CS4-7)Clinical Features of Gingivitis and Acute Gingival Infections- Prof. Dr. TOLGA TOZUM (1).pdf

Prof. Dr. TOLGA TOZUM YAKINDOĞU ÜNİVERSİTESİ DİŞHEKİMLİĞİ FAKÜLTESİ Learning outcomes: 1- Will be able to define periodontal health, gingival health and gingivitis, clinically distinguish periodontal health and gingivitis. 2-Will be able to explain and clinically distinguish between biofilm-induce...

Prof. Dr. TOLGA TOZUM YAKINDOĞU ÜNİVERSİTESİ DİŞHEKİMLİĞİ FAKÜLTESİ Learning outcomes: 1- Will be able to define periodontal health, gingival health and gingivitis, clinically distinguish periodontal health and gingivitis. 2-Will be able to explain and clinically distinguish between biofilm-induced and non-biofilm-induced gingivitis. 3- Will be able to explain the color changes in the gingiva except gingival inflammation and distinguish them clinically. 4-Will be able to list acute gingival diseases, distinguish them from each other according to their causes, and determine clinically. 5- Explain the treatments of gingivitis and acute gingival diseases . Clinical Features of Gingivitis Experimental gingivitis studies provided the first empiric evidence that the accumulation of microbial biofilm on clean tooth surfaces results in the development of an inflammatory process around gingival tissue. Research has also shown that the local inflammation will persist as long as the microbial biofilm is present adjacent to the gingival tissues and that the inflammation may resolve subsequent to a meticulous removal of the biofilm.The prevalence of gingivitis is evident worldwide. For example, epidemiologic studies indicate that more than 82% of adolescents in the United States have overt gingivitis and signs of gingival bleeding. A similar or higher prevalence of gingivitis is reported for children and adolescents in other parts of the world.A significant percentage of adults also show signs of gingivitis; more than half of the US adult population is estimated to exhibit gingival bleeding, and other populations show even higher levels of gingival inflammation. Whereas plaque remains the primary etiological factor that causes gingivitis, other factors may affect the development of periodontal diseases. Recent experimental gingivitis studies suggest an important role of the host response in the development and degree of gingival inflammation.In general, clinical features of gingivitis may be characterized by the presence of any of the following clinical signs: redness and sponginess of the gingival tissue, bleeding on provocation, changes in contour, and the presence of calculus or plaque with no radiographic evidence of crestal bone loss. The histologic examination of inflamed gingival tissue reveals ulcerated epithelium. The presence of inflammatory mediators negatively affects epithelial function as a protective barrier. Repair of this ulcerated epithelium depends on the proliferative or regenerative activity of the epithelial cells. Removal of the etiologic agents that triggered the gingival breakdown is essential. Course and Duration Gingivitis can occur with sudden onset and short duration, and it can be painful. A less severe phase of this condition can also occur. Chronic gingivitis is slow in onset and of long duration. It is painless, unless it is complicated by acute or subacute exacerbations, and it is the type that is most often encountered.Chronic gingivitis is a fluctuating disease in which inflammation persists or resolves and in which normal areas become inflamed.Recurrent gingivitis reappears after having been eliminated by treatment or disappearing spontaneously. Description Localized gingivitis is confined to the gingiva of a single tooth or group of teeth, whereas generalized gingivitis involves the entire mouth. Marginal gingivitis involves the gingival margin, and it may include a portion of the contiguous attached gingiva. Papillary gingivitis involves the interdental papillae, and it often extends into the adjacent portion of the gingival margin. Papillae are involved more frequently than the gingival margin, and the earliest signs of gingivitis often occur in the papillae. Diffuse gingivitis affects the gingival margin, the attached gingiva, and the interdental papillae. Gingival disease in individual cases is described by combining the preceding terms as follows: • Localized marginal gingivitis is confined to one or more areas of the marginal gingiva . • Localized diffuse gingivitis extends from the margin to the mucobuccal fold in a limited area. • Localized papillary gingivitis is confined to one or more inter- dental spaces in a limited area. • Generalized marginal gingivitis involves the gingival margins in relation to all the teeth. The interdental papillae are usually affected . • Generalized diffuse gingivitis involves the entire gingiva. The alveolar mucosa and the attached gingiva are affected, so the mucogingival junction is sometimes obliterated. Systemic conditions can be involved in the cause of generalized diffuse gingivitis and should be evaluated if they are suspected as an etiologic cofactor. Clinical Findings A systematic approach is required for the evaluation of the clinical features of gingivitis. The clinician should focus on subtle tissue alterations, because these may be of diagnostic significance. A systematic clinical approach requires an orderly examination of the gingiva for color, contour, consistency, position, and ease and severity of bleeding and pain. This section discusses these clinical characteristics and the microscopic changes that are responsible for each. Gingival Bleeding on Probing The two earliest signs of gingival inflammation that precede established gingivitis are as follows: (1) increased gingival crevicular fluid production rate; and (2) bleeding from the gingival sulcus on gentle probing discusses gingival crevicular fluid in detail. Gingival bleeding varies with regard to severity, duration, and ease of provocation. Bleeding on probing is easily detected clini cally and therefore is of value for the early diagnosis and prevention of more advanced gingivitis. It has been shown that bleeding on probing appears earlier than a change in color or other visual signs of inflammation; in addition, the use of bleeding rather than color changes to diagnose early gingival inflammation is advantageous in that bleeding is a more objective sign that requires less subjective estimation by the examiner. For example, it is estimated that 53.2 million (50.3%) US adults who are 30 years old and older exhibit gingival bleeding. Probing pocket depth measurements by themselves are of limited value for the assessment of the extent and severity of gingivitis. For example, gingival recession may result in a reduction of the probing depth and thus cause an inaccurate assessment of the periodontal status.4 Therefore, bleeding on probing is widely used by clinicians and epidemiolo- gists to measure disease prevalence and progression, to measure outcomes of treatment, and to motivate patients to perform necessary home care.In general, gingival bleeding on probing indicates an inflammatory lesion both in the epithelium and in the connective tissue that exhibits specific histologic differences as compared with health gingiva. Even though gingival bleeding on probing may not be a good diagnostic indicator for clinical attachment loss, its absence is an excellent negative predictor of future attachment loss.Therefore, the absence of gingival bleeding on probing is desirable and implies a low risk of future clinical attachment loss. Longitudinal findings revealed that sites with consistent bleeding (gingivval index = 2) had 70% more attachment loss than sites that were noninflamed over a 26-year period in 565 males. Thus, persistent gingivitis can be considered as a risk factor for periodontal attach ment loss that may lead to tooth loss. Interestingly, numerous studies have shown that current cigarette smoking suppresses the gingival inflammatory response, and smoking was found to exert a strong, chronic, dose-dependent suppressive effect on gingival bleeding with probing in the Third National Health and Nutrition Examination Survey.In addition, recent research reveals an increase in gingival bleeding with probing in patients who quit smoking. Thus, people who are com mitted to a smoking cessation program should be informed about the possibility of an increase in gingival bleeding associated with smoking cessation. Gingival Bleeding Caused by Local Factors Factors that contribute to plaque retention and that may lead to gingivitis include anatomic and developmental tooth variations, caries, frenum pull, iatrogenic factors, malpositioned teeth, mouth breathing, overhangs, partial dentures, lack of attached gingiva, and recession. In addition, orthodontic treatment and fixed retainers were associated with increased plaque retention and increased bleeding on probing.Chronic and Recurrent Bleeding. The most common cause of abnormal gingival bleeding on probing is chronic inflammation. The bleeding is chronic or recurrent, and it is provoked by mechanical trauma (e.g., from toothbrushing, toothpicks, or food impaction) or by biting into solid foods (e.g., apples). Gingival Bleeding Associated with Systemic Changes With some systemic disorders, gingival hemorrhage occurs spontaneously or after irritation, and it is excessive and difficult to control. These hemorrhagic diseases represent a wide variety of conditions that vary with regard to etiologic factors and clinical manifestations. Such conditions have the common feature of a hemostatic mechanism failure and result in abnormal bleeding in the skin, the internal organs, and other tissues, including the oral mucosa.Hemorrhagic disorders in which abnormal gingival bleeding is encountered include vascular abnormalities (vitamin C deficiencyallergy [e.g., Henoch–Schönlein purpura]), platelet disorders(thrombocytopenic purpura), hypoprothrombinemia (vitamin K deficiency), other coagulation defects (hemophilia, leukemia, Christmas disease), deficient platelet thromboplastic factor as a result of uremia, multiple myeloma, and postrubella purpura. The effects of hormonal replacement therapy, oral contraceptives, pregnancy, and the menstrual cycle are also reported to affect gingival bleeding. In addition, in women, long-term depression-related stress exposure may increase concentrations of interleukin-6 in gingival crevicular fluid and worsen periodontal conditions with elevated gingival inflammation and increased pocket depths.In addition, changes in androgenic hormones have long been established as significant modifying factors in gingivitis, especially among adolescents. Several reports have shown notable effects of fluctuating estrogen and progesterone levels on the periodontium, starting as early as puberty. Among pathologic endocrine changes, diabetes is an endocrine condition with a well-characterized effect on gingivitis. In diabetes, marked inflammation affects both the epithelial and connective tissues, which leads to the degeneration of the dermal papilla, an increase in the number of inflammatory cells, the destruction of reticulin fibers, and an accumulation of dense collagen fibers that causes fibrosis. Several medications have also been found to have adverse effects on the gingiva. For example, anticonvulsants, antihypertensive calcium channel blockers, and immunosuppressant drugs are known to cause gingival enlargement , which secondarily can cause gingival bleeding. The American Heart Association has recommended over-the-counter aspirin as a therapeutic agent for cardiovascular disease, and aspirin is often prescribed for rheumatoid arthritis, osteoarthritis, rheumatic fever, and other inflammatory joint diseases. Thus, it is important to consider aspirin’s effect on bleeding during a routine dental examination to avoid false-positive readings, which could result in an inaccurate patient diagnosis.67 (Chapter 11 discusses periodontal involvement in hematologic disorders.) Color Changes in the Gingiva The color of the gingiva is determined by several factors, including the number and size of blood vessels, the epithelial thickness, the quantity of keratinization, and the pigments within the epithelium. Color Changes with Gingivitis. Change in color is an important clinical sign of gingival disease. The normal gingival color is “coral pink,” and it is produced by the tissue’s vascularity and modified by the overlying epithelial layers. For this reason, the gingiva becomes red when vascularization increases or when the degree of epithelial keratinization is reduced or disappears. The color becomes pale when vascularization is reduced (in association with fibrosis of the corium) or when epithelial keratinization increases. Thus, chronic inflammation intensifies the red or bluish red color as a result of vascular proliferation and a reduction of keratinization. In addition, venous stasis will contribute a bluish hue. The gingival color changes with increasing chronicity of the inflammatory process. The changes start in the interdental papillae and the gingival margin and then spread to the attached gingiva. Proper diagnosis and treatment require an understanding of the tissue changes that alter the color of the gingiva at the clinical level. Color changes in acute gingival inflammation differ with regard to both nature and distribution from those in patients with chronic gingivitis. The color changes may be marginal, diffuse, or patch- like, depending on the underlying acute condition. With acute necrotizing ulcerative gingivitis, the involvement is marginal; with herpetic gingivostomatitis, it is diffuse; and with acute reactions to chemical irritation, it is patchlike or diffuse. Color changes vary with the intensity of the inflammation. Initially, there is an increase in erythema. If the condition does not worsen, this is the only color change until the gingiva reverts to normal. With severe acute inflammation, the red color gradually becomes a dull, whitish gray. The gray discoloration produced by tissue necrosis is demarcated from the adjacent gingiva by a thin, sharply defined erythematous zone. provides detailed descriptions of the clinical and pathologic features of the various forms of acute gingivitis. Metallic Pigmentation. Heavy metals (i.e., bismuth, arse- nic, mercury, lead, and silver) that are absorbed systemically as a result of therapeutic use or occupational or household environments may discolor the gingiva and other areas of the oral mucosa These changes are rare, but they should still be ruled out in suspected cases. Metals typically produce a black or bluish line in the gingiva that follows the contour of the margin The pigmenta- tion may also appear as isolated black blotches involving the inter dental marginal and attached gingiva. This differs from the tattooing produced by the accidental embedding of amalgam or other metal fragments. Gingival pigmentation from systemically absorbed metals results from the perivascular precipitation of metallic sulfides in the subepithelial connective tissue. Gingival pigmentation is not a result of systemic toxicity. It occurs only in areas of inflammation in which the increased permeability of irritated blood vessels permits the seepage of the metal into the surrounding tissue. In addition to inflamed gingiva, mucosal areas that are irritated by biting or abnormal chewing habits (e.g., inner surface of lips, cheek at level of occlusal line, lateral border of tongue) are common sites of pigmentation. Pigmentation can be eliminated by treating the inflammatory changes without necessarily discontinuing the metalcontaining medication. Color Changes Associated with Systemic Factors Many systemic diseases may cause color changes in the oral mucosa, including the gingiva.In general, these abnormal pigmentations are nonspecific, and they should stimulate further diagnostic efforts or referral to the appropriate specialist.Endogenous oral pigmentations can be caused by melanin, bilirubin, or iron. Melanin oral pigmentations can be normal physiologic pigmentations, and they are often found in highly pigmented ethnic groups). Diseases that increase melanin pigmentation include the following: • Addison’s disease is caused by adrenal dysfunction, and it produces isolated patches of discoloration that vary from bluish black to brown. • Peutz-Jeghers syndrome produces intestinal polyposis and melanin pigmentation in the oral mucosa and the lips. • Albright’s syndrome (polyostotic fibrous dysplasia) and von Recklinghausen’s disease (neurofibromatosis) produce areas of oral melanin pigmentation. The skin and the mucous membranes can also be stained by bile pigments. Jaundice is best detected via the examination of the sclera, but the oral mucosa may also acquire a yellowish color. The deposition of iron in hemochromatosis may produce a blue-gray pigmentation of the oral mucosa. Several endocrine and metabolic disturbances, including diabetes and pregnancy, may result in color changes. Blood dyscrasias such as anemia, polycythemia, and leukemia may also induce color changes. Exogenous factors that are capable of producing color changes in the gingiva include atmospheric irritants, such as coal and metal dust, and coloring agents in food or lozenges. Tobacco causes hyperkeratosis of the gingiva, and it may also induce a significant increase in melanin pigmentation of the oral mucosa.56 Localized bluish-black areas of pigment are often caused by amalgam implanted in the mucosa During recent years, the need for aesthetics in dentistry has increased, with a growing demand for a pleasing smile. This has made many individuals more aware of their gingival pigmentation, which may be apparent during smiling and speech.20,21 Tradition- ally, gingival depigmentation has been carried out with the use of nonsurgical and surgical procedures, including chemical, cryosurgical, and electrosurgical techniques. However, those techniques were met with skepticism because of their varying degrees of success. More recently, lasers have been used to ablate cells that produce the melanin pigment; a nonspecific laser beam destroys the epithelial cells, including those at the basal layer. In addition, selective ablation with the use of a laser beam with a wavelength that is specifically absorbed in melanin effectively destroys the pigmented cells without damaging the nonpigmented cells. In both cases, radiation energy is transformed into ablation energy, thereby resulting in cellular rupture and vaporization with minimal heating of the surrounding tissue. Changes in the Consistency of the Gingiva Both chronic and acute inflammations produce changes in the normal firm and resilient consistency of the gingiva. As previously noted, in patients with chronic gingivitis, both destructive (edematous) and reparative (fibrotic) changes coexist, and the consistency of the gingiva is determined by their relative predominance . Calcified Masses in the Gingiva. Calcified microscopic masses may be found in the gingiva. These can occur alone or in groups, and they vary with regard to size, location, shape, and structure. Such masses may be calcified material that has been removed from the tooth and traumatically displaced into th gingiva during scaling, root remnants, cementum fragments, or cementicles. Chronic inflammation and fibrosis, an occasional foreign body, and giant cell activity occur in relation to these masses. They are sometimes enclosed in an osteoidlike matrix. Crystalline foreign bodies have also been described in the gingiva, but their origin has not been determined. Toothbrushing. Toothbrushing has various effects on the con- sistency of the gingiva, such as promoting keratinization of the oral epithelium, enhancing capillary gingival circulation, and thickening alveolar bone. In animal studies, mechanical stimulation by toothbrushing was found to increase the proliferative activity of the junctional basal cells in dog gingiva by 2.5 times as compared with the use of a scaler. These findings may indicate that toothbrushing causes an increased turnover rate and desquamation of the junctional epithelial surfaces. This process may repair small breaks in the junctional epithelium and prevent direct access to the underlying tissue by periodontal pathogens. Changes in the Surface Texture of the Gingiva The surface of normal gingiva usually exhibits numerous small depressions and elevations that give the tissue an orange-peel appearance referred as stippling.13 Stippling is restricted to the attached gingiva and predominantly localized to the subpapillary area, but it extends to a variable degree into the interdental papilla.Although the biologic significance of gingival stippling is not known, some investigators conclude that the loss of stippling is an early sign of gingivitis However, clinicians must take into consideration that its pattern and extent vary in different mouth areas, among patients, and with age. In patients with chronic inflammation, the gingival surface is either smooth and shiny or firm and nodular, depending on whether the dominant changes are exudative or fibrotic. Smooth surface texture is also produced by epithelial atrophy in atrophic gingivitis, and peeling of the surface occurs with chronic desquamative gingivitis. Hyperkeratosis results in a leathery texture, and druginduced gingival overgrowth produces a nodular surface. Changes in the Position of the Gingiva Traumatic Lesions. One of the unique features of the most recent gingival disease classification is the recognition of nonplaque-induced traumatic gingival lesions as distinct gingival conditions. Traumatic lesions—whether they are chemical, physical,or thermal—are among the most common lesions in the mouth. Sources of chemical injuries include aspirin, hydrogen peroxide, silver nitrate, phenol, and endodontic materials. Physical injuries can include lip, oral, and tongue piercings, which can result in gingival recession. Thermal injuries can result from hot drinks and foods. In acute cases, the appearance of slough (necrotizing epithelium), erosion, or ulceration and the accompanying erythema are common features. In chronic cases, permanent gingival defects are usually present in the form of gingival recession. Typically, the localized nature of the lesions and the lack of symptoms readily eliminate them from the differential diagnosis of systemic conditions that may be present with erosive or ulcerative oral lesions. Gingival Recession. Gingival recession is a common finding. The prevalence, extent, and severity of gingival recession increase with age, and this condition is more prevalent among males.Positions of the Gingiva. By clinical definition, recession is the exposure of the root surface by an apical shift in the position of the gingiva. To understand recession, it helps to distinguish between the actual and apparent positions of the gingiva. The actual position is the level of the coronal end of the epithelial attachment on the tooth, whereas the apparent position is the level of the crest of the gingival margin. The severity of recession is determined by the actual position of the gingiva and not by its apparent position. For example, in periodontal disease, the inflamed pocket wall covers part of the denuded root; thus, some of the recession is hidden, and some may be visible. The total amount of recession is the sum of the two. Recession refers to the location of the gingiva rather than to its condition. Receded gingiva can be inflamed, but it may be normal except for its position Standard oral hygiene procedures, whether they involve tooth- brushing or flossing, may lead to frequent transient and minimal gingival injury.18,62 Although toothbrushing is important for gingival health, faulty toothbrushing technique or brushing with hard bristles may cause significant injury. This type of injury may present as lacerations, abrasions, keratosis, and recession, with the facial marginal gingiva being the most affected.59 Thus, in these cases, recession tends to be more frequent and severe in patients Changes in Gingival Contour Changes in gingival contour are primarily associated with gingival enlargement , but such changes may also occur with other conditions. Of historical interest are the descriptions of indentations of the gingival margin referred to as Stillman’s clefts and the McCall festoons. The term Stillman’s clefts has been used to describe a specific type of gingival recession that consists of a narrow, triangular-shaped gingival recession. As the recession progresses apically, the cleft becomes broader, thereby exposing the cementum of the root surface. When the lesion reaches the mucogingival junction, the apical border of oral mucosa is usually inflamed because of the difficulty with maintaining adequate plaque control at this site. The term McCall festoons has been used to describe a rolled, thickened band of gingiva that is usually seen adjacent to the cuspids when recession approaches the mucogingival junction. Initially, Stillman’s clefts and McCall festoons were attributed to traumatic occlusion, and the recommended treatment was occlusal adjustment. However, this association was never proved, and these indentations merely represent peculiar inflammatory changes of the marginal gingiva. Acute Gingival Infections Necrotizing Ulcerative Gingivitis Necrotizing ulcerative gingivitis (NUG) is a microbial disease of the gingiva in the context of an impaired host response. It is characterized by the necrosis and sloughing of gingival tissue, and it presents with characteristic signs and symptoms. Clinical Features NUG is usually identified as an acute disease. However, the term acute in this case is a clinical descriptor and should not be used as a diagnosis, because there is no chronic form of the disease. Although the acronym ANUG is frequently used, it is a misnomer. NUG often undergoes a diminution in severity without treatment, thereby leading to a subacute stage with milder clinical symptoms. Thus, patients may have a history of repeated remissions and exacerbations, and the condition can also recur in previously treated patients. Involvement may be limited to a single tooth or group of teeth, or it may be widespread throughout the mouth. NUG can cause tissue destruction that involves the periodontal attachment apparatus, especially in patients with long-standing disease or severe immunosuppression. When bone loss occurs, thecondition is called necrotizing ulcerative periodontitis (NUP).History. NUG is characterized by its sudden onset, sometimes after an episode of debilitating disease or acute respiratory tract infection. A change in living habits, protracted work without adequate rest, poor nutrition, tobacco use, and psychological stress are frequent features of the patient’s history. Oral Signs. Characteristic lesions are punched-out, craterlike depressions at the crest of the interdental papillae that subsequently extend to the marginal gingiva and rarely to the attached gingiva and oral mucosa. The surface of the gingival craters is covered by a gray, pseudomembranous slough that is demarcated from the remainder of the gingival mucosa by a pronounced linear erythema . In some cases, the lesions are denuded of the surface pseudomembrane, thereby exposing the gingival margin, which is red, shiny, and hemorrhagic. The characteristic lesions may progressively destroy the gingiva and the underlying periodontal tissues. Spontaneous gingival hemorrhage or pronounced bleeding after the slightest stimulation are additional characteristic clinical signs. Other signs that are often found include a fetid odor and increased salivation. NUG can occur in otherwise disease-free mouths, or it can be superimposed on chronic gingivitis or periodontal pockets. However, NUG or NUP does not usually lead to periodontal pocket formation, because the necrotic changes involve the junctional epithelium; a viable junctional epithelium is needed for pocket deepening. It is rare in edentulous mouths, but isolated spherical lesions occasionally occur in the soft palate.56 Oral Symptoms. The lesions are extremely sensitive to touch, and the patient often complains of a constant radiating, gnawing pain that is intensified by eating spicy or hot foods and chewing. There is a “metallic” foul taste, and the patient is conscious of an excessive amount of “pasty” saliva. Extraoral and Systemic Signs and Symptoms. Patients are usually ambulatory and have a minimum of systemic symptoms. Local lymphadenopathy and a slight elevation in temperature are common features of the mild and moderate stages of the disease. In severe cases, there may be high fever, increased pulse rate, leukocytosis, loss of appetite, and general lassitude. Systemic reactions are more severe in children. Insomnia, constipation, gastrointestinal disorders, headache, and mental depression sometimes accompany the condition. In very rare cases, severe sequelae such as gangrenous stomaitis and noma have been described. Clinical Course. The clinical course can vary. If untreated, NUG may lead to a progressive destruction of the periodontium as well as gingival recession accompanied by an increase in the severity of systemic complications. It is noteworthy that the microscopic appearance of NUG is nonspecific. Comparable changes result from trauma, chemical irritation, or the application of caustic medications. Relation of Bacteria to the Necrotizing Ulcerative Gingivitis Lesion Light and electron microscopy have been used to study the relationship of bacteria to the characteristic lesion of NUG. Light microscopy shows that the exudate on the surface of the necrotic lesion contains microorganisms that morphologically resemble cocci, fusiform bacilli, and spirochetes. The layer between the necrotic and living tissue contains enormous numbers of fusiform bacilli and spirochetes in addition to leukocytes and fibrin. Spirochetes and other bacteria invade the underlying living tissue. Spirochetes have been found as deep as 300 μm from the surface. The majority of spirochetes in the deeper zones are morphologically different from cultivated strains of Treponema microdentium. They occur in non-necrotic tissue before other types of bacteria, and they may be present in high concentrations intercellularly in the epithelium adjacent to the ulcerated lesion and in the connective tissue. Smears from the lesions show scattered bacteria (predominantly spirochetes and fusiform bacilli), desquamated epi- thelial cells, and occasional PMNs. Spirochetes and fusiform bacteria are usually seen with other oral spirochetes, vibrios, and filaments. Diagnosis Diagnosis is based on clinical findings of gingival pain, ulceration, and bleeding. A bacterial smear is not necessary or definitive, because the bacterial picture is not appreciably different from that of patients with marginal gingivitis, periodontal pockets, pericoronitis, or primary herpetic gingivostomatitis. However, bacterial studies are useful for the differential diagnosis of NUG and specific infections of the oral cavity (e.g., diphtheria, thrush, actinomycosis,streptococcal stomatitis). The microscopic examination of a biopsy specimen is not sufficiently specific to be diagnostic. It can be used to differentiate NUG from specific infections (e.g., tuberculosis) or from neoplastic disease, but it does not differentiate between NUG and other necrotizing conditions of nonspecific origin, such as those produced by trauma or caustic medications. Vincent’s angina is a fusospirochetal infection of the oropharynx and throat as distinguished from NUG, which affects the marginal gingiva. Patients with Vincent’s angina have a painful membranous ulceration of the throat, with edema and hyperemic patches breaking down to form ulcers that are covered with pseudomembranous material. The process may extend to the larynx and the middle ear. NUG in the patient with leukemia is not produced by leukemia itself, but it may result from the reduced host defense mechanisms seen with leukemia. In addition, NUG may be superimposed on the gingival tissue alterations caused by leukemia. The differential diagnosis consists not of distinguishing between NUG and leukemic gingival changes but rather of determining whether leukemia is a predisposing factor in the mouth of a patient with NUG. For example, if a patient with necrotizing involvement of the gingival margin also has generalized diffuse discoloration and edema of the attached gingiva, the possibility of an underlying systemically induced gingival change should be considered. Leukemia is one of the conditions that would need to be ruled out. NUG in the patient with human immunodeficiency virus infection has the same clinical features, although it often follows an extremely destructive course that leads to NUP, with a loss of soft tissue and bone and the formation of bony sequestra. Etiology Role of Bacteria. Plaut51 in 1894 and Vincent73 in 1896 pos- tulated that NUG was caused by specific bacteria: fusiform bacillus and a spirochetal organism. Opinions still differ with regard to whether bacteria are the primary causative factors of NUG. Several observations support this concept, including that spirochetal organisms and fusiform bacilli are always found in patients with the disease, with other organisms also involved. Rosebury and colleagues55 described a fusospirochetal complex that consists of T. microdentium, intermediate spirochetes, vibrios, fusiform bacilli, and filamentous organisms in addition to several Borrelia species. Loesche and colleagues38 described a predominant constant flora and a variable flora associated with NUG. The constant flora is composed of Prevotella intermedia in addition to Fusobacterium, Treponema, and Selenomonas species. The variable flora consists of a heterogeneous array of bacterial types. Treatment with metronidazole results in a significant reduction of Treponema species, Prevotella intermedia, and Fusobacterium, with resolution of the clinical symptoms. The antibacterial spectrum of this drug provides evidence for the anaerobic members of the flora as etiologic agents. These bacteriologic findings have been supported by immunologic data that demonstrated increased immunoglobulin G and M antibody titers for medium-sized spirochetes and P. intermedia in patients with NUG as compared with titers in those patients with chronic gingivitis and healthy controls. Role of the Host Response. Regardless of whether specific bacteria are implicated in the etiology of NUG, the presence of these organisms appears to be insufficient to cause the disease. In the first place, the fusiform–spirochete flora is frequently found in patients who do not have NUG. In addition, exudates from NUG lesions produce fusospirochetal abscesses rather than typical NUG when such exudates are inoculated subcutaneously into experimental animals.The role of an impaired host response in NUG has long been recognized. Even in the early descriptions of the disease, NUG was associated with physical and emotional stress, as well as decreased resistance to infection. NUG has not been produced experimentally in humans or animals by only the inoculation of bacterial exudates from the lesions. In the animal model, local or systemic immunosuppression with glucocorticoids (e.g., ketoconazole) results in more characteristic lesions of NUG in infected animals. Swenson and Muhler used Scillaren B, an amorphous glucoside, which reduced tissue resistance to create oral fusospirochetal infections in dogs.68 Furthermore, NUG is not found in well-nourished individuals with a fully functional immune system. All of the predisposing factors for NUG are associated with immunosuppression. Cogen and colleaguesdescribed a depression in host defense mechanisms, particularly in PMN chemotaxis and phagocytosis, in patients with NUG. (For further details regarding host–bacteria interactions in patients with NUG, It is essential for the clinician to determine the predisposing factors that lead to immunodeficiency in patients with NUG to address the continued susceptibility of the patient and to determine whether an underlying systemic disease is present. Immunodeficiency may be related to varying levels of nutritional deficiency, fatigue caused by chronic sleep deprivation, other health habits (e.g., alcohol or drug abuse), psychosocial factors, or systemic disease. Importantly, NUG may be the presenting symptom for patients with immunosuppression related to human immunodeficiency virus infection. Local Predisposing Factors. Preexisting gingivitis, injury to the gingiva, and smoking are important predisposing factors.Although NUG may appear in an otherwise disease-free mouth, it most often occurs superimposed on preexisting chronic gingival disease and periodontal pockets. Deep periodontal pockets and pericoronal flaps are particularly vulnerable areas, because they offer a favorable environment for the proliferation of anaerobic fusiform bacilli and spirochetes. Areas of the gingiva that are traumatized by opposing teeth in malocclusion (e.g., the palatal surface behind the maxillary incisors, the labial gingival surface of the mandibular incisors) may predispose an individual to the development of NUG. The relationship between NUG and smoking has often been mentioned in the literature. Pindborg reported that 98% of his patients with NUG were smokers and that the frequency of this disease increases with increasing exposure to tobacco smoke. The effect of smoking on periodontal disease in general has been the subject of numerous studies during the past two decades, and smoking has been established as a high risk factor for disease. Systemic Predisposing Factors. NUG is not found in a well-nourished individual with a fully functional immune system. Therefore, it is important for the clinician to determine the predisposing factors that lead to immunodeficiency. Again, immunodeficiency may be related to varying levels of nutritional deficiency; fatigue caused by chronic sleep deficiency; other health habits (e.g., alcohol or drug abuse); and systemic disease (e.g., diabetes, debili tating infection). Nutritional Deficiency. Necrotizing gingivitis has been produced in animals by giving them nutritionally deficient diets.Several researchers found an increase in the fusospirochetal flora in the mouths of the experimental animals, but the bacteria were regarded as opportunists that proliferate only when the tissues were altered by the deficiency. A poor diet has been cited as a predisposing factor for NUG and its sequelae in developing African countries, although the effects appear primarily to diminish the effectiveness of the immune response.Nutritional deficiencies (e.g., vitamin C, vitamin B2) accentuate the severity of the pathologic changes induced when the fusospirochetal bacterial complex is injected into animals.Debilitating Disease. Debilitating systemic disease may predispose patients to the development of NUG. Such systemic disturbances include chronic diseases (e.g., syphilis, cancer), severe gastrointestinal disorders (e.g., ulcerative colitis), blood dyscrasias (e.g., leukemia, anemia), and acquired immunodeficiency syndrome. Nutritional deficiency that results from debilitating disease may be an additional predisposing factor. Experimentally induced leukopenia in animals may produce ulcerative gangrenous stomatitis. Ulceronecrotic lesions appear in the gingival margins of hamsters that are exposed to total body irradiation; these lesions can be prevented with systemic antibiotics. Psychosomatic Factors. Psychologic factors appear to be important in the etiology of NUG. The disease often occurs in association with stressful situations (e.g., induction into the armed forces, school examinations).23 Psychologic disturbances as well as increased adrenocortical secretion62 are also common in patients with the disease. A significant correlation between disease incidence and two personality traits—dominance and abasementsuggests the presence of a NUG-prone personality. The mechanisms whereby psychologic factors create or predispose an individual to gingival damage have not been established,but alterations in digital and gingival capillary responses that Primary Herpetic Gingivostomatitis Primary herpetic gingivostomatitis is an infection of the oral cavity caused by herpes simplex virus (HSV) type 1.14,42,43,58 It occurs most often among infants and children who are less than 6 years old,5,58,61 but it is also seen in adolescents and adults. It occurs with equal frequency in male and female patients. In most individuals, however, the primary infection is asymptomatic. As part of the primary infection, the virus ascends through the sensory and autonomic nerves, where it persists as latent HSV in neuronal ganglia that innervate the site. In approximately one third of the world’s population, secondary manifestations result from various stimuli, such as sunlight, trauma, fever, and stress. These secondary manifestations include herpes labialis , herpetic stomatitis, herpes genitalis, ocular herpes, and herpetic encephalitis. Secondary herpetic stomatitis can occur on the palate, on the gingiva , or on the mucosa as a result of dental treatment that traumatizes or stimulates the latent virus in the ganglia that innervate the area; it may present as pain away from the site of treatment 2 to 4 days ater. Careful inspection for characteristic vesicles may be diagnostic Clinical Features Oral Signs. Primary herpetic gingivostomatitis appears as a diffuse, erythematous, shiny involvement of the gingiva and the adjacent oral mucosa, with varying degrees of edema and gin gival bleeding. During its initial stage, it is characterized by the presence of discrete, spherical gray vesicles, which may occur on the gingiva, the labial and buccal mucosae, the soft palate, the pharynx, the sublingual mucosa, and the tongue.After approximately 24 hours, the vesicles rupture and form painful small ulcers with red, elevated, halo-like margins and depressed yellowish or grayish-white central portions. These occur either in widely separated areas or in clusters where confluence occurs Occasionally, primary herpetic gingivitis may occur without overt vesiculation. The clinical picture consists of diffuse, erythematous, shiny discoloration and edematous enlargement of the gingivae with a tendency toward bleeding. The course of the disease is limited to 7 to 10 days. The diffuse gingival erythema and edema that appear early during the course of the disease persist for several days after the ulcerative lesions have healed. Scarring does not occur in the areas of healed ulcerations. Oral Symptoms. The disease is accompanied by generalized “soreness” of the oral cavity, which interferes with eating, drinking, and oral hygiene. The ruptured vesicles are the focal sites of pain; they are particularly sensitive to touch, thermal changes, foods such as condiments and fruit juices, and the action of coarse foods. In infants, the disease is marked by irritability and refusal to take food. Extraoral and Systemic Signs and Symptoms. Cervical adenitis, fever as high as 101°F to 105°F (38°C to 40.6°C), and generalized malaise are common. Diagnosis It is critical to arrive at a diagnosis as early as possible in a patient with a primary herpetic infection. Treatment with antiviral medications can dramatically alter the course of the disease by reducing symptoms and potentially reducing recurrences. The diagnosis is usually established from the patient’s history and the clinical findings. Material may be obtained from the lesions and submitted to the laboratory for confirmatory tests, including virus culture an immunologic tests that involve the use of monoclonal antibodies or deoxyribonucleic acid hybridization techniques. This should not delay treatment if strong clinical evidence exists for primary gingivostomatitis. Pericoronitis The term pericoronitis refers to inflammation of the gingiva in relation to the crown of an incompletely erupted tooth . It occurs most often in the mandibular third molar area. Pericoronitis may be acute, subacute, or chronic. Clinical Features The partially erupted or impacted mandibular third molar is the most common site of pericoronitis. The space between the crown of the tooth and the overlying gingival flap (operculum) is an ideal area for the accumulation of food debris and bacterial growth. Even in patients with no clinical signs or symptoms, the gingival flap is often chronically inflamed and infected, and it has varying degrees of ulceration along its inner surface. Acute inflammatory involvement is a constant possibility; it may be exacerbated by trauma, occlusion, or a foreign body trapped underneath the tissue flap(e.g., popcorn husk, nut fragment). Acute pericoronitis is identified by varying degrees of inflammatory involvement of the pericoronal flap and adjacent structures as well as by systemic complications. The inflammatory fluid and cellular exudate increase the bulk of the flap, which then may interfere with complete closure of the jaws and which can be traumatized by contact with the opposing jaw, thereby aggravating the inflammatory involvement. The resultant clinical picture is a red, swollen, suppurating lesion that is exquisitely tender, with radiating pains to the ear, the throat, and the floor of the mouth. The patient is extremely uncomfortable as a result of pain, a foul taste, and an inability to close the jaws. Swelling of the cheek in the region of the angle of thejaw and lymphadenitis are common findings. Trismus may also be a presenting complaint. In addition, the patient may have systemic complications such as fever, leukocytosis, and malaise. Complications Involvement may be localized in the form of a pericoronal abscess. It may spread posteriorly into the oropharyngeal area and medially to the base of the tongue, thereby making it difficult for the patient to swallow. Depending on the severity and extent of the infection, there may be involvement of the submaxillary, posterior cervical, deep cervical, and retropharyngeal lymph nodes.30,48 Peritonsillar abscess formation, cellulitis, and Ludwig’s angina are infrequent but potential sequelae of acute pericoronitis. 1-Newman M, Takei H, Klokkevold P, Carranza F. Newman and Carranza (2019); Clinical Periodontology, 13th Ed., Elsevier.