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

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 periodontitis of some form is a very common condition. The prevalence of periapical periodontitis is generally reported to vary according to age group, e.g. 33% in those aged 20–30, 40% in 30- to 40-year-olds, 48% in 40- to 50-year-olds, 57% in 50- to 60-year-olds and 62% in those over the age of 60. Most epidemiologic data has been generated in European countries, especially Scandinavia. Millions of root canal treatments are carried out in the United States each year, although the total number of root canal treatments is an imperfect indicator of the prevalence of periapical periodontitis, since not always is it performed due to the presence of periapacial periodontitis, and not all cases of asymptomatic periodontitis will be treated in this manner, either due to lack of patient attendance or watchful waiting.

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.

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.

Dental caries is an infectious disease caused primarily by "Streptococcus mutans", characterized by acid demineralization of the enamel, which can progress to further breakdown of the more organic, inner dental tissue (dentin). Everybody is susceptible to caries but the probability of development depends on the patient’s individual disease indicators, risk factors and preventive factors. Factors that are considered high-risk for developing carious lesions on the teeth include:

- Low fluoride exposure

- Time, length, and frequency of sugar consumption

- Quality of tooth cleaning

- Fluctuations in salivary flow rates and composition

- Behavior of the individual

- Socioeconomic status of the individual

- Quality and composition of biofilms

Organic acids released from dental plaque lead to demineralization of the adjacent tooth surface, and consequently to dental caries. Saliva is also unable to penetrate the build-up of plaque and thus cannot act to neutralize the acid produced by the bacteria and remineralize the tooth surface.

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.

Periodontitis is an infection of the gums which leads to bone destruction around the teeth in the jaw. Periodontitis occurs after gingivitis has been established, but not all individuals who have gingivitis will get periodontitis. Plaque accumulation is vital in the progression of periodontitis as the bacteria in plaque release enzymes which attack the bone and cause it to break down, and at the same time osteoclasts in the bone break down the bone as a way to prevent further infection. This can be treated with strict oral hygiene such as tooth brushing and cleaning in between the teeth as well as surgical debridement completed by a dental professional.

Overall, the incidence of dry socket is about 0.5–5% for routine dental extractions, and about 25–30% for impacted mandibular third molars (wisdom teeth which are buried in the bone).

Females are more frequently affected than males, but this appears to be related to oral contraceptive use rather than any underlying gender predilection. The majority of dry sockets occur in individuals aged between 20 and 40 which is when most dental extractions occur, although for any given individual it is more likely to occur in with increasing age.

Other possible risk factors include periodontal disease, acute necrotizing ulcerative gingivitis, local bone disease, Paget's disease of bone, osteopetrosis, cemento-osseous dysplasia, a history of previously developing a dry socket with past extractions and inadequate oral hygiene. Other factors in the postoperative period that may lead to loss of the blood clot include forceful spitting, sucking through a straw, and coughing or sneezing.

Chronic periapical periodontitis, also termed chronic apical periodontitis, chronic periradicular periodontitis, or assymptomatic periapical periodontitis

A periapical granuloma (also termed an apical granuloma or a radicular granuloma) is mass of chronically inflamed granulation tissue that forms at the apex of the root of a nonvital (dead) tooth. However, a periapical granuloma does not contain granulomatous inflammation, and therefore is not a true granuloma, but the term "periapical granuloma" is in common use.

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.

Untreated, the infection may lead to rapid destruction of the periodontium and can spread, as necrotizing stomatitis or noma, into neighbouring tissues in the cheeks, lips or the bones of the jaw. As stated, the condition can occur and be especially dangerous in people with weakened immune systems. This progression to noma is possible in malnourished susceptible individuals, with severe disfigurement possible.

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.

In developed countries, this disease occurs mostly in young adults. In developing countries, NUG may occur in children of low socioeconomic status, usually occurring with malnutrition (especially inadequate protein intake) and shortly after the onset of viral infections (e.g. measles).

Predisposing factors include smoking, viral respiratory infections and immune defects, such as in HIV/AIDS. Uncommon, except in lower socioeconomic classes, this typically affects adolescents and young adults, especially in institutions, armed forces, etc., or people with HIV/AIDS. The disease has occurred in epidemic-like patterns, but it is not contagious.

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 of gingival bleeding. The main cause of gingival bleeding is the formation and accumulation of plaque at the gum line due to improper brushing and flossing of teeth. The hardened form of plaque is calculus. An advanced form of gingivitis as a result of formation of plaque is periodontitis. Other causes that can exacerbate gingival bleeding include:

- placement of new dentures

- tooth or gum infection

- diabetes mellitus

- idiopathic thrombocytopenic purpura

- leukemia

- malnutrition

- use of aspirin and anticoagulants(blood thinners) such as warfarin and heparin

- hormonal imbalances during puberty and pregnancy

- iron overload

Other less common causes are:

- vitamin C deficiency (scurvy) and vitamin K deficiency

- dengue fever

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 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.

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.

An examination by the dentist or dental hygienist should be sufficient to rule out the issues such as malnutrition and puberty. Additional corresponding diagnosis tests to certain potential disease may be required. This includes oral glucose tolerance test for diabetes mellitus, blood studies, human gonadotrophin levels for pregnancy, and X-rays for teeth and jaw bones.

In order to determine the periodontal health of a patient, the dentist or dental hygienist records the sulcular depths of the gingiva and observes any bleeding on probing. This is often accomplished with the use of a periodontal probe. Alternatively, dental floss may also be used to assess the Gingival bleeding index. It is used as an initial evaluation on patient's periodontal health especially to measure gingivitis. The number of bleeding sites is used to calculate the gingival bleeding score.

Peer-reviewed dental literature thoroughly establishes that bleeding on probing is a poor positive predictor of periodontal disease, but conversely lack of bleeding is a very strong negative predictor. The clinical interpretation of this research is that while BOP presence may not indicate periodontal disease, continued absence of BOP is a strong predictor (approximately 98%) of continued periodontal health.

Can be caused by many things. A way to remember the causes is "PIG ON TAP"

Local factors-

- Occlusal Trauma

- Trauma

- Non-functional tooth

- Unopposed tooth (and impacted teeth, embedded teeth, teeth without antagonists)

Systemic factors-

- Idiopathic

- Pituitary Gigantism

- Paget's Disease

- Acromegaly

- Periapical granuloma

- Arthritis

- Calcinosis

- Rheumatic fever

It may be one of the complications of Paget's disease of bone in the form of generalized hypercementosis.

It may also be a compensatory mechanism in response to attrition to increase occlusal tooth height.

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.

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

Plaque accumulation causes the gingiva to become irritated and inflamed, and this is referred to as gingivitis. When the gingiva become so irritated that there is a loss of the connective tissue fibers that attach the gums to the teeth and bone that surrounds the tooth, this is known as periodontitis. Dental plaque is not the sole cause of periodontitis, however it is many times referred to as a primary aetiology. Plaque that remains in the oral cavity long enough will eventually calcify and become calculus. Calculus is detrimental to gingival health because it serves as a trap for increased plaque formation and retention; thus, calculus, along with other factors that cause a localized build-up of plaque, is referred to as a secondary aetiology of periodontitis.

When plaque is supragingival, the bacterial content contains a great proportion of aerobic bacteria and yeast, or those bacteria which utilize and can survive in an environment containing oxygen. Subgingival plaque contains a higher proportion of anaerobic bacteria, or those bacteria which cannot exist in an environment containing oxygen. Several anaerobic plaque bacteria, such as "Porphyromonas gingivalis", secrete antigenic proteins that trigger a strong inflammatory response in the periodontium, the specialized tissues that surround and support the teeth. Prolonged inflammation of the periodontium leads to bone loss and weakening of the gingival fibers that attach the teeth to the gums, two major hallmarks of periodontitis. Supragingival calculus formation is nearly ubiquitous in humans, but to differing degrees. Almost all individuals with periodontitis exhibit considerable subgingival calculus deposits. Dental plaque bacteria have been linked to cardiovascular disease and mothers giving birth to pre-term low weight infants, but there is no conclusive evidence yet that periodontitis is a significant risk factor for either of these two conditions.

Necrotic pulp is a finding in dentistry to describe dental pulp within a tooth which has become necrotic. Directly meaning, death of the pulp. It is a finding of interest to dentists as the process of pulp death may be painful causing a toothache.

Sequelae of a necrotic pulp include acute apical periodontitis, dental abscess or radicular cyst and discolouration of the tooth.

Tests for a necrotic pulp include: vitality testing using a thermal test or an electric pulp tester. Discolouration may be visually obvious, or more subtle.

Treatment usually involves endodontics or extraction.