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

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.

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.

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.

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.

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.

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.

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.

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.

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.

Regular use of a mouthguard during sports and other high-risk activities (such as military training) is the most effective prevention for dental trauma. Custom made mouthguard is preferable as it fits well, provides comfort and adequate protection. However, studies in various high-risk populations for dental injuries have repeatedly reported low compliance of individuals for the regular using of mouthguard during activities. Moreover, even with regular use, effectiveness of prevention of dental injuries is not complete, and injuries can still occur even when mouthguards are used as users are not always aware of the best makes or size, which inevitably result in a poor fit.

One of the most important measures is to impart knowledge and awareness about dental injury to those who are involved in sports environments like boxing and in school children in which they are at high risk of suffering dental trauma through an extensive educational campaign including lectures,leaflets,Posters which should be presented in an easy understandable way.

Dental trauma is most common in younger people, accounting for 17% of injuries to the body in those aged 0–6 years compared to an average of 5% across all ages. It is more frequently observed in males compared to females. Traumatic dental injuries are more common in permanent teeth compared to deciduous teeth and usually involve the front teeth of the upper jaw.

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.

In dentistry, calculus or tartar is a form of hardened dental plaque. It is caused by precipitation of minerals from saliva and gingival crevicular fluid (GCF) in plaque on the teeth. This process of precipitation kills the bacterial cells within dental plaque, but the rough and hardened surface that is formed provides an ideal surface for further plaque formation. This leads to calculus buildup, which compromises the health of the gingiva (gums). Calculus can form both along the gumline, where it is referred to as supragingival ("above the gum"), and within the narrow sulcus that exists between the teeth and the gingiva, where it is referred to as subgingival ("below the gum").

Calculus formation is associated with a number of clinical manifestations, including bad breath, receding gums and chronically inflamed gingiva. Brushing and flossing can remove plaque from which calculus forms; however, once formed, it is too hard and firmly attached to be removed with a toothbrush. Calculus buildup can be removed with ultrasonic tools or dental hand instruments (such as a periodontal scaler).

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.

Loss of attachment:

- By far the most common cause is periodontal disease (gum disease). This is painless, slowly progressing loss of bony support around teeth. It is made worse by smoking and the treatment is by improving the oral hygiene above and below the gumline.

- Dental abscesses can cause resorption of bone and consequent loss of attachment. Depending on the type of abscess, this loss of attachment may be restored once the abscess is treated, or it may be permanent.

- Many other conditions can cause permanent or temporary loss of attachment and increased tooth mobility. Examples include: Langerhans cell histiocytosis.

Increased forces on the tooth:

- Bruxism (abnormal clenching and grinding of teeth) can aggravate attachment loss and tooth mobility if periodontal disease is already present. The tooth mobility is typically reversible and the tooth returns to normal level of mobility once the bruxism is controlled.

- Dental trauma. Luxations, and root fractures of teeth can cause sudden mobility after a blow. Dental trauma may be isolated or associated with other facial trauma.

- Increased biting force on one tooth can cause temporary increased mobility until corrected. A common scenario is a new filling or crown which is a fraction of a millimeter too prominent in the bite, which after a few days causes periodontal pain in that tooth and/or the opposing tooth.

Skin abscesses are common and have become more common in recent years. Risk factors include intravenous drug use with rates reported as high as 65% in this population. In 2005 in the United States 3.2 million people went to the emergency department for an abscess. In Australia around 13,000 people were hospitalized in 2008 for the disease.

Closing an abscess immediately after draining it appears to speed healing without increasing the risk of recurrence. This may not apply to anorectal abscesses. While they heal faster, there may be a higher rate of recurrence than those left open.

Mobility is graded clinically by applying pressure with the ends of 2 metal instruments (e.g. dental mirrors) and trying to rock a tooth gently in a bucco-lingual direction (towards the tongue and outwards again). Using the fingers is not reliable as they are too compressible and will not detect small increases in movement. The location of the fulcrum may be of interest in dental trauma. Teeth which are mobile about a fulcrum half way along their root likely have a fractured root.

Normal, physiologic tooth mobility of about 0.25 mm is present in health. This is because the tooth is not fused to the bones of the jaws, but is connected to the sockets by the periodontal ligament. This slight mobility is to accommodate forces on the teeth during chewing without damaging them. Milk (deciduous) teeth also become looser naturally just before their exfoliation. This is caused by gradual resorption of their roots, stimulated by the developing permanent tooth underneath.

Abnormal, pathologic tooth mobility occurs when the attachment of the periodontal ligament to the tooth is reduced (attachment loss, see diagram), or if the periodontal ligament is inflamed. Generally, the degree of mobility is inversely related to the amount of bone and periodontal ligament support left.

Grace & Smales Mobility Index

- Grade 0: No apparent mobility

- Grade 1: Perceptible mobility <1mm in buccolingual direction

- Grade 2: 1mm< but <2mm

- Grade 3: 2mm< or depressibility in the socket

Miller Classification

- Class 1: < 1 mm(Horizontal)

- Class 2: >1 mm(Horizontal)

- Class 3: > 1 mm (Horizontal+vertical mobility)

As is often the case, there are diseases/conditions with signs and symptoms that are similar to actinomycosis. As such, misdiagnoses can occur. Some examples include abscesses caused by grass seeds, woody tongue, bottle jaw, cancerous growths, and irritation caused by lodged objects.

90% of cases are smokers, however only a very small fraction of smokers appear to develop this lesion. It has been speculated that either the direct toxic effect or hormonal changes related to smoking could cause squamous metaplasia of lactiferous ducts. It is not well established whether the lesion regresses after smoking cessation.

Extrapuerperal cases are often associated with hyperprolactinemia or with thyroid problems. Also diabetes mellitus may be a contributing factor in nonpuerperal breast abscess.

The newborn`s exposure to the maternal vaginal bacterial flora which contains aerobic and anaerobic bacterial flora can lead to the development of anaerobic bacterial infection. These infections include cellulitis of the site of fetal monitoring (caused by "Bacterodes" spp.), bacteremia, aspiration pneumonia (caused by "Bacterodes" spp.), conjunctivitis (caused by clostridia,) omphalitis (caused by mixed flora), and infant botulism. Clostridial species may play a role in necrotizing enterocolitis. Management of these infection necessitates treating of the underlying condition(s) when present, and administration of proper antimicrobial therapy

Some women (approximately 15%) will require antibiotic treatment for infection which is usually caused by bacteria from the skin or the baby's mouth that entering the milk ducts through skin lesions of the nipple or through the opening of the nipple. Infection is usually caused by "staphylococcus aureus". Infectious pathogens commonly associated with mastitis are "Staphylococcus aureus", "streptococcus" spp., gram-negative bacilli such as "Escherichia coli". "Salmonella spp.", mycobacteria, "candida", and Cryptococcus have been identified in rare instances.

Recent research suggests that infectious pathogens play a much smaller role in the pathogenesis than was commonly assumed only a few years ago. Most detected pathogens are very common species that are natural part of the breast fauna and simple detection of their presence is not sufficient to prove a causative role. Furthermore, there are indications that treatment with antibiotics may have minimal impact, and over-all there is insufficient evidence to confirm or refute the effectiveness of antibiotic therapy for treating lactational mastitis.

Condition predisposing to anaerobic infections include: exposure of a sterile body location to a high inoculum of indigenous bacteria of mucous membrane flora origin, inadequate blood supply and tissue necrosis which lower the oxidation and reduction potential which support the growth of anaerobes. Conditions which can lower the blood supply and can predispose to anaerobic infection are: trauma, foreign body, malignancy, surgery, edema, shock, colitis and vascular disease. Other predisposing conditions include splenectomy, neutropenia, immunosuppression, hypogammaglobinemia, leukemia, collagen vascular disease and cytotoxic drugs and diabetes mellitus. A preexisting infection caused by aerobic or facultative organisms can alter the local tissue conditions and make them more favorable for the growth of anaerobes. Impairment in defense mechanisms due to anaerobic conditions can also favor anaerobic infection. These include production of leukotoxins (by "Fusobacterium" spp.), phagocytosis intracellular killing impairments (often caused by encapsulated anaerobes and by succinic acid ( produced by "Bacteroides" spp.), chemotaxis inhibition (by "Fusobacterium, Prevotella" and "Porphyromonas" spp.), and proteases degradation of serum proteins (by Bacteroides spp.) and production of leukotoxins (by "Fusobacterium" spp.).

The hallmarks of anaerobic infection include suppuration, establishment of an abscess, thrombophlebitis and gangrenous destruction of tissue with gas generation. Anaerobic bacteria are very commonly recovered in chronic infections, and are often found following the failure of therapy with antimicrobials that are ineffective against them, such as trimethoprim–sulfamethoxazole (co-trimoxazole), aminoglycosides, and the earlier quinolones.

Some infections are more likely to be caused by anaerobic bacteria, and they should be suspected in most instances. These infections include brain abscess, oral or dental infections, human or animal bites, aspiration pneumonia and lung abscesses, amnionitis, endometritis, septic abortions, tubo-ovarian abscess, peritonitis and abdominal abscesses following viscus perforation, abscesses in and around the oral and rectal areas, pus-forming necrotizing infections of soft tissue or muscle and postsurgical infections that emerge following procedures on the oral or gastrointestinal tract or female pelvic area. Some solid malignant tumors, ( colonic, uterine and bronchogenic, and head and neck necrotic tumors, are more likely to become secondarily infected with anaerobes. The lack of oxygen within the tumor that are proximal to the endogenous adjacent mucosal flora can predispose such infections.