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 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.

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.

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.

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.

Periodontitis is an inflammation of the periodontium, i.e., the tissues that support the teeth. The periodontium consists of four tissues:

- gingiva, or gum tissue,

- cementum, or outer layer of the roots of teeth,

- alveolar bone, or the bony sockets into which the teeth are anchored, and

- periodontal ligaments (PDLs), which are the connective tissue fibers that run between the cementum and the alveolar bone.

The primary cause of gingivitis is poor or ineffective oral hygiene, which leads to the accumulation of a mycotic and bacterial matrix at the gum line, called dental plaque. Other contributors are poor nutrition and underlying medical issues such as diabetes. Diabetics must be meticulous with their homecare to control periodontal disease. New finger prick tests have been approved by the Food and Drug Administration in the US, and are being used in dental offices to identify and screen patients for possible contributory causes of gum disease, such as diabetes.

In some people, gingivitis progresses to periodontitis – with the destruction of the gingival fibers, the gum tissues separate from the tooth and deepened sulcus, called a periodontal pocket. Subgingival microorganisms (those that exist under the gum line) colonize the periodontal pockets and cause further inflammation in the gum tissues and progressive bone loss. Examples of secondary causes are those things that, by definition, cause microbic plaque accumulation, such as restoration overhangs and root proximity.

Smoking is another factor that increases the occurrence of periodontitis, directly or indirectly, and may interfere with or adversely affect its treatment.

Ehlers–Danlos syndrome is a periodontitis risk factor and so is the Papillon–Lefèvre syndrome also known as palmoplantar keratoderma.

If left undisturbed, microbial plaque calcifies to form calculus, which is commonly called tartar. Calculus above and below the gum line must be removed completely by the dental hygienist or dentist to treat gingivitis and periodontitis. Although the primary cause of both gingivitis and periodontitis is the microbial plaque that adheres to the tooth surfaces, there are many other modifying factors. A very strong risk factor is one's genetic susceptibility. Several conditions and diseases, including Down syndrome, diabetes, and other diseases that affect one's resistance to infection, also increase susceptibility to periodontitis.

Another factor that makes periodontitis a difficult disease to study is that human host response can also affect the alveolar bone resorption. Host response to the bacterial-mycotic insult is mainly determined by genetics; however, immune development may play some role in susceptibility.

According to some researchers periodontitis may be associated with higher stress. Periodontitis occurs more often in people from the lower end of the socioeconomic scale than people from the upper end of the socioeconomic scale.

The cause of plaque-induced gingivitis is bacterial plaque, which acts to initiate the body's host response. This, in turn, can lead to destruction of the gingival tissues, which may progress to destruction of the periodontal attachment apparatus. The plaque accumulates in the small gaps between teeth, in the gingival grooves and in areas known as "plaque traps": locations that serve to accumulate and maintain plaque. Examples of plaque traps include bulky and overhanging restorative margins, claps of removable partial dentures and calculus (tartar) that forms on teeth. Although these accumulations may be tiny, the bacteria in them produce chemicals, such as degradative enzymes, and toxins, such as lipopolysaccharide (LPS, otherwise known as endotoxin) or lipoteichoic acid (LTA), that promote an inflammatory response in the gum tissue. This inflammation can cause an enlargement of the gingiva and subsequent formation. Early plaque in health consists of a relatively simple bacterial community dominated by Gram-positive cocci and rods. As plaque matures and gingivitis develops, the communities become increasingly complex with higher proportions of Gram-negative rods, fusiforms, filaments, spirilla and spirochetes. Later experimental gingivitis studies, using culture, provided more information regarding the specific bacterial species present in plaque. Taxa associated with gingivitis included "Fusobacterium nucleatum" subspecies "polymorphum", "Lachnospiraceae" [G-2] species HOT100, "Lautropia" species HOTA94, and "Prevotella oulorum" (a species of "Prevotella" bacterium), whilst "Rothia dentocariosa" was associated with periodontal health. Further study of these taxa is warranted and may lead to new therapeutic approaches to prevent periodontal disease.

Research has shown that there are five million teeth knocked-out each year in the United States.

Up to 25% of school-aged children and military trainees and fighters experience some kind of dental trauma each year. The incidence of dental avulsion in school aged children ranges from 0.5 to 16% of all dental trauma. Many of these teeth are knocked-out during school activities or sporting events such as contact sports, football, basketball, and hockey.It is important for anyone whom is related, working, or witnessing sports that they be educated on this subject matter. Being educated could aid in minimizing injuries that could do further harm to the victim. Being informed and spreading awareness of dental avulsion in the state of knowledge, treatment, and prevention could make an impact.

Aetiology of CTS is multifactorial, the causative factors include:

- previous restorative procedures.

- occlusal factors

- developmental conditions/anatomical considerations.

- trauma

- others, e.g, aging dentition or presence of lingual tongue studs.

Most commonly involved teeth are mandibular molars followed by maxillary premolars, maxillary molars and maxillary premolars. in a recent audit, mandibular first molar thought to be most affected by CTS possibly due to the wedging effect of opposing pointy, protruding maxillary mesio-palatal cusp onto the mandibular molar central fissure.

There are many possible causes for gingival recession:

- By far the most common cause is gum disease (periodontal disease).

- Overaggressive brushing is often assumed to cause gum recession, however a systematic review of the literature concludes that "The data to support or refute the association between tooth brushing and gingival recession are inconclusive." A subsequent study found horizontal tooth brushing technique (versus Bass technique or circular methods), medium-hardness toothbrush use and brushing only once daily were associated with gingival recession.

- Hereditary thin, fragile or insufficient gingival tissue predisposes to gingival recession.

- Dipping tobacco, which affects the mucous membrane lining in the mouth and will cause receding gums over time

- Self-inflicted trauma, such as habits like digging a fingernail or pencil into the gum. This type of recession more commonly associated with children and persons with psychiatric disorders.

- Scurvy (lack of dietary vitamin C)

- Acute necrotizing ulcerative gingivitis

- Abnormal tooth position, such as tooth crowding, giving inadequate cover of one or more teeth by the jaw bone.

- Piercings in the lip or tongue that wear away the gum by rubbing against it.

- Intentional gingival retraction. For example, the adult tooth may not grow out of the gum, and to remedy this, a procedure called an exposure is done. It involves the gum tissue being cut open to allow the adult tooth to grow out. This is a less common cause of gum recession.

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.

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".

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.

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.

The long-term prognosis of replanted knocked out teeth is very variable. The treatment for knocked-out teeth has progressed from a success rate of 10% to over 90%.

However, this success rate can only be achieved with the institution of optimum care within fifteen minutes to an hour of the accident. In the case of knocked-out teeth, being prepared and knowing what to do can mean the difference between a person retaining or losing replanted knocked-out teeth for life. Teeth that have been knocked out when they are fully matured, that is, when the root has completely formed, have a much better prognosis than those teeth that are immature and not fully formed. This is due to the fragility of the root. When teeth have not fully formed, the walls of the root are thinner and thus more fragile. Another complication for the prognosis is the length of time that the tooth has been out of its socket. Teeth that are replanted within fifteen minutes of the accident have an excellent prognosis. Teeth that have been extra-oral and dry stored for more than one hour have a poor prognosis. Teeth that have been placed in an optimal storage medium within one hour of the accident also have an excellent prognosis. All teeth that have been knocked out should be replanted but watched carefully for the development of root resorption. Teeth that do not have root canal treatment within two weeks of replantation also have a poor prognosis.

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.

There are two views of the microbiology of periodontitis: the specific plaque hypothesis and the non-specific plaque hypothesis.

Consensus is that neither view is correct, but via a middle path, that damage is due to a shift in the relative populations of more and less dangerous bacteria in the plaque. This is called the ecological plaque hypothesis.

The disease is associated with a variable microbial pattern.

Anaerobic species of bacteria Porphyromonas gingivalis, Bacteroides forsythus, Treponema denticola, Prevotella intermedia, Fusobacterium nucleatum, Eubacterium sp. have all been implicated in chronic periodontitis.

Microaerophile bacteria Actinomyces actinomycetemcomitans, Campylobacter rectus, and Eikenella corrodens also may play a role in chronic periodontitis.

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.

Gingival recession, also known as receding gums, is the exposure in the roots of the teeth caused by a loss of gum tissue and/or retraction of the gingival margin from the crown of the teeth. Gum recession is a common problem in adults over the age of 40, but it may also occur starting from the age of a teenager, or around the age of 10. It may exist with or without concomitant decrease in crown-to-root ratio (recession of alveolar bone).

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.

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.

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.

There is no universally accepted treatment strategy, but, generally, treatments aim to prevent movement of the segments of the involved tooth so they do not move or flex independently during biting and grinding and so the crack is not propagated.

- Stabilization (core buildup) (a composite bonded restoration placed in the tooth or a band is placed around the tooth to minimize flexing)

- Crown restoration (to do the same as above but more permanently and predictably)

- Root Canal therapy (if pain persists after above)

- Extraction

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).

Toothpaste with zinc citrate has been shown to produce a statistically significant reduction in plaque accumulation, but it is so modest that its clinical importance is questionable. Some calculus may form even without plaque deposits, by direct mineralisation of the pellicle.