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

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

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

This type of gingival enlargement is sometimes termed "drug induced gingival enlargement" or "drug influenced gingival enlargement", abbreviated to "DIGO". Gingival enlargement may also be associated with the administration of three different classes of drugs, all producing a similar response: Gingival overgrowth is a common side effect of phenytoin, termed "Phenytoin-induced gingival overgrowth" (PIGO).

- anticonvulsants (such as phenytoin, phenobarbital, lamotrigine, vigabatrin, ethosuximide, topiramate and primidone NOT common for valproate)

- calcium channel blockers (antihypertensives such as nifedipine, amlodipine, and verapamil). The dihydropyridine derivative isradipidine can replace nifedipine and does not induce gingival overgrowth.

- cyclosporine, an immunosuppresant.

Of all cases of DIGO, about 50% are attributed to phenytoin, 30% to cyclosporins and the remaining 10-20% to calcium channel blockers.

Drug-induced enlargement has been associated with a patient's genetic predisposition, and its association with inflammation is debated. Some investigators assert that underlying inflammation is necessary for the development of drug-induced enlargement, while others purport that the existing enlargement induced by the drug effect compounds plaque retention, thus furthering the tissue response. Careful attention to oral hygiene may reduce the severity of gingival hyperplasia. In most cases, discontinuing the culprit drug resolves the hyperplasia.

It is commonly seen in Boxer dogs and other brachycephalic breeds, and in the English Springer Spaniel. It usually starts around middle age and progresses. Some areas of the gingiva can become quite large but have only a small attachment to the rest of the gingiva, and it may completely cover the teeth. Infection and inflammation of the gingiva is common with this condition. Under anesthesia, the enlarged areas of gingiva can be cut back with a scalpel blade or CO laser, but it often recurs. Gingival enlargement is also a potential sequela of gingivitis. As in humans, it may be seen as a side effect to the use of ciclosporin.

This condition occurs in association with denture wearing, and so those affected tend to be middle aged or older adults. 66-75% are estimated to occur in women. Epulis fissuratum is the third most common reactive lesion that occurs in the mouth, after peripheral giant cell granuloma and pyogenic granuloma.

Bleeding on probing which is also known as bleeding gums or gingival bleeding is a term used by dentists and dental hygienists when referring to bleeding that is induced by gentle manipulation of the tissue at the depth of the gingival sulcus, or interface between the gingiva and a tooth. Bleeding on probing, often abbreviated BOP, is a sign of inflammation and indicates some sort of destruction and erosion to the lining of the sulcus or the ulceration of sulcular epithelium. The blood comes from lamina propria after the ulceration of the lining.

If the causative factor persists, tissue will become more fibrous over time.

OFG is uncommon, but the incidence is increasing. The disease usually presents in adolescence or young adulthood. It may occur in either sex, but males are slightly more commonly affected.

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.

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

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.

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.

Plasma cell gingivits is rare, and plasma cell cheilitis is very rare. Most people with plasma cell cheilitis have been elderly.

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.

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.

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.

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.

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.

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.

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.

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.

Recent advances have seen the introduction of platelet derived growth factor (PDGF) infused bone graft material. This material is usually combined with the cellular matrix to form a soft bone paste that is then covered by the allograft. The development of this type of bone and tissue cellular matrix (also known as ortho filler) results in greater osseointegration with the patient's healthy bone and soft tissue.

Healing from such procedures requires 2–4 weeks. After a few months the results can be evaluated and in some cases the new tissue needs to be reshaped in a very minor procedure to get an optimal result. In cases where recession is not accompanied by periodontal bone loss, complete or near complete coverage of the recession area is achievable.

Periodontal disease is the most common disease found in dogs and affects more than 80% of dogs aged three years or older. Its prevalence in dogs increases with age, but decreases with increasing body weight; i.e., toy and miniature breeds are more severely affected. Recent research undertaken at the Waltham Centre for Pet Nutrition has established that the bacteria associated with gum disease in dogs are not the same as in humans. Systemic disease may develop because the gums are very vascular (have a good blood supply). The blood stream carries these anaerobic micro-organisms, and they are filtered out by the kidneys and liver, where they may colonize and create microabscesses. The microorganisms traveling through the blood may also attach to the heart valves, causing vegetative infective endocarditis (infected heart valves). Additional diseases that may result from periodontitis include chronic bronchitis and pulmonary fibrosis.

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.