bacterial plaque.
Bacterially generated acid in the mouth is usually neutralized by the alkaline secretions of the salivary tissue. However, when the acid is made by bacteria in plaque, the physical density of the plaque prevents saliva from reaching the enamel surface of the tooth.
The acid dissolves the calcium hydroxyapatite of the enamel and progressively penetrates the full thickness of the enamel, decalcifying it as it goes.
This produces a visible cavity in the tooth. 
As the cavity forms, bacteria can penetrate deeper into the tooth until the dentine is
reached, and then penetrate the dentine layer through the hollow dentinal tubules  which become distended with bacteria and tissue debris. This, combined with the continuing demineralizing effect of the acid, leads to liquefaction of the dentine.
Eventually the dentine layer may be fully penetrated, and both bacteria and acid reach the soft central dental pulp. 

Along the line of attack, the enamel and dentine are destroyed and the odontoblasts die.
Although there is limited capacity for tissue reaction because the tissues are poorly 
cellular, in chronic lesions the odontoblasts may produce secondary dentine in an attempt at repair and restitution.

The consequences of carious attack are a pit or crater in the enamel, a penetrating 
destruction of the dentine and, when the dentine is fully penetrated, acute pulpitis
due to bacterial and acid damage to the soft tissues of the pulp.

The most important complications of dental caries are pulpitis and periapical inflammation or abscess.

Spread of bacteria and acid into the soft pulp space through carious penetration leads 
to necrosis of some of the pulp tissues, with an associated acute inflammatory reaction
(mainly vessel dilatation, oedema, and neutrophil infiltration).
When there is extensive tissue necrosis a pulp abscess may form.
The combination of bacterial and acid necrosis with increased intra-pulp pressure due to inflammatory oedema leads to extensive necrosis of all the pulp tissues.
Inflammatory stimulation of the nerve twigs in the pulp produces severe pain, localized or diffuse toothache being the main symptom of acute pulpitis.

Where the penetration of the enamel and dentine has been through a narrow carious channel, the pulp cavity remains largely isolated from the mouth cavity (closed pulpitis).
However, where there has been extensive destruction of the enamel and dentine, the pulp cavity may be exposed to the oral cavity (open pulpitis).
In these cases the pulp cavity is often completely replaced by inflammatory granulation tissue, which progresses through the phases of vascular granulation tissue, fibrous granulation tissue, and fibrous scar.
The scarred pulp forms a polypoid protrusion into the oral cavity, which may become re-epithelialized.

Inflammation and death of the pulp is often followed by apical periodontal infection, 
the inflammation initially being confined to the small space beneath the apex, between the tooth apex and the surrounding bone.
At first the infection is acute, with a predominantly acute inflammatory reaction that is rich in neutrophils, and there is often abscess formation (periapical abscess).
The inflammation eventually becomes chronic, with a heavy infiltrate of lymphocytes and plasma cells, and granulation tissue formation (chronic periapical periodontitis).

The enlarging inflammatory mass often erodes the bone around the apex of the tooth, producing an osteolytic, rounded lesion composed of chronic inflammatory granulation tissue, which may contain small neutrophil accumulations.
This is sometimes called a 'periapical granuloma' and is the most common cause of teeth-related cystic lesions in the bone .

Expansion of acute or chronic inflammatory lesions at the apex of abnormal teeth may produce inflammation in surrounding tissues with, for example, abscesses in the mandible pointing through the skin of the neck or producing sublingual cellulitis.
 
Similar lesions in the upper jaw can break through the floor of the maxillary sinus to produce chronic sinus inflammation.

Periodontal disease, not associated with apical abnormality, is usually a consequence of gingivitis.

GINGIVITIS

Some form of gingivitis (inflammation of the gums) is present in almost every mouth, 
and is usually the result of neglected oral and dental hygiene.
Acute gingivitis particularly affects young men, manifesting as swelling and soreness of the gums, often with bleeding and ulceration.
Large numbers of bacteria are present in the ulcerated areas, and are probably causative.

Chronic gingivitis occurs as a result of accumulation of bacterial plaque.
It usually begins in childhood, when it is asymptomatic.
Regular brushing of teeth, beginning in childhood, minimizes the accumulation of bacterial plaque and reduces the likelihood of significant gingivitis in later life. Bacterial plaque becomes calcified in adults, separating the gingiva from the tooth. There is chronic inflammation in the gingival epithelium and sub-mucosa, with large numbers of lymphocytes and plasma cells.

Chronic periodontitis results from the consequences of chronic gingival inflammation in relation to the presence of calculous plaque between the gingiva and the tooth. These are: 

• Destruction of the periodontal ligament, leading to loosening of the tooth in its   socket.

• Progressive deepening of the pocket between tooth and gingiva, which contains ever-increasing amounts of sub-gingival plaque.

• Progressive inflammatory destruction of the alveolar bone, leading to severe gingival recession.

• Periodontal abscess formation. if the chronic inflammatory process becomes accelerated by acute bacterial infection. This accelerates destruction of the alveolar bone, and pus may extrude into the alveolar cavity or alongside the tooth in the sub-gingival pocket.

Cysts related to the teeth can produce osteolytic lesions in the bones of the jaw

DENTAL CYSTS

Dental cysts can be simply classified into those due to a developmental abnormality, 
and those that are secondary to inflammatory disease associated with the teeth.
The most important inflammatory cyst is the radicular cyst.
It is far more common than the developmental cysts, and usually occurs in adults in association with dental caries of the permanent dentition.
Most commonly involving the upper lateral incisors, it follows the development of a periapical granuloma resulting from caries.
Cords of squamous epithelium grow into the chronic inflammatory mass, and central dissolution of the epithelial masses leads to cyst formation.
The wall is characteristically inflamed, and cholesterol clefts are frequent, often with associated foreign body giant cells.
The associated tooth dies, and the cyst may persist after extraction of the tooth.
As the chronic inflammatory cyst enlarges, the surrounding bone may be eroded, producing a well-defined area of lucency on radiology.

Among the most important  developmental cystsare odontogenic keratocysts, which usually occur in young males and are related to the mandibular molar region. 
They may be asymptomatic or may present with an intraoral swelling.
Lined by stratified squamous epithelium, with a variable keratin layer that is sometimes parakeratotic, they may be multilocular and are occasionally multiple.
Treatment is difficult, and they tend to recur after incomplete removal.
Dentigerous cysts mostly involve the third molars or the canine teeth.
A typical cyst envelops the crown of an unerupted or displaced tooth and is attached to its neck.
The cyst is lined by stratified squamous epithelium, usually only a few cell layers thick,supported on a thick fibrous wall.
At its junction with the neck of the tooth, the cyst epithelium merges with the reduced remnants of the enamel epithelium.
The cyst contains yellow fluid, which is usually clear. However, metaplasia of the squamous epithelium lining the cyst can occasionally lead to the production of keratin and mucin, which may render the cyst contents mucoid or pasty.
These cysts are derived from the dental follicle of the unerupted tooth and are unilocular.

As their name implies, lateral periodontal cysts lie alongside the tooth.
Their origin is uncertain. They are frequently asymptomatic, mainly being detected in routine dental X-rays as a round, osteolytic lesion that is discrete from, and lateral to, the root of a canine or premolar tooth. The cyst is lined by thin, non-keratinized squamous epithelium, with a surrounding fibrous wall. 

The cyst is lined by stratified squamous epithelium.
The cyst is related to the neck of a displaced tooth, and is lined by a thin layer of stratified squamous epithelium.

Tumours derived from dental precursor tissues are rare

The most common tumour derived from odontogenic epithelium is the ameloblastoma.
It is benign and does not metastasize.
Tumours are mainly seen in the mandible of middle-aged adults, the vast majority developing at the angle of the mandible.
They are slow-growing lesions, which locally invade the bone, tumour expansion often
leading to separation of the teeth and, occasionally, to loosening.
They are composed of islands of odontogenic epithelium, often with a mixed fibrous stroma.
The odontogenic epithelium forms islands with peripheral, tall ameloblastic epithelial cells surrounding loose epithelium, resembling the stellate reticulum of the developing tooth.
Squamous metaplasia may occur, which is a source of potential confusion with invasive squamous carcinoma. The tumour may resemble a unilocular or multilocular cyst radiologically.