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.

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.

Risk factors associated with gingivitis include the following:

- age

- osteoporosis

- low dental care utilization (fear, financial stresses, etc.)

- poor oral hygiene

- overly aggressive oral hygiene such as brushing with stiff bristles

- mouth-breathing during sleep

- medications that dry the mouth

- cigarette smoking

- genetic factors

- pre-existing conditions

The periapical cyst (also termed radicular cyst or inflammatory cyst) is the most common odontogenic cyst. Periapical is defined as "the tissues surrounding the apex of the root of a tooth" and a cyst is "a pathological cavity lined by epithelium, having fluid or gaseous content that is not created by the accumulation of pus." Most frequently located in the maxillary anterior region, it is caused by pulpal necrosis secondary to dental caries or trauma. The cyst has lining that is derived from the epithelial cell rests of Malassez which proliferate to form the cyst. Highly common in the oral cavity, the periapical cyst is asymptomatic, but highly significant because a secondary infection can cause pain and damage. In radiographs, it appears a radiolucency (dark area) around the apex of a tooth's root.

There is only very weak evidence linking to coronary heart disease.

There is little evidence linking progression of periodontal disease to low birth weight or preterm birth:

"In these women with periodontitis and within this study's limitations, disease progression was not associated with an increased risk for delivering a pre-term or a low birthweight infant."

There is recently emerged evidence linking chronic periodontitis with head and neck squamous cell carcinoma: "Patients with periodontitis were more likely to have poorly differentiated oral cavity SCC than those without periodontitis (32.8% versus 11.5%; P = 0.038)".

There is evidence to suggest that periodontal disease may play a role in the pathogenesis of Alzheimer's Disease.

Periapical cysts comprise approximately 75% of the types of cysts found in the oral region. The ratio of individuals diagnosed with periapical cysts is 3:2 male to female, as well as individuals between 20 and 60 years old. Periapical cysts occur worldwide.

Types of Periapical cysts:

Apical: 70%

Lateral: 20%

Residual: 10%

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.

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.

The lateral periodontal cyst is a non-inflammatory developmental cyst that arises from the epithelial post-functional dental lamina, which is a remnant from odontogenesis. It is more common in middle-aged males. Usually asymptomatic, it presents as a regular well-corticated radiolucency on the side of a mandibular canine or premolar root. Histologically, the cyst appears similar to the gingival cyst of the adult, having a non-keratinized squamous epithelial lining. The involved tooth is usually vital and has no indication for root canal treatment unless the signs of non-vital or necrotic pulpal tissue were confirmed. The cysts arise from epithelial rest cells in the periodontal ligament, although it is unknown whether from the cell rests of Malassez, reduced enamel epithelium or dental lamina remnants, and are generally treated by surgical enucleation.

The aetiology of dental abrasion can be due to a single stimuli or, as in most cases, multi-factorial. The most common cause of dental abrasion, is the combination of mechanical and chemical wear.

Tooth brushing is the most common cause of dental abrasion, which is found to develop along the gingival margin, due to vigorous brushing in this area. The type of toothbrush, the technique used and the force applied when brushing can influence the occurrence and severity of resulting abrasion. Further, brushing for extended periods of time (exceeding 2-3 min) in some cases, when combined with medium/hard bristled toothbrushes can cause abrasive lesions.

Different toothbrush types are more inclined to cause abrasion, such as those with medium or hard bristles. The bristles combined with forceful brushing techniques applied can roughen the tooth surface and cause abrasion as well as aggravating the gums. Repetitive irritation to the gingival margin can eventually cause recession of the gums. When the gums recede, the root surface is exposed which is more susceptible to abrasion.

Comparatively, electric toothbrushes have less abrasive tendencies.

Types of toothpastes can also damage enamel and dentine due to the abrasive properties. Specific ingredients are used in toothpaste to target removal of the bio-film and extrinsic staining however in some cases can contribute to the pastes being abrasive.

Whitening toothpastes are found to be one of the most abrasive types of toothpastes, according to the RDA Scale, detailed below. In-home and clinical whitening have been proven to increase the likelihood of an individual experiencing dental abrasion. It is believed that dental abrasion due to the whitening process is caused by a combination of both mechanical and chemical irritants, for example, using whitening toothpaste and at home bleaching kits together. However, if an individual is regimented in their after-whitening care then they can avoid loss of dentine minerals and in turn abrasion can be avoided. (that contribute to developing abrasion).

Another factor that can contribute to abrasion is alteration of pH levels in the saliva. This can be sugary/ acidic foods and liquids. The reasoning behind this is that an increase in acidity of saliva can induce demineralization and therefore compromising the tooth structure to abrasive factors such as tooth brushing or normal wear from mastication. When the tooth structure is compromised, this is where the mineral content of the saliva can create shallow depressions in the enamel and thus, when brushed can cause irreparable damage on tooth surface. The dental abrasion process can be further stimulated and accelerated through the effects of dental Acid erosion.

Daily oral hygiene measures to prevent periodontal disease include:

- Brushing properly on a regular basis (at least twice daily), with the patient attempting to direct the toothbrush bristles underneath the gumline, helps disrupt the bacterial-mycotic growth and formation of subgingival plaque.

- Flossing daily and using interdental brushes (if the space between teeth is large enough), as well as cleaning behind the last tooth, the third molar, in each quarter

- Using an antiseptic mouthwash: Chlorhexidine gluconate-based mouthwash in combination with careful oral hygiene may cure gingivitis, although they cannot reverse any attachment loss due to periodontitis.

- Using periodontal trays to maintain dentist-prescribed medications at the source of the disease: The use of trays allows the medication to stay in place long enough to penetrate the biofilms where the microorganism are found.

- Regular dental check-ups and professional teeth cleaning as required: Dental check-ups serve to monitor the person's oral hygiene methods and levels of attachment around teeth, identify any early signs of periodontitis, and monitor response to treatment.

- Microscopic evaluation of biofilm may serve as a guide to regaining commensal health flora.

Typically, dental hygienists (or dentists) use special instruments to clean (debride) teeth below the gumline and disrupt any plaque growing below the gumline. This is a standard treatment to prevent any further progress of established periodontitis. Studies show that after such a professional cleaning (periodontal debridement), microbial plaque tends to grow back to precleaning levels after about three to four months. Nonetheless, the continued stabilization of a patient's periodontal state depends largely, if not primarily, on the patient's oral hygiene at home, as well as on the go. Without daily oral hygiene, periodontal disease will not be overcome, especially if the patient has a history of extensive periodontal disease.

Periodontal disease and tooth loss are associated with an increased risk, in male patients, of cancer.

Contributing causes may be high alcohol consumption or a diet low in antioxidants.

Teeth are constantly subject to both horizontal and vertical occlusal forces. With the center of rotation of the tooth acting as a fulcrum, the surface of bone adjacent to the pressured side of the tooth will undergo resorption and disappear, while the surface of bone adjacent to the tensioned side of the tooth will undergo apposition and increase in volume.

In both primary and secondary occlusal trauma, tooth mobility might develop over time, with it occurring earlier and being more prevalent in secondary occlusal trauma. To treat mobility due to primary occlusal trauma, the cause of the trauma must be eliminated. Likewise for teeth subject to secondary occlusal trauma, though these teeth may also require splinting together to the adjacent teeth so as to eliminate their mobility.

In primary occlusal trauma, the cause of the mobility was the excessive force being applied to a tooth with a normal attachment apparatus, otherwise known as a "periodontally-uninvolved tooth". The approach should be to eliminate the cause of the pain and mobility by determining the causes and removing them; the mobile tooth or teeth will soon cease exhibiting mobility. This could involve removing a high spot on a recently restored tooth, or even a high spot on a non-recently restored tooth that perhaps moved into hyperocclusion. It could also involve altering one's parafunctional habits, such as refraining from chewing on pens or biting one's fingernails. For a bruxer, treatment of the patient's primary occlusal trauma could involve selective grinding of certain interarch tooth contacts or perhaps employing a nightguard to protect the teeth from the greater than normal occlusal forces of the patient's parafunctional habit. For someone who is missing enough teeth in non-strategic positions so that the remaining teeth are forced to endure a greater "per square inch" occlusal force, treatment might include restoration with either a removable prosthesis or implant-supported crown or bridge.

In secondary occlusal trauma, simply removing the "high spots" or selective grinding of the teeth will not eliminate the problem, because the teeth are already periodontally involved. After splinting the teeth to eliminate the mobility, the cause of the mobility (in other words, the loss of clinical attachment and bone) must be managed; this is achieved through surgical periodontal procedures such as soft tissue and bone grafts, as well as restoration of edentulous areas. As with primary occlusal trauma, treatment may include either a removable prosthesis or implant-supported crown or bridge.

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).

An impacted tooth is one that fails to erupt into the dental arch within the expected developmental window.

Because impacted teeth do not erupt, they are retained throughout the individual's lifetime unless extracted or exposed surgically. Teeth may become impacted because of adjacent teeth, dense overlying bone, excessive soft tissue or a genetic abnormality. Most often, the cause of impaction is inadequate arch length and space in which to erupt. That is the total length of the alveolar arch is smaller than the tooth arch (the combined mesiodistal width of each tooth). The wisdom teeth (third molars) are frequently impacted because they are the last teeth to erupt in the oral cavity. Mandibular third molars are more commonly impacted than their maxillary counterparts. As a general rule, all impacted teeth must be removed, except canine teeth; canines do not need surgery and may just remain buried and give no further problems.

Radicular cysts are by far the most common cyst occurring in the jaws.

Secondary occlusal trauma occurs when "normal or excessive occlusal forces" are placed on teeth with "compromised periodontal attachment", thus contributing harm to an already damaged system. As stated, secondary occlusal trauma occurs when there is a compromised periodontal attachment and, thus, a "pre-existing periodontal condition".

Repair with cementum or dentin occurs after partial root resorption, fusing the tooth with the bone. It may occur following dental trauma, especially occlusal trauma, or after periapical periodontitis caused by pulp necrosis. Ankylosis itself is not a reason to remove a permanent tooth, however teeth which must be removed for other reasons are made significantly more difficult to remove if they are ankylosed.

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.

Dentists and dental hygienists measure periodontal disease using a device called a periodontal probe. This thin "measuring stick" is gently placed into the space between the gums and the teeth, and slipped below the gumline. If the probe can slip more than below the gumline, the patient is said to have a gingival pocket if no migration of the epithelial attachment has occurred or a periodontal pocket if apical migration has occurred. This is somewhat of a misnomer, as any depth is, in essence, a pocket, which in turn is defined by its depth, i.e., a 2-mm pocket or a 6-mm pocket. However, pockets are generally accepted as self-cleansable (at home, by the patient, with a toothbrush) if they are 3 mm or less in depth. This is important because if a pocket is deeper than 3 mm around the tooth, at-home care will not be sufficient to cleanse the pocket, and professional care should be sought. When the pocket depths reach in depth, the hand instruments and cavitrons used by the dental professionals may not reach deeply enough into the pocket to clean out the microbial plaque that causes gingival inflammation. In such a situation, the bone or the gums around that tooth should be surgically altered or it will always have inflammation which will likely result in more bone loss around that tooth. An additional way to stop the inflammation would be for the patient to receive subgingival antibiotics (such as minocycline) or undergo some form of gingival surgery to access the depths of the pockets and perhaps even change the pocket depths so they become 3 mm or less in depth and can once again be properly cleaned by the patient at home with his or her toothbrush.

If patients have 7-mm or deeper pockets around their teeth, then they would likely risk eventual tooth loss over the years. If this periodontal condition is not identified and the patients remain unaware of the progressive nature of the disease, then years later, they may be surprised that some teeth will gradually become loose and may need to be extracted, sometimes due to a severe infection or even pain.

According to the Sri Lankan tea laborer study, in the absence of any oral hygiene activity, approximately 10% will suffer from severe periodontal disease with rapid loss of attachment (>2 mm/year). About 80% will suffer from moderate loss (1–2 mm/year) and the remaining 10% will not suffer any loss.

Gingival and periodontal pockets are dental terms indicating the presence of an abnormal depth of the gingival sulcus near the point at which the gingival tissue contacts the tooth.

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.

The prognosis depends upon the type, size and location of a cyst. Most cysts are entirely benign, and some may require no treatment. Rarely, some cystic lesions represent locally aggressive tumors that may cause destruction of surrounding bone if left untreated. This type of cyst are usually removed with a margin of healthy bone to prevent recurrence of new cysts. If a cyst expands to a very large size, the mandible may be weakened such that a pathologic fracture occurs.

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.

Treatment for TRs is limited to tooth extraction because the lesion is progressive. Amputation of the tooth crown without root removal has also been advocated in cases demonstrated on a radiograph to be type 2 resorption without associated periodontal or endodontic disease because the roots are being replaced by bone. However, X-rays are recommended prior to this treatment to document root resorption and lack of the periodontal ligament.

Tooth restoration is not recommended because resorption of the tooth will continue underneath the restoration. Use of alendronate has been studied to prevent TRs and decrease progression of existing lesions.

True dental caries is uncommon among companion animals. Although it has not been accurately documented in cats, the incidence of caries in dogs has been estimated at approximately 5%. The term "feline cavities" is commonly used to refer to TRs; however, sacchrolytic acid-producing bacteria are not involved in this condition.