History

In 1999 the American Academy of Periodontology assembled an International Workshop for a Classification of Periodontal Diseases and Conditions; this resulted in what became known as the 1999 Armitage Classification. In 2014 an AAP task force looking at the classification determined three areas of concern; attachment level (although clinical attachment level (CAL) is important for research it proved to be overly time consuming in everyday clinical practice); chronic versus aggressive periodontitis; and localized versus generalized periodontitis. In 2017 World Workshop on the Classification of Periodontal Disease and Peri-Implant Conditions was formed to update and standardize the previous 1999 classification and to develop a similar classification for peri-implant diseases and conditions.

The main differences between the 1999 and the 2017 classifications are: Firstly, different statuses of periodontal and gingival health were described. Secondly, that three forms of periodontitis were identified: necrotizing periodontitis, periodontitis as a manifestation of systemic disease, and periodontitis (comprising the forms of disease previously recognized as “chronic” or “aggressive”). Thirdly, this new classification system encompasses a multidimensional view of periodontitis using a staging and grading system. Fourthly, a change in the classification gingival recessions, and the change of terminology of periodontal biotype for periodontal phenotype. Finally, there was a significant expansion in the descriptions of peri-implant health, peri-implant mucositis, and peri-implantitis.

1. Periodontal Health, Gingival Diseases and Conditions
   1. Periodontal Health and Gingival Health

The 2017 world workshop for the classification of periodontal diseases (Chapple et al. 2018) defined periodontal health and gingival health into three different entities based on the history of periodontal disease of the patient and presence or absence of clinical attachment level: intact periodontium, reduced periodontium in a non-periodontitis patient, and reduced periodontium in a successfully treated stable periodontitis patient (Table 2.1).

It is important to mention that there is certain level of tolerance between the definition of periodontal health on an intact periodontium and gingivitis (dental plaque induced) of less than 10% bleeding on probing on all the sites. If there is any presence of loss in the clinical attachment level the correct term to use would be of a reduced periodontium while the differences on bleeding on probing will determine the health status of the periodontium.

Interestingly, patients with a reduced periodontium due to periodontitis successfully treated previously can present with increased probing depths of up to 4 mm, this is due that probing depths of <3 mm are rarely achieved on a 100% of treated sites, therefore it could lead to overtreatment as any non-bleeding site of >3 mm would not be considered “health” and would require further treatment instead of monitoring and supportive care. Yet, in the case of gingivitis patients the maximum allowed probing depth was set to 3 mm irrespective of the previous periodontal history of the patient.

• b) Gingivitis: Dental Biofilm-Induced
  1. I) Associated with dental biofilm alone

As explained before, based on the history of periodontal disease of the patient, there are three possible entities to diagnose dental biofilm-induced gingivitis which can be seen in Table 2.1.

Whether they are associated with hormonal imbalances, mediations, systemic disorders, or malnutrition, these gingival diseases have the following characteristics in common (Mariotti 1999; Trombelli et al. 2018):

• The signs and symptoms are confined to the gingiva.
• Plaque is the main etiological factor which will initiate or exacerbate the gingival lesions.
• Inflammation of the gingival tissues will produce changes in color (transition to a red/bluish-red hue), shape (enlarged gingival contours due to edema or fibrosis), texture, bleeding upon stimulation, and elevated sulcular temperature (Figure 2.2).
  

  

• There is no alveolar bone loss and pocket depth; clinical attachment levels around teeth are stable.
• This is a reversible condition which resolves upon removal of the etiological factors.
• Possible role as a precursor to attachment loss around teeth.

Gingivitis primarily induced by dental plaque includes the following disease subdivisions:

1. Gingivitis associated with dental biofilm only: Signs and symptoms typical of gingivitis can be observed at all ages of dentate populations and this disease has been considered to be the most common form of periodontal disease (Page 1985). The disease can be observed in a child as young as five years of age, progress with a peak during puberty, and remain present throughout life at various extents. Plaque is present at the gingival margin and a positive correlation exists between gingivitis and plaque accumulation.

   There is no pathognomonic flora associated with gingivitis, although the dental plaque in gingivitis differs from that present in gingival health (Ranney 1993). Note that gingivitis may also occur on a reduced periodontium (decreased amount of alveolar bone height and connective tissue support around teeth) which was previously surgically treated for a periodontitis. This situation is encountered when there is a recurrence of inflammation of the marginal gingiva on a periodontium with previous attachment loss but without any evidence of progressive attachment loss (no indication of active disease) (Mariotti 1999; Trombelli et al. 2018).

• II) Mediated by systemic or local risk factors
  1. Systemic risk factor (modifying factors)

• i) Smoking

  Smoking is one of the major risk factors for periodontitis, due to its effects upon gingival tissues. Among the effects we can identify: microvascular vasoconstriction and fibrosis. These can mask clinical signs of inflammation, such as bleeding on probing, despite the presence of a significant underlying pathological inflammatory response in the gingival tissues.

• ii) Hyperglycemia

  Diabetes-mellitus-associated gingivitis: Diabetes mellitus is a complex disease with varying degrees of systemic and oral complications involving abnormalities in insulin production, fat, proteins, and sugar metabolism, and resulting in an impaired vascular and immune system as well as an inadequate inflammatory response. Diabetes mellitus is categorized as Type 1 and Type 2. Type 1 develops due to impaired production of insulin and Type 2 is caused by deficient utilization of insulin. There is evidence to suggest that uncontrolled Type 1 diabetes in children is associated with exaggerated response of the gingival tissues to dental plaque (Lindhe 2003). It is a reversible condition once the diabetes is under control and the dental plaque is removed.

• iii) Nutritional factors

  Ascorbic acid deficiency gingivitis: Nutritional deficiencies such as ascorbic acid (vitamin C deficiency) can significantly exacerbate the response of the gingiva to plaque bacteria (Mariotti 1999). The clinical description of severe vitamin C deficiency or scurvy consists of bulbous, spongy, hemorrhagic, swollen, and erythematous gingival lesions (Charbeneau et al. 1983). The result of compromised antioxidant micronutrient defenses to oxidative stress and impacts negatively collagen synthesis, resulting in weakened capillary blood vessel walls and consequent enhanced gingival bleeding. This condition is unusually seen in areas of adequate food supply but can potentially affect infants of low socioeconomic families, institutionalized elderly individuals, and alcoholics.

• iv) Pharmacological agents (prescription, nonprescription and recreational)

1. Oral contraceptives: Studies have shown that women taking oral contraceptive drugs have a higher incidence of gingival enlargement in comparison to women who do not take the medications (Kaufman 1969). Pronounced inflammation (change in gingival contour, color, exudate) is seen and is reversible upon removal of medications (Figure 2.3).
   

   

2. Other. In general any drug that may alter the salivary flow, impact endocrine function, and/or produce gingival enlargement (Trombelli et al. 2018).

• v) Sex steroid hormones
  1. Puberty

     Puberty-associated gingivitis: A rise in gingival inflammation and gingival volume is noted during puberty in both sexes without necessarily seeing a rise in the quantity of plaque (Sutcliffe 1972). The incidence of the severity of gingivitis in adolescence is not only related to the rise in steroid hormones but is also influenced by a variety of factors such as dental caries, mouth breathing, teeth crowding, and tooth eruption (Stamm 1986). These changes are reversible after puberty. More specifically, hyperplastic gingivitis often seen during the adolescence period can be associated with:

• — Orthodontic treatment: Note that fibrotic tissue tends to recur if surgical removal is attempted during orthodontic treatment. It is recommended to wait until orthodontic appliances are removed before surgically removing excess tissue (Figure 2.4).
  

  

• — Mouth breathing: Mouth breathing, which often accompanies Angle’s classification 2 division 1 malocclusion, is considered to be an exacerbating factor to gingivitis (Lindhe 2003). Gingival hyperplasia tends to affect mostly the anterior superior region and is also prone to recurrence if surgical removal is performed without any correction of the actual mouth breathing through orthodontic treatment or cessation of habit.

2. Menstrual cycle

   Menstrual-cycle-associated gingivitis: The most common sign is a minor gingival inflammation during ovulation; gingival exudate has been shown to increase at least 20% in 75% of women (Hugoson 1971). This situation is reversible after ovulation.

   Note: Hormonal gingivitis or postmenopausal gingivitis can be seen in women taking hormone replacement therapy. Signs and symptoms may involve atrophic, thin, erythematous gingival tissues, and patient complaints of gingival sensitivity to spicy foods and acidic beverages. Palliative treatment is suggested.

3. Pregnancy
   1. Gingivitis: A combination of pregnancy hormones and dental plaque may increase the severity of gingivitis in women sensitive to local irritants. In addition to the typical gingivitis signs, severe inflammation can develop in the presence of relatively low amounts of dental plaque (Hugoson 1971). It will usually affect pregnant women in their second or third trimester, and is reversible after child delivery.
   2. Pyogenic granuloma: This refers to a mass of hyperplastic gingival tissue principally found in the interdental maxillary regions. It is not a tumor but an exaggerated inflammatory response to irritation resulting in a solitary polyploid capillary hemangioma which can easily bleed upon mild provocation (Sills et al. 1996). Pregnancy-associated pyogenic granuloma presents clinically as a painless protuberant exophytic mass attached by a sessile or pedunculated base from the gingival margin. It has been reported to occur in 0.5–5% of pregnancies and can develop as early as the first trimester (Mariotti 1999). It usually regresses or completely disappears following parturition. If needed, surgical excision can be performed postpartum. The treatment for pregnancy-associated gingivitis and pyogenic granuloma during pregnancy is an impeccable control of the etiological factors (scaling, prophylaxis, and chlorhexidine rinses). This condition can also be classified under Epulides in the Reactive processes of non-dental plaque associated gingival conditions (Holmstrup et al. 2018).

4. Oral contraceptives

• iv) Hematological conditions

1. Leukemia-associated gingivitis: Leukemia is a progressive malignant hematological disease characterized by the development of abnormal leukocytes and leukocytes precursors in the blood and bone marrow. Leukemia is classified according to disease progression (acute or chronic), cell types involved (myeloid or lymphoid), and cell numbers in blood (leukemic or aleukemic). The oral manifestations are acute, consisting of cervical adenopathies, petechia, gingival enlargements, and mucous ulcers. Dental plaque can exacerbate the gingival inflammatory changes which include swelling, redness/blueness, sponginess, and glazed appearance of the gingiva which is infiltrated with leukemic cells (Lindhe 2003). Persistent and unexplained gingival bleeding may indicate an underlying thrombocytopenia associated with the leukemic condition. Lesions are often found in the acute monocytic type, and consist of a modified gingival volume and bleeding of gingiva upon touch. Symptoms lessen when antiseptic mouthwashes are used and plaque volume is reduced.
2. Other
   • b) Local risk factors
     1. i) Dental plaque biofilm retention factors
     2. ii) Oral dryness
     3. iii) Drug-influenced gingival enlargement

Drug-induced gingival enlargement: Three commonly used classes of medications create these lesions:

• Anti-convulsant drug used for treatment of epilepsy: Dilantin (Phenytoin sodium), 50% incidence (Angelopoulos et al. 1972)
• Immunosuppressant drug used to avoid host rejection of grafted tissues: Cyclosporine A, 25–30% incidence (Over time, this drug is tapered and the gingival enlargements become easier to control.) (Romito et al. 2004)
• Calcium channels blocking agents used as hypertensive drugs: Nifedipine, Verapamil, Diltiazem, 15–20% incidence (Barclay et al. 1992)

Over the years more medications have been described to induce gingival enlargement, such as (Bharti et al. 2013):

• Anticonvulsants

• – Ethosuximide
• – Ethotoin
• – Mephenytoin
• – Methsuximide
• – Phenobarbital
• – Phenytoin
• – Primidone
• – Sodium valproate
• – Vigabatrin

• Immunosuppressants

• – Cyclosporine
• – Sirolimus
• – Tacrolimus

• Calcium channel blockers

• – Amlodipine
• – Diltiazem
• – Felodipine
• – Manidipine
• – Nicardipine
• – Nifedipine
• – Nimodipine
• – Nisoldipine
• – Nitrendipine
• – Verapamil

Individuals taking these medications may develop gingival enlargements leading to pseudopockets. Characteristics of drug-influenced gingival enlargement include (Mariotti 1999):

• Predilection of anterior gingiva; starts interproximally and expands
• Higher prevalence in children
• Onset within the first three months of taking the drug
• Enlargement of the gingival contours appears
• Stippling is present in the gingiva
• Pronounced inflammatory response in relation to the plaque volume
• Not associated with attachment loss but can be found in periodonitums with and without bone loss

Treatment consists of control of etiological factors followed by full mouth gingivectomy. Gingivectomy (full mouth or local) may need to be performed annually. If possible, the drugs can also be changed or dosages adjusted to improve the oral condition.

• c) Gingival Diseases: Non-Dental Biofilm-Induced

Although these gingival lesions are not produced by plaque and do not disappear when plaque is removed, it should be noted that the severity of the clinical manifestation can often be related to the presence of bacterial plaque (Holmstrup et al. 2018).

1. Genetic/developmental disorders
   1. Hereditary gingival fibromatosis

      This gingival hyperplasia (gingival overgrowth) is an uncommon condition of genetic origin. Of idiopathic etiology, this condition develops irrespective of effective plaque removal. Hereditary gingival fibromatosis can be an isolated condition or part of a syndrome or systemic condition (Gorlin et al. 1990) (Figure 2.5).

• b) Specific infections
  • i) Bacterial origin

These types of gingivitis and stomatitis can be found in immunocompromised and immunocompetent individuals. They occur when the microorganisms surpass innate host resistance. Clinical signs may range from painful, edematous ulcerations to asymptomatic cancers, mucosal patches, or atypical non-ulcerated inflamed gingiva. Lesions elsewhere on the body may also be present. Gingival lesions may occur due to infections with Neisseria gonorrhea, Treponema pallidum, streptococci, or other organisms.

1. Neisseria gonorrhoeae (Gonorrhea)

   Gonorrhea is a sexually transmitted disease which can affect the oropharyngeal region in approximately 20% of infected individuals (Neville 2002). Diffuse erythema, small erosive pustules, and edema can be seen in this region as well as on tonsils and uvula. Gingivitis and stomatitis, as well as a sore throat and a cervical or submandibular lymphadenopathy, may also be present.

• 2) Treponema pallidum (Syphilis)

  Syphilis is a chronic infection produced by Treponema pallidum. The primary modes of transmission are sexual contact or mother to fetus. The infection undergoes a characteristic evolution that classically proceeds through three stages: In primary syphilis, an asymptomatic contagious chancre appears three to four weeks post contact at the site of inoculation. When affecting the oral cavity, it can affect the lips, gingiva, tonsils, tongue, and palate. It leaves a scar and heals spontaneously. In secondary syphilis, whitish mucous patches as well as maculopalular cutaneous rashes are often present and are still contagious at this point. In tertiary syphilis, a noncontagious granulomatous inflammation (gumma) reaction appears which can often cause necrosis and perforation of the tongue or palate. Serious systemic conditions are involved (Neville et al. 2002).

• 3) Mycobacterium tuberculosis (Tuberculosis)
• 4) Streptococcal gingivitis

  An upper respiratory tract infection usually causes fever and accompanies a diffuse gingivitis, tonsillitis, pharyngitis, and ulceration of the oral mucosa. One of the most common species involved is the group A, β-hemolytic streptococci (Neville et al. 2002).

• ii) Viral origin

  Several viral infections are known to cause gingivitis. Most of them enter the body during childhood and may give rise to the disease followed by periods of latency.

1. Coxsackie virus (Hand-Foot-Mouth disease)
2. Herpes simplex I and II (primary or recurrent)
   • – Primary herpetic gingigostomatitis: Herpes simplex virus type 1 (and occasionally type 2) is responsible for causing the primary infection which involves painful severe gingivitis with ulcerations (on keratinized and non-keratinized tissues) and edema followed by stomatitis. High fever and malaise is generally present. Vesicles on lips can produce a crusty lips appearance after rupturing (Miller 1992) (Figure 2.6).
     

     

   • – Palliative treatment only is required. The infection lasts approximately 10 days. During this period, the patient must be well hydrated with liquids and topical application of anesthetic agents is also indicated. Chlorhexidine and an antibiotic may be needed to prevent a super-infection. In the adult infection, antiviral drugs such as Zovirax, #70, 200 mg, 1 tabqid, for 2 weeks can be prescribed.
   • – Recurrent oral herpes: Reactivation of the virus resulting in recurrent infections occurs in 20–40% of individuals with the primary infection (Greenberg 1996). These lesions (vesicles which become ulcers) usually only affect the keratinized tissues and are usually present unilaterally or locally. The treatment, if any, can consist of topical antiviral ointment or tablets.

• 3) Varicella zoster (chickenpox—Shingles—V nerve)

Varicella-zoster virus causes varicella (chickenpox) as the primary self-limiting infection. The virus then remains latent and can be reactivated resulting in the herpes zoster infection. This painful unilateral infection is often seen in older individuals and is accompanied by cutaneous lesions of the affected nervous territory (Miller 1996).

• 4) Molluscum contagiosum
• 5) Human papilloma virus (squamous cell papilloma, condyloma acuminatum, verruca vulgaris, focal epithelial hyperplasia)

• iii) Fungal origin

The most frequent oral fungal infections consist of candidosis and histoplasmosis.

1. Candidosis

   Candida-species infections: C. albicans is one of the most frequent candida species affecting the oral cavity. It is considered an opportunistic infection occurring when the host resistance is diminished. Most subtypes of candidosis can be treated with antifungal medications (Ketoconazole 200 mg, 1 tab/day, 10 days, or Fluconazole 100 mg, 1 tab/ day, 14 days).

1. Generalized gingival candidosis include:
   • Acute types:
     • Pseudomembranous candidosis: This type of infection produces soft white patches disseminated throughout the oral mucosa. These patches can be removed with an instrument leaving behind an erythematous mucosal surface.
     • Atrophic or erythematous candidosis: This type of infection produces red lesions spreading all over the oral mucosa. They are associated with severe pain and discomfort.
   • Chronic types:
     • Hyperplasic candidosis: Typically, the lesion is longstanding and presents itself as a thick white patch which cannot be rubbed off (leukoplakia correlation).
     • Mucocutaneous: This type of candidosis mostly affects the skin, scalp, and nails; much more rarely it affects the gingiva.
   • Prosthetic stomatitis (types 1,2,3)
   • Linear gingival erythema: This disease was initially termed “HIV-related gingivitis.” It mostly affects immunocompromised individuals or HIV patients. The unusual pattern of inflammation appears as a distinctive linear band of erythema which involves 2–3 mm of marginal gingival (Neville et al. 2002). Redness can be circumscribed or diffused and can spread until it passes the mucogingival junction. It is often generalized in the oral cavity, but can be localized to just a few teeth. The main characteristic is that it does not respond to conventional treatment (SRP and plaque control).

Note: the HIV patient is also more prone to:

• Hyperplasic candidosis
• Pseudomembranous candidosis
• Cheilitis
• Ulcerative necrotizing gingivitis, ulcerative necrotizing periodontitis
• Hairy leukoplakia
• Kaposi’s sarcoma
  • 2) Other mycoses (Histoplasmosis; Aspergillosis)

    Histoplasmosis is a granulomatous disease caused by Histoplasma capsulatum and represents one of the most frequent systemic mycoses in the United States. The frequently seen subclinical development of infection usually includes either a pulmonary chronic histoplasmosis (30% have oral manifestations) or a disseminated form found primarily in HIV patients (60% have oral manifestations). Oral findings can consist of painful granulomatous ulcerations (Holmstrup 1999).

• c) Inflammatory and immune conditions
  1. Hypersensitivity reactions
     1. 1) Contact allergy

        Contact allergy is a rare condition, but it is an inflammatory reaction of the gingival tissue mostly to dental restorative materials, dentifrices, mouthwashes, and foods. Their presentation is associated to a type IV hypersensitivity reaction.

• 2) Plasma cell gingivitis

  Clinically it presents as an erythematous gingival with velvety texture, usually affecting the maxillary anterior gingiva, and histopathologically presents a dense infiltrate of plasma cells in the lamina propia. It is of uncertain etiology.

• 3) Erythema multiforme

  Erythema multiforme is an acute vesiculobullous disease affecting mucous membranes and skin. This inflammatory reaction produces bullae which rupture and leave extensive ulcers covered by yellowish fibrinous exudates, sometimes described as pseudomembranes, on the gingival tissues. Another characteristic oral lesion is the typically swollen lips with crust formation of the vermillion border. “Target lesions,” which can be described as a central bulla surrounded by an erythematous halo, can be found on the skin of the hands and feet (Lozada-Nur et al. 1989). The pathogenesis of this disease remains obscure, but an autoimmune reaction is suspected as the main underlying etiological factor. Two main forms of the disease have been described, minor form (limited affection) and major form (Stevens-Johnson syndrome).

• iii) Autoimmune diseases of the skin and mucus membranes

  Mucocutaneous disorders: Many dermatologic diseases present with gingival manifestations in the form of desquamative, ulcerative, or erythematous gingival lesions. The most relevant ones are presented as follows:

• 1) Pemphigus vulgaris

  Pemphigus is a group of autoimmune diseases characterized by the formation of intraepithelial bulla in skin and mucous membranes. One of the most common and serious subtypes of this disease is pemphigus vulgaris. Clinically, it presents as painful desquamative lesions of the gingiva, as erosions or ulcerations which are remains of ruptured bullae (Sciubba 1996). As a diagnostic tool, the histological analysis can reveal that the bullae contain non-adhering free epithelial cells (Tzank cells). It also will respond positively to the Nicholski test. Direct immunofluorescence will reveal presence of immunoglobulin G (IgG) antibodies and occasionally components of the complement system, more specifically component complement 3 (C3), in the intercellular spaces between the epithelial cells resulting in a “chicken wire” pattern. This disease can be fatal if left untreated.

• 2) Pemphigoid

  Pemphigoid is a group of disorders in which autoantibodies are directed toward components of the basement membrane, resulting in the detachment of the epithelium from the connective tissue. This may occur on the skin (bullous pemphigoid) and mucous membranes. When only mucous membranes are involved, it is termed benign mucous membrane pemphigoid. The main manifestation is desquamative lesions of the gingiva, presenting intensely erythematous lesions. This type of benign epithelial lesion arises from underneath the basement membrane, producing a desquamation more resistant to detachment during the clinical examination. Direct immunofluorescence will reveal a linear deposition of IgG, IgA, or C3 along the epithelial basement membrane zone.

• 3) Lichen planus

  Lichen planus is one of the most common dermatological diseases affecting the oral cavity. Of autoimmune etiology, it can be classified according to the following subtypes: reticular, atrophic, plaque, erosive, and bullous. The characteristic clinical appearance resembles desquamative chronic gingivitis with the presence of white papules and white striations which often form a reticular pattern, also known as the Wickam striae (Thorn et al. 1988) (Figure 2.7). Histopathologic analysis will reveal epithelial rete ridges with a pointed or “saw-toothed” shape, additionally there will be degenerating keratinocytes (civatte bodies) and presence of a band of inflammatory infiltrate (mainly lymphocytes) in the superficial part of the connective tissue.

• 4) Lupus erythematosus

Lupus erythematosus represents a group of autoimmune connective tissue disorders in which antibodies are directed toward the individual’s cellular components. Two major forms exist: the discoid form (chronic type) and the systemic form. The typical lesions that can be seen on the gingiva appear as small, white dots of central atrophy surrounded by irradiating fine white striae with a periphery of telangiectasia. The characteristic “butterfly” skin lesions are photosensitive, scaly, erythematous macules located on the bridge of the nose and cheeks (Schiodt 1984).

1. Systemic lupus erythematosus
2. Discoid lupus erythematosus

• iii) Granulomatous inflammatory condition (orofacial granulomatosis)
  1. 1) Chron disease
  2. 2) Sarcoidosis

• d) Reactive processes
  1. Epulides

Epulides is a nonspecific term defined as an exophytic process originating from the gingiva, therefore histopathology is necessary to define a more specific diagnosis. Usually it does not have symptoms associated to it, and it affects most frequently the attached gingiva (64%) (Holmstrup et al. 2018).

• 1) Fibrous epulis

  Also known as focal fibrous hyperplasia or irritation fibroma, it presents as an exophytic smooth surfaced pink mass of fibrous consistency. The primary etiologic factor is presumably continued physical trauma/irritation.

• 2) Calcifying fibroblastic granuloma

  Also described as ossifying fibroid epulis or peripheral ossifying fibroma. Clinically it presents as a pedunculated or sessile red to pink mass usually originating from the interproximal papilla. It occurs exclusively in the gingiva. Histopathologic it is characterized by a highly fibroblastic tissue with a lobulated mass of calcified cementum-like tissue.

• 3) Pyogenic granuloma (vascular epulis)

  In the literature it has also been described as telangietatic granuloma, pregnancy granuloma, pregnancy tumor, and vascular epulis. It is common, often associated to pregnancy, and with a high predilection for gingiva. Clinically presents as a pedunculated mass, often ulcerated, smooth, red to pink, and variable in size. Histopathologically presents as a discontinuous hyperplasic parakeratinized stratified squamous epithelium and an increased amount of endothelial cells in the connective tissue.

• 4) Peripheral giant cell granuloma (or central)

  Other names attributed to this lesion are giant cell epulis and peripheral giant cell reparative granuloma. Clinically, presents as a well-defined sessile or pedunculated mass, soft in consistency, sometimes ulcerated, and with a wide variety of color (purple, bluish to brown). Its name is attributed to the histopathological finding of multiple giant cells.

• e) Neoplasms
  1. Premalignant
     1. 1) Leukoplakia
     2. 2) Erythroplakia
  2. Malignant
     1. 1) Squamous cell carcinoma
     2. 2) Leukemia
     3. 3) Lymphoma (Hodgkin and non-Hodgkin)
• f) Endocrine, nutritional, and metabolism diseases
  1. Vitamin deficiencies
     1. 1) Fat soluble vitamins (Vitamins A, D, and E)
     2. 2) Water soluble vitamins (Complex Band Vitamin C)
• g) Traumatic lesions
  1. Physical/mechanical insults

     Physical or mechanical trauma: Gingival recessions or artefacta gingivitis can be the result of physical traumatic events or bad oral habits (Figures 2.8, 2.9, and 2.10).

1. 1) Frictional keratosis
2. 2) Mechanical induced gingival ulceration
3. 3) Factitious injury (self-harm)

• ii) Chemical

  Chemical injury or toxic reaction: Toxic gingival reaction can be caused by chemical injury of the mucosa as seen in surface etching of the tissue by toxic products. For example, chlorhexidine can cause desquamation of mucosa; paraformaldehyde can give rise to inflammation and tissue necrosis. Other reactions can be attributed to aspirin, cocaine, or toothpaste rubbed on the gingival tissues (Figure 2.11).