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The terms gingival hyperplasia and gingival hypertrophy have been used to describe this topic in the past. These are not precise descriptions of gingival enlargement because these terms are strictly histologic diagnoses, and such diagnoses require microscopic analysis of a tissue sample. Hyperplasia refers to an increased number of cells, and hypertrophy refers to an increase in the size of individual cells. As these identifications obviously cannot be performed with a clinical examination and evaluation of the tissue, the term "gingival enlargement" is more properly applied. Gingival enlargement has been classified according to cause into 5 general groups:
- Inflammatory enlargement
- Drug induced enlargement
- Enlargement associated with systemic diseases or conditions
- Neoplastic enlargement
- False enlargement.
Gingival enlargement may be caused by a multitude of causes. The most common is chronic inflammatory gingival enlargement, when the gingivae are soft and discolored. This is caused by tissue edema and infective cellular infiltration caused by prolonged exposure to bacterial plaque, and is treated with conventional periodontal treatment, such as scaling and root planing.
Gingivitis and gingival enlargement are often seen in mouth breathers, as a result of irritation brought on by surface dehydration, but the manner in which it is caused has not been demonstrated.
The accumulation and retention of plaque is the chief cause of inflammatory gingival enlargement. Risk factors include poor oral hygiene, as well as physical irritation of the gingiva by improper restorative and orthodontic appliances.
The lesion is usually painless. The usual appearance is of two excess tissue folds in alveolar vestibule/buccal sulcus, with the flange of the denture fitting in between the two folds. It may occur in either the maxillary or mandibular sulci, although the latter is more usual. Anterior locations are more common than posterior. Less commonly there may be a single fold, and the lesion may appear on the lingual surface of the mandibular alveolar ridge.
The swelling is firm and fibrous, with a smooth, pink surface. The surface may also show ulceration or erythema. The size of the lesion varies from less than 1 cm to involving the entire length of the sulcus.
The cause is usually pressure from the flange of a denture which causes chronic irritation and a hyperplastic response in the soft tissues. Women during pregnancy can also present with an epulis, which will resolve after birth. Fibroepithelial polyps, pedunculated lesions of the palate beneath an upper denture, are associated with this condition. A cobble-stone appearance similar to an epulis fissuratum in a patient without dentures can be diagnostic of Crohn's disease. Epulis fissuratum can also appear around dental implants.
Signs and symptoms may include:
- Persistent or recurrent enlargement of the lips, causing them to protrude. If recurrent, the interval during which the lips are enlarged may be weeks or months. The enlargement can cause midline fissuring of the lip ("median cheilitis") or angular cheilitis (sores at the corner of the mouth). The swelling is non-pitting (c.f. pitting edema) and feels soft or rubbery on palpation. The mucous membrane of the lip may be erythemaous (red) and granular. One or both lips may be affected.
- Oral ulceration (mouth ulcers) which may be aphthous like, or be more chronic and deep with raised margins. Alternatively, lesions similar to pyostomatitis vegetans may occur in OFG, but this is uncommon.
- "Full width" gingivitis (compare with marginal gingivitis).
- Gingival enlargement (swelling of the gums).
- Fissured tongue (grooves in the tongue).
- Enlargement of the mucous membrane of the mouth, which may be associated with cobblestoning and mucosal tags (similar lesions often occur on the intestinal mucosa in Crohn's disease).
- Enlargement of the perioral and periorbital soft tissues (the tissues of the face around the mouth and the eyes). The facial skin may be dry, exfoliative (flaking) or erythematous.
- Cervical lymphadenopathy (enlarged lymph nodes in the neck).
- Facial palsy (weakness and altered sensation of the face).
The enlargement of the tissues of the mouth, lips and face seen in OFG is painless. Melkersson-Rosenthal syndrome is where OFG occurs with fissured tongue and paralysis of the facial nerve. The cause of the facial paralysis is thought to be caused by the formation of granulomas in the facial nerve, which supplies the muscles of facial expression.
OFG could be classified as a type of cheilitis (lip inflammation), hence the alternative names for the condition using the word cheilitis, and a granulomatous condition.
This type of epulis is neither pyogenic ("pus producing") nor a true granuloma, but it is a vascular lesion. About 75% of all pyogenic granulomas occur on the gingiva, although they may also occur elsewhere in the mouth or other parts of the body (where the term epulis is inappropriate). This common oral lesion is thought to be a reaction to irritation of the tissues and poor oral hygiene. It is more common in younger people and in females, and appears as a red-purple swelling and bleeds easily.
This is a fibrous hyperplasia of excess connective tissue folds that takes place in reaction to chronic trauma from an ill fitting denture. It usually occurs in the mandibular labial sulcus. Sometimes the term "epulis" is used synonymously with epulis fissuratum, but this is technically incorrect as several other lesions could be described as epulides.
Acute periapical periodontitis, also termed acute apical periodontitis, acute periradicular periodontitis, or symptomatic periapical periodontitis.
The type of periapical periodontitis is usually classified according to whether it is an acute/symptomatic process or a chronic/asymptomatic process.
There may or may not be any evidence of history of HGF in the family nor any usage of taking long-term medicines for any particular disease when it comes to diagnosing HGF. There also may or may not be any signs of medical and/or family history of mental retardation, hypertrichosis, nor clinical symptoms that can be associated with gingival enlargement. Although, enlargement of gingiva, interdental papilla, hindered speech, and secondary inflammatory changes taking place in the mouth commonly at the marginal gingiva are all very indicative of this condition. Commonly the patient will have mandiblular and maxilliary inflammation and overgrowth as opposed to the traditional pink, firm, and fleshy consistency of healthy gingiva. The patient's jaw may also appear distorted because of the gingiva englargements. Overgrowth of the gingiva can range from slightly covering the surface of teeth or it can even completely cover the surrounding teeth. The patient can also experience damage or loss of teeth.
The symptoms of gingivitis are somewhat non-specific and manifest in the gum tissue as the classic signs of inflammation:
- Swollen gums
- Bright red or purple gums
- Gums that are tender or painful to the touch
- Bleeding gums or bleeding after brushing and/or flossing
- Bad breath (halitosis)
Additionally, the stippling that normally exists in the gum tissue of some individuals will often disappear and the gums may appear shiny when the gum tissue becomes swollen and stretched over the inflamed underlying connective tissue. The accumulation may also emit an unpleasant odor. When the gingiva are swollen, the epithelial lining of the gingival crevice becomes ulcerated and the gums will bleed more easily with even gentle brushing, and especially when flossing.
Plasma cell gingivitis appears as mild gingival enlargement and may extend from the free marginal gingiva on to the attached gingiva. Sometimes it is blended with a marginal, plaque induced gingivitis, or it does not involve the free marginal gingiva. It may also be found as a solitude red area within the attached gingiva (pictures). In some cases the healing of a plaque-induced gingivitis or a periodontitis resolves a plasma cell gingivitis situated a few mm from the earlier plack-infected marginal gingiva. In case of one or few solitary areas of plasma cell gingivitis, no symptoms are reported from the patient. Most often solitary entities are therefore found by the dentist.
The gums are red, friable, or sometimes granular, and sometimes bleed easily if traumaticed. The normal stippling is lost. There is not usually any loss of periodontal attachment. In a few cases a sore mouth can develop, and if so pain is sometimes made worse by toothpastes, or hot or spicy food. The lesions can extend to involve the palate.
Plasma cell cheilitis appears as well defined, infiltrated, dark red plaque with a superficial lacquer-like glazing. Plasma cell cheilitis usually involves the lower lip. The lips appear dry, atrophic and fissured. Angular cheilitis is sometimes present.
Where the condition involves the tongue, there is an erythematous enlargement with furrows, crenation and loss of the normal dorsal tongue coating.
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.
In the early stages some patients may complain of a feeling of tightness around the teeth. Three signs/symptoms must be present to diagnose this condition:
- Severe gingival pain.
- Profuse gingival bleeding that requires little or no provocation.
- Interdental papillae are ulcerated with necrotic slough. The papillary necrosis of NUG has been described as "punched out".
Other signs and symptoms may be present, but not always.
- Oral malodor (intraoral halitosis).
- Bad taste (metallic taste).
Malaise, fever and/or cervical lymph node enlargement are rare (unlike the typical features of herpetic stomatitis). Pain is fairly well localized to the affected areas. Systemic reactions may be more pronounced in children. Cancrum oris (noma) is a very rare complication, usually in debilitated children. Similar features but with more intense pain may be seen in necrotizing periodontitis in HIV/AIDS.
It is one of the seven destructive periodontal diseases as listed in the 1999 classification.
Gum recession is generally not an acute condition. In most cases, receding of gums is a progressive condition that occurs gradually over the years. This is one reason that it is common over the age of 40. Because the changes in the condition of the gums from one day to another are minimal, patients get used to the gums' appearance and tend not to notice the recession visually. Receding gums may remain unnoticed until the condition starts to cause symptoms.
The following signs and symptoms may indicate gum recession:
- Tooth mobility
- Dentin hypersensitivity (over-sensitive teeth) - short, sharp pain is triggered by hot, cold, sweet, sour, or spicy food and drink. If the cementum covering the root is not protected anymore by the gums, it is easily abraded exposing the dentin tubules to external stimuli.
- Teeth may also appear longer than normal (a larger part of the crown is visible if gums are receding)
- The roots of the tooth are exposed and visible
- The tooth feels notched at the gum line
- Change in the tooth’s color (due to the color difference between enamel and cementum)
- Spaces between teeth seem to grow (the space is the same, but it seems larger because the gums do not fill it any more)
- Cavities below the gum line
If the gum recession is caused by gingivitis, the following symptoms may also be present:
- Puffy, red, or swollen (inflamed) gums
- Gum bleeding while brushing or flossing
- Bad breath (halitosis)
In some cases, it is the treatment of gingivitis that reveals a gum recession problem, that was previously masked by the gums swelling.
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."
Necrotizing gingivitis is part of a spectrum of disease termed necrotizing periodontal diseases. It is the most minor form of this spectrum, with more advanced stages being termed necrotizing periodontitis, necrotizing stomatitis and the most extreme, cancrum oris.
Acute necrotizing ulcerative gingivitis (ANUG) refers to the clinical onset of NUG. The word acute is used because usually the onset is sudden. Other forms of NUG may be chronic or recurrent.
Necrotizing ulcerative periodontitis (NUP) is where the infection leads to attachment loss, and involves only the gingiva, periodontal ligament and alveolar ligament. Progression of the disease into tissue beyond the mucogingival junction characterizises necrotizing stomatitis.
Clinical signs of TRs are often minimal since the discomfort can be minor. However, some authors have described discomfort while chewing, anorexia, dehydration, weight loss, and tooth fracture. The lower third premolar is the most commonly affected tooth.
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.
Hereditary gingival fibromatosis (HGF), also known as idiopathic gingival hyperplasia, is a rare condition of gingival overgrowth. HGF is characterized as a benign, slowly progressive, nonhemorrhagic, fibrous enlargement of keratinized gingiva. It can cover teeth in various degrees, and can lead to aesthetic disfigurement. Fibrous enlargement is most common in areas of maxillary and mandibular tissues of both arches in the mouth. Phenotype and genotype frequency of HGF is 1:175,000 where males and females are equally affected but the cause is not entirely known. It mainly exists as an isolated abnormality but can also be associated with a multi-system syndrome.
Gingivitis is a non-destructive disease that occurs around the teeth. The most common form of gingivitis, and the most common form of periodontal disease overall, is in response to bacterial biofilms (also called plaque) that is attached to tooth surfaces, termed "plaque-induced gingivitis".
While some cases of gingivitis never progress to periodontitis, data indicates that periodontitis is always preceded by gingivitis.
Gingivitis is reversible with good oral hygiene; however, without treatment, gingivitis can progress to periodontitis, in which the inflammation of the gums results in tissue destruction and bone resorption around the teeth. Periodontitis can ultimately lead to tooth loss. The term means "inflammation of the gum tissue".
In the early stages, periodontitis has very few symptoms, and in many individuals the disease has progressed significantly before they seek treatment.
Symptoms may include:
- 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
- Spitting out blood after brushing teeth
- 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 toothbrush.)
- 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)
Patients should realize gingival inflammation and bone destruction are largely painless. Hence, people may wrongly assume painless bleeding after teeth cleaning is insignificant, although this may be a symptom of progressing periodontitis in that patient.
Drug-related gingival hyperplasia is a cutaneous condition characterized by enlargement of the gums noted during the first year of drug treatment. There are three drug classes that are associated with this condition namely, anticonvulsants (such as phenyotoin and phenobartibal), calcium channel blocker (such as amlopidine, nifedipine and verapamil) and ciclosporin, an immunosuppressant Although the mechanism of drug related gingival hyperplasia is not well understood, some risk factors for the condition include the duration of drug use and poor oral hygiene. In most cases, alternative drugs are given, in order to avoid this side effect.