Smoking and tobacco use of any kind are associated with increased risk of dry socket. This may be partially due to the vasoconstrictive action of nicotine on small blood vessels. Abstaining from smoking in the days immediately following a dental extraction reduces the risk of a dry socket occurring.

Vasoconstrictors are present in most local anesthetics, and are intended to increase the length of analgesia by reducing blood supply to the region which reduces the amount of local anesthetic solution that is absorbed into the circulation and carried from the local tissues. Hence, use of local anesthetics with vasoconstrictors is associated with an increased risk of dry socket occurring. However, frequently use of local anesthetic without vasoconstrictors would not provide sufficient analgesia, especially in the presence of acute pain and infection, meaning that the total dose of local anesthetic may need to be increased. Adequate pain control during the extraction is balanced against an increased risk of dry socket.

Pericoronitis usually occurs in young adults, around the time when wisdom teeth are erupting into the mouth. If the individual has reached their twenties without any attack of pericoronitis, it becomes substantially less likely one will occur thereafter.

Once the plaque stagnation area is removed either through further complete tooth eruption or tooth removal then pericoronitis will likely never return. A non-impacted tooth may continue to erupt, reaching a position which eliminates the operculum. A transient and mild pericoronal inflammation often continues while this tooth eruption completes. With adequate space for sustained improved oral hygiene methods, pericoronitis may never return. However, when relying on just oral hygiene for impacted and partially erupted teeth, chronic pericoronitis with occasional acute exacerbation can be expected.

Dental infections such as a pericoronal abscess can develop into septicemia and be life-threatening in persons who have neutropenia. Even in people with normal immune function, pericoronitis may cause a spreading infection into the potential spaces of the head and neck. Rarely, the spread of infection from pericoronitis may compress the airway and require hospital treatment (e.g. Ludwig's angina), although the majority of cases of pericoronitis are localized to the tooth. Other potential complications of a spreading pericoronal abscess include peritonsillar abscess formation or cellulitis.

Chronic pericoronitis may be the etiology for the development of paradental cyst, an inflammatory odontogenic cyst.

The prognosis for impacted wisdom teeth depends on the depth of the impaction. When they lack a communication to the mouth, the main risk is the chance of cyst or neoplasm formation which is relatively uncommon.

Once communicating with the mouth, the onset of disease or symptoms cannot be predicted but the chance of it does increase with age. Less than 2% of wisdom teeth are free of either periodontal disease or caries by age 65. Further, several studies have found that between 30% – 60% of people with previously asymptomatic impacted wisdom teeth will have them extracted due to symptoms or disease, 4–12 years after initial examination.

Extraction of the wisdom teeth removes the disease on the wisdom tooth itself and also appears to improve the periodontal status of the second molar, although this benefit diminishes beyond the age of 25.

A periodontal abscess most commonly occurs as a complication of advanced periodontal disease (which is normally painless). A periodontal pocket contains dental plaque, bacteria and subgingival calculus. Periodontal pathogens continually find their way into the soft tissues, but normally they are held in check by the immune system. A periodontal abscess represents a change in this balance, related to decreased local or systemic resistance of the host. An inflammatory response occurs when bacteria invade and multiply within the soft tissue of the gingival crevice/periodontal pocket. A pus-filled abscess forms when the immune system responds and attempts to isolate the infection from spreading.

Communication with the oral environment is maintained via the opening of the periodontal pocket. However, if the opening of a periodontal pocket becomes obstructed, as may occur if the pocket has become very deep (e.g. with furcation involvement), then plaque and calculus are trapped inside. Food packing may also obstruct a periodontal pocket. Food packing is usually caused by failure to accurately reproduce the contact points when dental restorations are placed on the interproximal surfaces of teeth. Another potential cause occurs when a periodontal pocket is scaled incompletely. Following this procedure, the gingival cuff tightens around the tooth, which may be enough to trap the bacteria left in the pocket. A gingival retraction cord which is accidentally left "in situ" is an occasional cause of a periodontal abscess.

Penetrating injury to the gingiva e.g. with a toothbrush bristle, fishbone, toothpick or periodontal instrument may inoculate bacteria into the tissues. Trauma to the tissues, e.g. caused by an impact on a tooth, or excessive pressure exerted on teeth during orthodontic treatment. Occlusal overload may also be involved in the development of a periodontal abscess, but this is rare and usually in combination with other factors. Bruxism is a common cause of excessive occlusal forces.

Systemic immune factors such as diabetes can predispose to the formation of periodontal abscesses.

Perforation of a root canal during endodontic therapy can also lead to a periodontal abscess.

Most dental pain can be treated with routine dentistry. In rare cases, toothache can be a symptom representing a life-threatening condition, such as a deep neck infection (compression of the airway by a spreading odontogenic infection) or something more remote like a heart attack.

Dental caries, if left untreated, follows a predictable natural history as it nears the pulp of the tooth. First it causes reversible pulpitis, which transitions to irreversible pulpitis, then to necrosis, then to necrosis with periapical periodontitis and, finally, to necrosis with periapical abscess. Reversible pulpitis can be stopped by removal of the cavity and the placement of a sedative dressing of any part of the cavity that is near the pulp chamber. Irreversible pulpitis and pulp necrosis are treated with either root canal therapy or extraction. Infection of the periapical tissue will generally resolve with the treatment of the pulp, unless it has expanded to cellulitis or a radicular cyst. The success rate of restorative treatment and sedative dressings in reversible pulpitis, depends on the extent of the disease, as well as several technical factors, such as the sedative agent used and whether a rubber dam was used. The success rate of root canal treatment also depends on the degree of disease (root canal therapy for irreversible pulpitis has a generally higher success rate than necrosis with periapical abscess) and many other technical factors.

If left untreated, a severe tooth abscess may become large enough to perforate bone and extend into the soft tissue eventually becoming osteomyelitis and cellulitis respectively. From there it follows the path of least resistance and may spread either internally or externally. The path of the infection is influenced by such things as the location of the infected tooth and the thickness of the bone, muscle and fascia attachments.

External drainage may begin as a boil which bursts allowing pus drainage from the abscess, intraorally (usually through the gum) or extraorally. Chronic drainage will allow an epithelial lining to form in this communication to form a pus draining canal (fistula). Sometimes this type of drainage will immediately relieve some of the painful symptoms associated with the pressure.

Internal drainage is of more concern as growing infection makes space within the tissues surrounding the infection. Severe complications requiring immediate hospitalization include Ludwig's angina, which is a combination of growing infection and cellulitis which closes the airway space causing suffocation in extreme cases. Also infection can spread down the tissue spaces to the mediastinum which has significant consequences on the vital organs such as the heart. Another complication, usually from upper teeth, is a risk of septicaemia (infection of the blood) from connecting into blood vessels, brain abscess (extremely rare), or meningitis (also rare).

Depending on the severity of the infection, the sufferer may feel only mildly ill, or may in extreme cases require hospital care.

Few studies have looked at the percentage of the time wisdom teeth are present or the rate of wisdom teeth eruption. The lack of up to five teeth (excluding third molars, i.e. wisdom teeth) is termed hypodontia. Missing third molars occur in 9-30% of studied populations.

One large scale study on a group of young adults in New Zealand showed 95.6% had at least 1 wisdom tooth with an eruption rate of 15% in the maxilla and 20% in the mandible. Another study on 5000 army recruits found 10,767 impacted wisdom teeth. The frequency of impacted lower third molars has been found to be 72% and the frequency of retained impacted wisdom teeth that are free of disease and symptoms is estimated at 11.6% to 29% which drops with age.

The incidence of wisdom tooth removal was estimated to be 4 per 1000 person years in England and Wales prior to the 2000 NICE guidelines.

Successful treatment of a dental abscess centers on the reduction and elimination of the offending organisms.

This can include treatment with antibiotics and drainage. If the tooth can be restored, root canal therapy can be performed. Non-restorable teeth must be extracted, followed by curettage of all apical soft tissue.

Unless they are symptomatic, teeth treated with root canal therapy should be evaluated at 1- and 2-year intervals after the root canal therapy to rule out possible lesional enlargement and to ensure appropriate healing.

Abscesses may fail to heal for several reasons:

- Cyst formation

- Inadequate root canal therapy

- Vertical root fractures

- Foreign material in the lesion

- Associated periodontal disease

- Penetration of the maxillary sinus

Following conventional, adequate root canal therapy, abscesses that do not heal or enlarge are often treated with surgery and filling the root tips; and will require a biopsy to evaluate the diagnosis.

A periodontal abscess (also termed lateral abscess, or parietal abscess), is a localized collection of pus (i.e. an abscess) within the tissues of the periodontium. It is a type of dental abscess. A periodontal abscess occurs alongside a tooth, and is different from the more common periapical abscess, which represents the spread of infection from a dead tooth (i.e. which has undergone pulpal necrosis). To reflect this, sometimes the term "lateral (periodontal) abscess" is used. In contrast to a periapical abscess, periodontal abscesses are usually associated with a vital (living) tooth. Abscesses of the periodontium are acute bacterial infections classified primarily by location.

Toothache may occur at any age, in any gender and in any geographic region. Diagnosing and relieving toothache is considered one of the main responsibilities of dentists. Irreversible pulpitis is thought to be the most common reason that people seek emergency dental treatment. Since dental caries associated with pulpitis is the most common cause, toothache is more common in populations that are at higher risk of dental caries. The prevalence of caries in a population is dependent upon factors such as diet (refined sugars), socioeconomic status, and exposure to fluoride (such as areas without water fluoridation). In the United States, an estimated 12% of the general population reported that they suffered from toothache at some point in the six months before questioning. Individuals aged 18–34 reported much higher experience of toothache than those aged 75 or over. In a survey of Australian schoolchildren, 12% had experienced toothache before the age of five, and 32% by the age of 12. Dental trauma is extremely common and tends to occur more often in children than adults.

Erupted teeth that are adjacent to impacted teeth are predisposed to periodontal disease. Since the most difficult tooth surface to be cleaned is the distal surface of the last tooth, in the presence of an impacted tooth there is always gingival inflammation around the second molar that is invariably present. Even this minor amount of inflammation can provide bacteria access to a larger portion of the root surface that results in early formation of periodontitis compromising the tooth.

Even in situations in which no obvious communication exists between the mouth and the impacted third molar there may be enough communication to initiate dental caries (tooth decay).

Pericoronitis is an infection of the soft tissue that covers the crown of an impacted tooth and is usually caused by the normal oral microbiota. For most people there exists a balance between the host defenses and the oral micriobiota but if the host defenses are compromised like during minor illness such as influenza or an upper respiratory tract infection, pericoronitis results. Another common cause is entrapment of food beneath the gum flap (also called an operculum). Pericoronitis can present as a mild infection or severe infection. In its mildest form it is just a localized tissue swelling and soreness whereas in severe forms the swelling is slightly larger even sometimes creating trismus (difficulty opening the mouth).

Occasionally, an impacted tooth causes sufficient pressure on the roots of adjacent teeth causing it to resorb.

An impacted tooth occupies space that is usually filled with bone. This weakens that area of bone and renders the jaw more susceptible to fracture.

When impacted teeth are retained completely within the alveolar process, the associated follicular sac is also retained along with it. Though in most persons the dental follicle maintains its original size sometimes it may undergo cystic degeneration and become a dentigerous cyst or a keratocyst.

Dental infections account for approximately 80% of cases of Ludwig's angina. Mixed infections, due to both aerobes and anaerobes, are of the cellulitis associated with Ludwig's angina. Typically, these include alpha-hemolytic streptococci, staphylococci and bacteroides groups.

The route of infection in most cases is from infected lower molars or from pericoronitis, which is an infection of the gums surrounding the partially erupted lower (usually third) molars. Although the widespread involvement seen in Ludwig's usually develops in immunocompromised persons, it can also develop in otherwise healthy individuals. Thus, it is very important to obtain dental consultation for lower-third molars at the first sign of any pain, bleeding from the gums, sensitivity to heat/cold or swelling at the angle of the jaw.

There has been a single case reported where Ludwig's angina was thought to be caused by a recent Tongue piercing. In addition, Filipino boxer Pancho Villa (1901–1925) died after contracting Ludwig's Angina following a bout with Jimmy McLarnin.

Treatment involves appropriate antibiotic medications, monitoring and protection of the airway in severe cases, and, where appropriate, urgent Otolaryngology-Head and Neck Surgery, maxillo-facial surgery and/or dental consultation to incise and drain the collections. The antibiotic of choice is from the penicillin group.

Incision and drainage of the abscess may be either intraoral or external. An intraoral incision and drainage procedure is indicated if the infection is localized to the sublingual space. External incision and drainage is performed if infection involves the perimandibular spaces.

A nasotracheal tube is sometimes warranted for ventilation if the tissues of the mouth make insertion of an oral airway difficult or impossible.

In cases where the patency of the airway is compromised, skilled airway management is mandatory. Fiberoptic intubation is common.

Ludwig's angina is a life-threatening condition, and carries a fatality rate of about 5%.