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Gingivitis is an inflammatory condition of the gingival tissue most commonly caused by bacterial infection. Unlike periodontitis, there is no attachment loss and therefore no migration of the junctional epithelium; inflammation remains confined to the soft tissues of the gums without destruction of the periodontal ligament or alveolar bone. Clinically, gingivitis presents with redness, swelling, bleeding on probing, tenderness, and occasionally bad breath. The most common form is plaque-induced gingivitis, which results from the accumulation of bacterial biofilm at the gumline. This condition is reversible with early detection, professional care, and consistent oral hygiene practices. This activity describes the evaluation and management of gingivitis and highlights the role of the interprofessional team in managing patients with this condition. The course provides participants with a thorough understanding of gingivitis, including its causes, clinical signs, assessment methods, and effective management strategies. Participants gain practical knowledge in recognizing symptoms, conducting evaluations, and implementing preventive and therapeutic measures such as scaling and improved oral hygiene routines. The course also emphasizes the importance of interprofessional collaboration in patient care. Coordinated efforts among dental professionals, nurses, physicians, pharmacists, and behavioral health specialists contribute to more effective patient education, early detection of related health issues, and comprehensive care planning. This team-based approach improves patient outcomes by ensuring that oral health is integrated into the broader context of overall health, supporting early intervention and long-term disease prevention. Objectives: Identify the etiology and pathogenesis of gingivitis. Assess the clinical signs and symptoms of gingivitis. Differentiate the treatment options for patients with gingivitis. Outline the importance of improving care coordination among the interprofessional team to enhance the delivery of care for patients affected by gingivitis. Access free multiple choice questions on this topic.

Gingivitis is an inflammatory condition of the gingival tissue, most commonly caused by bacterial infection. Unlike periodontitis, there is no attachment loss and therefore no migration of the junctional epithelium. The condition is restricted to the soft-tissue area of the gingival epithelium and connective tissue.[1] Among all the periodontal diseases, gingivitis is considered to be the most common. There are various forms of gingivitis based on clinical appearance, duration of infection, severity, and etiology. However, the chronic form of gingivitis that is caused by plaque is considered to be the most frequent variant. Clinically, the gingival tissues are characterized by swelling, redness, tenderness, a shiny surface, and bleeding upon gentle probing. Gingivitis seldom generates spontaneous bleeding and is commonly painless; therefore, many patients do not recognize the disease and fail to seek attention.[2]

Gingivitis is caused by the microbial plaque deposits located in or close to the gingival sulcus. The microorganisms more strongly associated with the etiology of gingivitis include species of Streptococcus, Fusobacterium, Actinomyces, Veillonella, and Treponema. Bacteroides, Capnocytophaga, and Eikenella are also potentially linked to the etiology of the disease. There may be other local or systemic etiologic factors that intensify plaque deposition or the vulnerability of the tissue to microbial attack.[3] Gingivitis can be categorized into four main types based on its underlying causes: 1. Plaque-induced gingivitis This is the most common cause of gingivitis. Plaque is a thin film that forms on the tooth surface due to poor oral hygiene. If not regularly removed, it can harden up and form calculus. As plaque harbors a large number of bacteria, inflammation can occur in the gingival tissue. Some local factors can contribute to the formation of plaque, such as crowding of teeth, which makes plaque removal difficult. As misaligned teeth often require orthodontic correction, cleaning difficulty increases, resulting in the accumulation of more plaque. Furthermore, a dental prosthesis that does not have an adequate fit or is not properly finished can also act as a nidus for plaque accumulation. In children, tooth eruption is frequently associated with gingivitis as plaque accumulation tends to increase in the area where primary teeth are exfoliating, and permanent teeth are erupting, as oral hygiene may be difficult to maintain in these areas. This is referred to as eruptive gingivitis. 2. Nutritional gingivitis This may occur due to a deficiency of vitamin C. It has been found that a modern lifestyle with the intake of an increased amount of refined carbohydrates and an increased ratio of omega-6 to omega-3 fatty acids can promote the inflammatory process.[4] The mechanism by which carbohydrates with a high glycemic index promote the inflammatory process is through activation of NFkB and oxidative stress.[5][6] 3. Hormonal gingivitis

This may occur due to a deficiency of vitamin C. It has been found that a modern lifestyle with the intake of an increased amount of refined carbohydrates and an increased ratio of omega-6 to omega-3 fatty acids can promote the inflammatory process.[4] The mechanism by which carbohydrates with a high glycemic index promote the inflammatory process is through activation of NFkB and oxidative stress.[5][6] 3. Hormonal gingivitis During pregnancy, there are not only changes in hormone levels but also a greater predisposition to dilating blood vessels. These factors contribute to an exaggerated inflammatory response by the gingival tissues, even to a minor quantity of plaque accumulation. It has been suggested that the levels of estrogen determine the severity of gingival inflammation created against the biofilm at the gingival margin.[7][8] The hormonal alterations that occur during puberty influence how the gingival tissue reacts to plaque accumulation, causing what is known as puberty gingivitis. It has been found that in the cytoplasm of the cells of the gingiva, receptors for both estrogens and testosterone that have a high affinity for these hormones are present. The receptors for estrogen are specifically present in the basal and spinous layers of the epithelium. In the connective tissue, such receptors are found in the fibroblasts and endothelial cells of small vessels. Therefore, the gingiva is an easy target organ for these steroid hormones, resulting in gingivitis. It has been observed that during adolescence, gingivitis appears earlier in girls (11 to 13 years) than in boys (13 to 14 years).[9] 4. Drug-induced gingivitis

During pregnancy, there are not only changes in hormone levels but also a greater predisposition to dilating blood vessels. These factors contribute to an exaggerated inflammatory response by the gingival tissues, even to a minor quantity of plaque accumulation. It has been suggested that the levels of estrogen determine the severity of gingival inflammation created against the biofilm at the gingival margin.[7][8] The hormonal alterations that occur during puberty influence how the gingival tissue reacts to plaque accumulation, causing what is known as puberty gingivitis. It has been found that in the cytoplasm of the cells of the gingiva, receptors for both estrogens and testosterone that have a high affinity for these hormones are present. The receptors for estrogen are specifically present in the basal and spinous layers of the epithelium. In the connective tissue, such receptors are found in the fibroblasts and endothelial cells of small vessels. Therefore, the gingiva is an easy target organ for these steroid hormones, resulting in gingivitis. It has been observed that during adolescence, gingivitis appears earlier in girls (11 to 13 years) than in boys (13 to 14 years).[9] 4. Drug-induced gingivitis Various drugs used for systemic conditions can cause gingivitis as a side effect, such as phenytoin (used for epileptic seizures), calcium channel blockers (used for angina, high blood pressure), anticoagulants, fibrinolytic agents, oral contraceptive agents, protease inhibitors, vitamin A, and analogs. The mechanism behind this gingival inflammation is thought to be the ability of the metabolites of these drugs to induce the proliferation of fibroblasts. An imbalance between the synthesis and the degradation of the extracellular matrix leads to the accumulation of immature proteins in the extracellular matrix, particularly collagen. This, in turn, results in gingivitis.[10] Apart from the already mentioned, various risk and influencing factors can contribute to the development of gingivitis. These include smoking and tobacco chewing, systemic conditions, genetic factors (hereditary gingival fibromatosis), and local conditions (dry mouth, crowded teeth).

Gingivitis is the most common of periodontal diseases. It is more prevalent in males than in females, as research has shown that females tend to follow better oral care regimes. It is commonly seen in children and adults. Studies have found gingivitis to be more prevalent in people with low socioeconomic status, as people with high socioeconomic status tend to show a more positive attitude towards the maintenance of oral hygiene. Also, they have better access to health care options. Studies reveal that gingivitis is more prevalent in pregnant women than in non-pregnant women. Moreover, more severe forms of gingivitis have been more often seen in pregnant women.[11] The most frequently seen types of gingivitis are plaque-induced, hormonal, acute ulcerative necrotizing, drug-induced, or spontaneously presenting hyperplastic gingivitis. Categorically, the more predominant form of gingivitis is plaque-induced. This type accounts for far more cases than all other variants combined.[12]

Periodontal disease undergoes 4 different stages that were first explained by Page and Schroeder in 1976.[13] Pathophysiologically, gingivitis has been divided into initial, early, and established stages, and periodontitis has been indicated as the advanced stage. 1. Initial lesion This stage is characterized by an acute exudative inflammatory response, a raised gingival fluid flow, and the migration of neutrophils from the blood vessel of the subgingival plexus located in the gingival connective tissue to the gingival sulcus. An alteration of the matrix of the connective tissue located next to vessels results in the accumulation of fibrin in the area. The initial lesion is seen within 4 days of the initiation of plaque accumulation. There is a destruction of collagen caused by collagenase and other enzymes secreted by the neutrophils. About 5% to 10% of the connective tissue is occupied by the inflammatory infiltrate in this stage.[12] 2. Early lesion The early lesion is consistent with delayed hypersensitivity. It usually appears after 1 week from the beginning of plaque deposition. In this stage, the clinical signs of gingivitis, such as redness and bleeding from the gingiva, start appearing. The inflammatory cells that predominate in this lesion are lymphocytes, accounting for 75% of the total, and macrophages. A small number of plasma cells are also seen. Along with the inflammatory infiltration that occupies 5% to 15% of the connective tissue of the gingival margin, there is a loss of collagen in the affected area that reaches 60% to 70%. Furthermore, the local fibroblasts undergo a series of pathological changes, and the gingival fluid flow and the number of leukocytes migrating to the region continue to increase. Neutrophils and mononuclear cells are also increased in the junctional epithelium. The duration of the early lesion has not yet been determined; it can remain for longer than previously expected.[12] 3. Established lesion

The early lesion is consistent with delayed hypersensitivity. It usually appears after 1 week from the beginning of plaque deposition. In this stage, the clinical signs of gingivitis, such as redness and bleeding from the gingiva, start appearing. The inflammatory cells that predominate in this lesion are lymphocytes, accounting for 75% of the total, and macrophages. A small number of plasma cells are also seen. Along with the inflammatory infiltration that occupies 5% to 15% of the connective tissue of the gingival margin, there is a loss of collagen in the affected area that reaches 60% to 70%. Furthermore, the local fibroblasts undergo a series of pathological changes, and the gingival fluid flow and the number of leukocytes migrating to the region continue to increase. Neutrophils and mononuclear cells are also increased in the junctional epithelium. The duration of the early lesion has not yet been determined; it can remain for longer than previously expected.[12] 3. Established lesion There is increased collagenolytic activity in this stage along with a rise in the number of macrophages, plasma cells, and T and B lymphocytes. However, the predominant cells are plasma cells and B lymphocytes. In this stage, a small gingival pocket lined with a pocket epithelium is created. The lesion exhibits a high degree of organization. It has been suggested that the severity of gingivitis correlates with a growth in the B cells and plasma cells population, and a decrease in the number of T cells. An established lesion may follow 2 paths: it can either remain stable for months or years, or progress to a more destructive lesion, which appears to be related to a change in the microbial flora or infection of the gingiva. This stage is reversible following effective periodontal therapy, which increases the number of microorganisms associated with periodontal health and correlates with a reduction in plasma cells and lymphocytes.[12] 4. Advanced lesion This stage is a transition to periodontitis. It is characterized by irreversible attachment loss. The inflammatory changes and bacterial infection affect the supporting tissues of the teeth and surrounding structures, including the gingiva, periodontal ligament, and alveolar bone, leading to their destruction and potentially resulting in tooth loss.[14][15]

Healthy gingival tissue looks pink or pigmented in dark-skinned patients, firm, with no signs of redness or swelling, and with no bleeding after gently passing a periodontal probe along the gingival crevice. On periodontal probing, healthy gingiva shows less than 3 mm crevices, and there is no bone loss on x-rays.In many instances, gingivitis may go unnoticed by the patient as the disease may exist and progress without any symptoms. When symptomatic, the patient usually gives a history of bleeding from the gingiva while brushing, flossing, and sometimes eating particularly hard food, along with halitosis that does not resolve even after performing oral hygiene. Physical examination of the oral cavity reveals the presence of an inflamed and tender gingiva that usually bleeds on gentle probing. The gingival margins that show a knife-edge appearance and the gingival tissue with a stippled aspect found in healthy gingiva are replaced by a more rounded and shiny aspect. Significant plaque and calculus deposits are usually seen. In chronic gingivitis, the size of the gingival tissue may be increased towards the incisal due to edema or hyperplasia, resulting in probing depths more than 3 mm; however, no attachment loss has occurred. These are known as false pockets. Gingival swelling can be graded into 4 types: Grade 0: No signs of gingival swelling. Grade I: Swelling that is confined to the interdental papilla region. Grade II: Swelling involving both the interdental papilla and the marginal gingiva. Grade III: Swelling that covers three-fourths or more of the crown structure. The Gingival Index The purpose of the gingival index is to indicate the quality of the gingival tissue, differentiating the severity of the lesion, and the location of the alteration concerning the 4 areas that form the perimeter of the marginal gingiva. The criteria included in the index are only related to qualitative changes in the gingiva. A score from 0 to 3 is given to each area of the tooth (mesial, distal, vestibular, palatine, or lingual); this is the gingival index for the area. The gingival index score per tooth is calculated by adding the scores from the 4 areas and then dividing the total by 4. The gingival index for the subject is obtained by adding the indices of each tooth and dividing them by the number of teeth that were examined.[16] Criteria for the gingival index system include: 0: Normal gingiva.

The purpose of the gingival index is to indicate the quality of the gingival tissue, differentiating the severity of the lesion, and the location of the alteration concerning the 4 areas that form the perimeter of the marginal gingiva. The criteria included in the index are only related to qualitative changes in the gingiva. A score from 0 to 3 is given to each area of the tooth (mesial, distal, vestibular, palatine, or lingual); this is the gingival index for the area. The gingival index score per tooth is calculated by adding the scores from the 4 areas and then dividing the total by 4. The gingival index for the subject is obtained by adding the indices of each tooth and dividing them by the number of teeth that were examined.[16] Criteria for the gingival index system include: 0: Normal gingiva. 1: Mild inflammation – a slight color change, slight edema. No bleeding on probing. 2: Moderate inflammation – redness, edema, and glazing. Bleeding on probing. 3: Severe inflammation – marked redness and edema, ulceration, and tendency to spontaneous bleeding.[16] Classification of gingivitis In the latest International Workshop for a Classification of Periodontal Diseases and Conditions in 2017, gingival diseases have been classified as follows: Gingivitis - dental biofilm-induced Associated with dental biofilm alone Mediated by systemic or local risk factors Drug-influenced gingival enlargement Gingival diseases - non-dental, biofilm-induced Genetic/ developmental disorders Specific infections Inflammatory and immune conditions Reactive processes Neoplasms Endocrine, nutritional, and metabolic diseases Traumatic lesions Gingival pigmentation [17]

As gingivitis is a soft tissue disease, radiographic evaluation is not usually necessary; however, it may be of help for differentiating gingivitis from periodontitis in some cases. Lab investigations are also routinely not required.

The prime objective of treating gingivitis is to reduce inflammation. This is achieved by the use of different instruments to remove dental plaque deposits.[18] Gingivitis, in its initial stages, can be easily managed if the patient starts following oral hygiene protocol, which includes regular tooth brushing with an appropriate technique and interproximal hygiene, such as dental flossing or the use of interproximal brushes. The removal of plaque and calculus is also professionally achieved by scaling and root planning according to the severity of the condition. If it is a drug-induced gingival overgrowth, the physician can change the medication to improve the outcome of treatment of the condition. If it is due to a nutritional deficiency, supplements can be prescribed. Medications in the form of antiseptic mouthwash that contains chlorhexidine can also be prescribed in conjunction with the mechanical removal of plaque. It has been suggested that the use of chlorhexidine mouthwashes in addition to the usual toothbrushing and interproximal cleaning leads to a significant decrease in the build-up of dental biofilm. The concentration of the chlorhexidine rinse does not affect its effectiveness.[19] There are studies on the effect of medicinal or herbal plants on the management of gingivitis. The mechanism of action of these plants on gingivitis is due to their anti-inflammatory property. Such medicinal plants include pomegranate, tea, and chamomile. The flavonoids and tannins present in these plants are potent anti-inflammatory and astringent phytochemicals. Therefore, they can resolve both gingival bleeding and inflammation.[20] Some studies have demonstrated a synergistic effect when herbal plants are prescribed in conjunction with conventional mechanical plaque removal procedures, such as scaling.[21]

Gingivitis can be differentiated from periodontitis by the attachment loss undergone in the latter, which can be clinically noticed during periodontal probing.[22] They can also be differentiated histologically and radiographically.

Gingivitis, if identified and treated, can easily be resolved as the condition is reversible and the altered tissues can return to normal once the dental biofilm has been removed. If gingivitis progresses to periodontitis, connective tissue attachment loss and bone destruction occur, which may ultimately result in tooth loss.

The most common complication or sequelae of chronic gingivitis is the progression of the inflammation towards the underlying tissue and bone, resulting in periodontitis. The ultimate consequence of such an event is tooth loss. Gingivitis is a precursor of periodontitis. However, gingivitis does not always progress to periodontitis.

The patient should be educated on the importance of maintaining good oral hygiene, which can prevent the formation of plaque and, thus, gingivitis. A correct brushing technique according to individual needs, frequency of brushing, and use of interproximal hygiene must be taught. Furthermore, the importance of regular dental visits should be emphasized. Finally, the use of mouthwash may also be advised.[23][24]

To improve the treatment outcome of gingivitis, an interprofessional approach is required to identify the causes of the disease and to intervene at an early stage. Also, a thorough knowledge of the epidemiological pattern is required for planning the public-health services, as plaque-induced gingivitis can be seen at any age of the dentate population. Periodontal disease is not just limited to the destruction of the periodontium; it also affects general systemic health. Thus, both dentists and physicians must be aware of the close link between periodontal disease and systemic diseases, such as diabetes mellitus, cardiovascular diseases, and preterm birth or low birth weight.[25][26][27]