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.

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.

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.

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.

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.

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.

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.

In the early stages, chronic periodontitis has few symptoms and in many individuals the disease has progressed significantly before they seek treatment.

Symptoms may include the following:

- Redness or bleeding of gums while brushing teeth, using dental floss or biting into hard food (e.g. apples) (though this may occur even in gingivitis, where there is no attachment loss)

- Gum swelling that recurs

- Halitosis, or bad breath, and a persistent metallic taste in the mouth

- Gingival recession, resulting in apparent lengthening of teeth. (This may also be caused by heavy-handed brushing or with a stiff tooth brush.)

- Deep pockets between the teeth and the gums (pockets are sites where the attachment has been gradually destroyed by collagen-destroying enzymes, known as "collagenases")

- Loose teeth, in the later stages (though this may occur for other reasons as well)

Gingival inflammation and bone destruction are often painless. Patients sometimes assume that painless bleeding after teeth cleaning is insignificant, although this may be a symptom of progressing chronic periodontitis in that patient.

Subgingival calculus is a frequent finding.

There is a slow to moderate rate of disease progression but the patient may have periods of rapid progression ("bursts of destruction"). Chronic periodontitis can be associated with local predisposing factors(e.g. tooth-related or iatrogenic factors). The disease may be modified by and be associated with systemic diseases (e.g. diabetes mellitus, HIV infection) It can also be modified by factors other than systemic disease such as smoking and emotional stress.

Major risk factors: Smoking, lack of oral hygiene with inadequate plaque biofilm control.

Measuring disease progression is carried out by measuring probing pocket depth (PPD) and bleeding indices using a periodontal probe. Pockets greater than 3mm in depth are considered to be unhealthy. Bleeding on probing is considered to be a sign of active disease. Discharge of pus, involvement of the root furcation area and deeper pocketing may all indicate reduced prognosis for an individual tooth.

Age is related to the incidence of periodontal destruction: "...in a well-maintained population who practises oral home care and has regular check-ups, the incidence of incipient periodontal destruction increases with age, the highest rate occurs between 50 and 60 years, and gingival recession is the predominant lesion before 40 years, while periodontal pocketing is the principal mode of destruction between 50 and 60 years of age."

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.

Among those in the intensive care unit, ulceration resulting in bleeding is very rare.

As the original sulcular depth increases and the apical migration of the junctional epithelium has simultaneously occurred, the pocket is now lined by pocket epithelium (PE) instead of junctional epithelium (JE). To have a true periodontal pocket, a probing measurement of 4 mm or more must be clinically evidenced. In this state, much of the gingival fibers that initially attached the gingival tissue to the tooth have been irreversibly destroyed. The depth of the periodontal pockets must be recorded in the patient record for proper monitoring of periodontal disease. Unlike in clinically healthy situations, parts of the sulcular epithelium can sometimes be seen in periodontally involved gingival tissue if air is blown into the periodontal pocket, exposing the newly denuded roots of the tooth. A periodontal pocket can become an infected space and may result in an abscess formation with a papule on the gingival surface. Incision and drainage of the abscess may be necessary, as well as systemic antibiotics; placement of local antimicrobial delivery systems within the periodontal pocket to reduce localized infections may also be considered.

It is classified as supra bony and infra bony based on its depth in relation to alveolar bone.

Risk factors for stress ulcer formation that have been identified are numerous and varied. However, two landmark studies and one position paper exist that addresses the topic of risk factors for stress ulcer formation:

- Non-critically ill medical patients with 2 or more of the following: respiratory failure, sepsis, heart failure, hepatic encephalopathy, jaundice, kidney failure, stroke, hypertension, previous gastrointestinal disease and treatment with corticosteroids, NSAIDS, heparin, or warfarin.

- In surgical critically ill patients, only those patients who are on a mechanical ventilator for more than 48 hours and/or those with a coagulopathy.

- The American Society of Health-System Pharmacists guideline recommends against the practice of stress ulcer prophylaxis in non-critically ill patients.

Nosebleeds are due to the rupture of a blood vessel within the richly perfused nasal mucosa. Rupture may be spontaneous or initiated by trauma. Nosebleeds are reported in up to 60% of the population with peak incidences in those under the age of ten and over the age of 50 and appear to occur in males more than females. An increase in blood pressure (e.g. due to general hypertension) tends to increase the duration of spontaneous epistaxis. Anticoagulant medication and disorders of blood clotting can promote and prolong bleeding. Spontaneous epistaxis is more common in the elderly as the nasal mucosa (lining) becomes dry and thin and blood pressure tends to be higher. The elderly are also more prone to prolonged nose bleeds as their blood vessels are less able to constrict and control the bleeding.

The vast majority of nose bleeds occur in the anterior (front) part of the nose from the nasal septum. This area is richly endowed with blood vessels (Kiesselbach's plexus). This region is also known as Little's area. Bleeding farther back in the nose is known as a posterior bleed and is usually due to bleeding from Woodruff's plexus, a venous plexus situated in the posterior part of inferior meatus. Posterior bleeds are often prolonged and difficult to control. They can be associated with bleeding from both nostrils and with a greater flow of blood into the mouth.

The causes of nosebleeds can generally be divided into two categories, local and general factors, although a significant number of nosebleeds occur with no obvious cause.

Causes include:

- acute pancreatitis, where methemalbumin formed from digested blood tracks around the abdomen from the inflamed pancreas

- bleeding from blunt abdominal trauma

- bleeding from aortic rupture

- bleeding from ruptured ectopic pregnancy

Importance of the sign is on a decline since better diagnostic modalities are now available.

They are removed under general anaesthesia . Most can be removed through anterior nares . Large ones need to be broken into pieces before removal . Some particularly hard and irregular ones may require lateral rhinotomy .

Treatment for light bruises is minimal and may include RICE (rest, ice, compression, elevation), painkillers (particularly NSAIDs) and, later in recovery, light stretching exercises. Particularly, immediate application of ice while elevating the area may reduce or completely prevent swelling by restricting blood flow to the area and preventing internal bleeding. Rest and preventing re-injury is essential for rapid recovery. Applying a medicated cream containing mucopolysaccharide polysulfuric acid (e.g., Hirudoid) may also speed the healing process. Other topical creams containing skin-fortifying ingredients, including but not limited to retinol or alpha hydroxy acids, such as DerMend, can improve the appearance of bruising faster than if left to heal on its own.

Very gently massaging the area and applying heat may encourage blood flow and relieve pain according to the gate control theory of pain, although causing additional pain may indicate the massage is exacerbating the injury. As for most injuries, these techniques should not be applied until at least three days following the initial damage to ensure all internal bleeding has stopped, because although increasing blood flow will allow more healing factors into the area and encourage drainage, if the injury is still bleeding this will allow more blood to seep out of the wound and cause the bruise to become worse.

In most cases hematomas spontaneously revert, but in cases of large hematomas or those localized in certain organs ("e.g.", the brain), the physician may optionally perform a puncture of the hematoma to allow the blood to exit.

The presence of bruises may be seen in patients with platelet or coagulation disorders, or those who are being treated with an anticoagulant. Unexplained bruising may be a warning sign of child abuse, domestic abuse, or serious medical problems such as leukemia or meningoccocal infection. Unexplained bruising can also indicate internal bleeding or certain types of cancer. Long-term glucocorticoid therapy can cause easy bruising. Bruising present around the navel (belly button) with severe abdominal pain suggests acute pancreatitis. Connective tissue disorders such as Ehlers-Danlos syndrome may cause relatively easy or spontaneous bruising depending on the severity.

During an autopsy, bruises accompanying abrasions indicate the abrasions occurred while the individual was alive, as opposed to damage incurred post mortem.

A rhinolith is a calculus present in the nasal cavity. The word is derived from the roots "" and "", literally meaning "nose stone". It is an uncommon medical phenomenon, not to be confused with dried nasal mucus. A rhinolith usually forms around the nucleus of a small exogenous foreign body, blood clot or secretion by slow deposition of calcium and magnesium salts. Over a period of time, they grow into large irregular masses that fill the nasal cavity. They may cause pressure necrosis of the nasal septum or lateral wall of nose. Rhinoliths can cause nasal obstruction, epistaxis, headache, sinusitis and epiphora. They can be diagnosed from the history with unilateral foul smelling blood stained nasal discharge or by anterior rhinoscopy. On probing probe can be passed around all its corners. In both CT and MRI rhinolith will appear like a radiopaque irregular material. Small rhinoliths can be removed by foreign body hook. Whereas large rhinoliths can be removed either by crushing with luc's forceps or by Moore's lateral rhinotomy approach.

Inadequate nutrition or the consumption of tainted food are suspected. Both IgG and IgM autoantibodies to platelet and to glycoprotein IIb/IIIa is found in majority of patients.

Cullen's sign is superficial edema and bruising in the subcutaneous fatty tissue around the umbilicus.

It is named for gynecologist Thomas Stephen Cullen (1869–1953), who first described the sign in ruptured ectopic pregnancy in 1916.

This sign takes 24–48 hours to appear and can predict acute pancreatitis, with mortality rising from 8–10% to 40%. It may be accompanied by Grey Turner's sign (bruising of the flank), which may then be indicative of pancreatic necrosis with retroperitoneal or intraabdominal bleeding.