Gingivitis

Etiology

Gingivitis most commonly results from the accumulation of dental plaque biofilm, which harbors a diverse microbial flora that initiates and sustains gingival inflammation. The microorganisms most strongly associated with gingivitis include species of Streptococcus, Fusobacterium, Actinomyces, Veillonella, and Treponema, with Bacteroides, Capnocytophaga, and Eikenella also implicated. Although microbial biofilm is the primary etiologic factor, additional local or systemic factors may intensify plaque deposition or increase tissue vulnerability to microbial attack.[3]

Gingivitis can be categorized into 4 main types based on its underlying etiology:

Plaque-Induced Gingivitis

The most common cause of plaque is a thin film that forms on the tooth surface due to poor oral hygiene. If not regularly removed, it can harden into calculus. Because plaque harbors numerous bacteria, inflammation can occur in the gingival tissue. Local factors can contribute to plaque formation, such as tooth crowding, which makes plaque removal difficult.

Because misaligned teeth often require orthodontic correction, cleaning becomes more difficult, leading to more plaque accumulation. Furthermore, an improperly fitted dental prosthesis can also serve as a nidus for plaque accumulation. In children, tooth eruption is frequently associated with gingivitis because plaque tends to accumulate in areas where primary teeth are exfoliating, and permanent teeth are erupting, making oral hygiene difficult to maintain. This phenomenon is referred to as eruptive gingivitis. 

Nutritional Gingivitis

Nutritional gingivitis refers to gingival disease caused or modified by nutritional deficiencies and is classified under Non-Plaque-Induced Gingival Diseases in the 2017 World Workshop classification as Endocrine, Nutritional and Metabolic Diseases. While plaque-induced gingivitis is the most common form, nutritional deficiencies, particularly vitamin C deficiency (ie, scurvy), can cause distinct gingival pathology that may occur independently of or be superimposed on plaque-induced inflammation.[3] Key nutritional deficiencies affecting the gingival tissues include:

Vitamin C deficiency (scurvy)

Vitamin C deficiency leads to scurvy-related periodontal issues characterized by decreased collagen formation and maintenance, increased periodontal inflammation, hemorrhage, and tooth loss.[4] Scurvy exhibits characteristic clinical findings of perifollicular petechiae, corkscrew hairs, gingivitis, swollen gums, and easy bruising.[5]

Other vitamin deficiencies

• Vitamin K deficiency causes gingival hemorrhage.
• Vitamin A insufficiency predisposes to abnormalities of oral epithelial keratinization.
• Vitamin D deficiency is linked to increased risk of periodontal disease and reduced oral immunity.
• B-complex deficiencies are associated with glossitis, angular cheilitis, and recurrent aphthous stomatitis.[4]

A modern lifestyle, characterized by increased intake of refined carbohydrates and a higher omega-6-to-omega-3 fatty acid ratio, can promote inflammation.[6] The mechanism by which high-glycemic-index carbohydrates promote inflammation involves activation of NF-κB and oxidative stress.[7][8] Nutritional gingivitis (particularly scorbutic gingivitis from vitamin C deficiency) is distinguished from other forms of gingivitis by its characteristic presentation:

• Purplish-red, spongy gingival swelling with spontaneous hemorrhage
• Occurrence independent of plaque levels
• Presence of pathognomonic systemic findings (eg, perifollicular petechiae, corkscrew hairs)
• Rapid resolution with vitamin supplementation rather than plaque removal

Hormonal Gingivitis

Pregnancy and puberty are associated with increased prevalence and severity of gingival inflammation due to elevated sex steroid hormones.[9] Estrogen and progesterone levels during pregnancy dramatically affect the periodontium through multiple mechanisms. These mechanisms include microbial changes, immune alterations, and clinical factors.

Pregnancy confers not only changes in hormone levels but also a greater predisposition to vasodilation. These alterations contribute to an exaggerated inflammatory response in the gingival tissues, even with minor plaque accumulation. Studies' results suggest that estrogen levels determine the severity of gingival inflammation induced by biofilm at the gingival margin.[10][11] Salivary estrogen levels increase significantly during the second and third trimesters. Individuals with both high estrogen and high visible plaque index levels demonstrate the highest frequency of pregnancy gingivitis, with simultaneously enhanced estrogen and plaque bringing additional risk beyond high plaque alone.

The hormonal alterations that occur during puberty also influence the way the gingival tissue responds to plaque accumulation, leading to puberty gingivitis. In the cytoplasm of gingival cells, receptors with high affinity for both estrogen and testosterone are present. The receptors for estrogen are specifically present in the basal and spinous layers of the epithelium.

In connective tissue, such receptors are found on fibroblasts and endothelial cells of small vessels. Therefore, the gingiva is an easy target organ for these steroid hormones, resulting in gingivitis. Clinicians have observed that during adolescence, gingivitis appears earlier in girls (11–13 years) than in boys (13–14 years).[12]

Drug-Induced Gingivitis

Various drugs used for systemic conditions can cause gingivitis as an adverse effect, including phenytoin (used for epileptic seizures), calcium channel blockers (used for angina and high blood pressure), anticoagulants, fibrinolytic agents, oral contraceptive agents, vitamin A and its analogs, and protease inhibitors. The mechanism behind this gingival inflammation is thought to be the ability of these drugs' metabolites to induce fibroblast proliferation. An imbalance between extracellular matrix synthesis and degradation leads to the accumulation of immature proteins, particularly collagen. This accumulation, in turn, results in gingivitis.[13] Apart from the aforementioned mechanism, various risk factors can contribute to the development of gingivitis. These factors include tobacco use (smoking and chewing), systemic conditions, genetic factors (eg, hereditary gingival fibromatosis), and local conditions (eg, dry mouth, crowded teeth).

Immunosuppressive therapies modify both clinical periodontal parameters and the subgingival microbiota, with effects that vary by agent and therapy duration.[14] Cyclosporine demonstrates the most significant impact on periodontal condition. Patients receiving cyclosporine show worse periodontal parameters compared to those without this medication (P < 0.05). 

Cyclosporine-induced gingival overgrowth affects 25% to 70% of patients and is often accompanied by gingival inflammation, whereas phenytoin-induced overgrowth typically forms fibrotic lesions.[15] Time under immunosuppression demonstrates heterogeneous effects on mean probing depth, clinical attachment loss, and prevalence of specific periodontal pathogens.[15] Patients after solid organ transplantation commonly present with gingivitis (60.5%), gingival recession (58%), and periodontitis (55.26%).[16]

Epidemiology

Gingivitis is the most common of periodontal diseases. The condition is more prevalent in males than in females, as research has shown that females tend to follow better oral care regimes. Gingivitis is common in both children and adults. The most common risk factors for gingivitis in pediatric populations include poor oral hygiene practices, increasing age, low socioeconomic status, infrequent toothbrushing, and malocclusion.[17] 

Studies' results have shown gingivitis to be more prevalent in individuals with low socioeconomic status, as individuals with high socioeconomic status tend to show a more positive attitude towards the maintenance of oral hygiene. This population also has better access to health care. In addition, the studies' results also reveal that gingivitis is more prevalent in pregnant individuals than in nonpregnant females. Additionally, pregnant individuals are more likely to develop more severe forms of gingivitis.[18]

The most frequently seen types of gingivitis are plaque-induced, hormonal, acute necrotizing ulcerative, drug-induced, or spontaneously presenting hyperplastic gingivitis. Categorically, the predominant form of gingivitis is plaque-induced. This type accounts for far more cases than all other variants combined.[19]

Pathophysiology

Gingivitis pathophysiology involves a complex interplay between bacterial biofilm accumulation and host immune-inflammatory responses, progressing through distinct histological stages. The disease represents a disruption of the homeostatic relationship between oral commensal bacteria and gingival tissue, leading to inflammation that is typically reversible with plaque removal. Gingival disease progresses through 4 stages, first described by Page and Schroeder in 1976.[20] Pathophysiologically, gingivitis is divided into initial, early, and established stages, with periodontitis representing the advanced stage.

Initial Lesion

This stage is characterized by an acute exudative inflammatory response, increased gingival fluid flow, and the migration of neutrophils from the subgingival plexus within the gingival connective tissue into the gingival sulcus. An alteration in the connective tissue matrix adjacent to vessels leads to fibrin accumulation in that area. The initial lesion is observed within 4 days of plaque accumulation. Collagen destruction is caused by collagenase and other enzymes secreted by neutrophils. In this stage, the inflammatory infiltrate occupies about 5% to 10% of the connective tissue.[19]

Early Lesion

The early lesion is consistent with delayed hypersensitivity, which typically appears after 1 week of plaque deposition. At this stage, clinical signs of gingivitis, such as gingival redness and bleeding, begin to appear. 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 inflammatory infiltrate occupying 5% to 15% of the connective tissue at the gingival margin, a loss of collagen is observed in the affected area, reaching 60% to 70%.

Furthermore, the local fibroblasts undergo a series of pathological changes as 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 may persist longer than previously expected.[19]

Established Lesion

This stage demonstrates increased collagenolytic activity, along with an increase 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. Studies' results suggest that the severity of gingivitis correlates with increases in B-cell and plasma cell populations and decreases in T-cell numbers. An established lesion may follow 2 paths: it can remain stable for months or years, or it may progress to a more destructive lesion, which appears to be related to gingival infection or a change in the microbial flora. 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.[19]

Advanced Lesion

This stage is a transition to periodontitis, characterized by irreversible attachment loss. 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 tooth loss.[21][22] Experimental gingivitis studies' results reinforce the concept of individual variation in host response. These studies suggest 3 distinct clinical inflammatory phenotypes: fast, low, and slow responders, each with its own set of characteristics.[23] 

The host immune response involves activation of multiple cell types, including keratinocytes, stromal cells, neutrophils, monocytes/macrophages, dendritic cells, and lymphocyte subsets, which release pro-inflammatory cytokines and chemokines. Low responders are characterized by low concentrations of host mediators despite similar bacterial accumulation to that of high responders. Slow responders show that interleukin (IL)-1β is not associated with clinical inflammation in this group, and they have significantly higher levels of certain bacterial species. 

Fast responders demonstrate a higher nonorganized response (IL-4, IL-6, IL-8, IL-12, IL-13) and lower organized response (IL-2, IL-10, tumor necrosis factor-α).[23] Although bacteria are necessary, a susceptible host is also required for periodontal disease. The immune-inflammatory response that develops results in the destruction of structural components through multiple mechanisms:

• Proteolytic enzymes released by both host cells and bacteria damage tissue.
• Chemotactic factors recruit polymorphonuclear leukocytes; sustained recruitment leads to the release of enzymes that break down tissue.
• Cytokine and prostanoid cascades mediate the breakdown of soft and hard tissues.
• Matrix metalloproteinases contribute to tissue degradation.
• Complement activation and arachidonic acid metabolites amplify inflammatory responses.

The host response is essentially protective, but both hypo-responsiveness and hyperresponsiveness in certain pathways can lead to enhanced tissue destruction. Histologically, nonprogressive inflammatory foci are composed predominantly of T lymphocytes and macrophages (suggesting that a cell-mediated response controls the disease), whereas destructive lesions are dominated by B lymphocytes and plasma cells (suggesting that humoral immunity is not always effective).[15]

Histopathology

The inflammatory infiltrate in gingivitis varies by stage and age. In adults, the early lesion is characterized by a predominance of T lymphocytes, while the established lesion shows a predominance of B lymphocytes and plasma cells. In children, the inflammatory infiltrate mainly consists of T lymphocytes, and it does not seem to progress to a B cell lesion.[19]

History and Physical

In many instances, gingivitis may go unnoticed by the patient, as the disease can exist and progress without 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. Healthy gingival tissue appears pink or pigmented, firm, with no signs of redness or swelling, and no bleeding after gently passing a periodontal probe along the gingival crevice.

On periodontal probing, healthy gingiva shows less than 3 mm crevices, with no bone loss visible on x-rays. In gingivitis, physical examination of the oral cavity reveals inflamed, 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 gingival tissue may enlarge towards the incisal edge due to edema or hyperplasia, resulting in probing depths greater 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 gingival index is used to assess the quality of the gingival tissue, determine the severity of the lesion, and locate the alteration within the 4 areas surrounding the marginal gingiva. The index criteria focus solely on qualitative changes in the gingiva. A score from 0 to 3 is assigned to each area of the tooth (mesial, distal, vestibular, palatine, or lingual), representing the gingival index for that area. The score for each tooth's gingival index is calculated by summing the scores across the 4 areas and dividing by 4. The overall gingival index for the patient is obtained by adding the indices of all examined teeth and dividing by the total number of teeth examined.[24]

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 a tendency toward spontaneous bleeding [24]

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: Nondental biofilm–induced
  • Genetic and developmental disorders
  • Specific infections
  • Inflammatory and immune conditions
  • Reactive processes
  • Neoplasms
  • Endocrine, nutritional, and metabolic diseases
  • Traumatic lesions
  • Gingival pigmentation [25]

Evaluation

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

Treatment / Management

The prime objective of treating gingivitis is to reduce inflammation. The fundamental method to achieve this outcome is the use of various instruments to remove dental plaque deposits.[26] Treatment for gingivitis and periodontitis should establish periodontal health, arrest disease progression, prevent recurrence, and preserve the dentition in a state of health, comfort, and function. 

The healing response is typically assessed 1 to 2 months after treatment. For patients with early or moderate disease, nonsurgical treatment (ie, scaling, oral hygiene instruction) is often sufficient. Successful long-term management requires behavior change to address lifestyle risk factors (especially smoking) and, most importantly, to attain and sustain high standards of lifelong daily plaque removal. 

Evidence regarding the ideal recall interval for dental check-ups shows no clinically significant differences among 6-month, 24-month, and risk-based recall intervals for adults in gingival bleeding, caries, or oral health-related quality of life over 4 years (high-certainty evidence).[27] For patients with gingivitis only (ie, no history of periodontitis), professional examination, prophylaxis, and oral hygiene instruction should be provided once or twice yearly, depending on the presence of other risk factors such as attachment loss, age, smoking, or abnormal tooth mobility. A single recall interval is not suitable for all patients; selection must be based on individual patient needs.(A1)

If the gingivitis is due to drug-induced gingival overgrowth, the dentist can consult with the prescribing clinician to change the offending medication to improve treatment outcomes. If the gingivitis is due to a nutritional deficiency, supplements can be prescribed. Medications, such as an antiseptic mouthwash containing chlorhexidine, can also be prescribed alongside mechanical plaque removal. Studies' results have suggested that using chlorhexidine mouthwash, in addition to regular toothbrushing and interproximal cleaning, leads to a significant reduction in dental biofilm buildup. The concentration of the chlorhexidine rinse does not affect its effectiveness.[28](A1)

Studies have examined the effect of medicinal or herbal plants on the management of gingivitis. The mechanism of action of these plants in gingivitis is their anti-inflammatory properties. Such medicinal plants include pomegranate, green tea, and chamomile. The flavonoids and tannins present in these plants are potent anti-inflammatory and astringent phytochemicals that can resolve both gingival bleeding and inflammation.[29] Some studies' results have demonstrated a synergistic effect when herbal plants are prescribed alongside conventional mechanical plaque-removal procedures, such as scaling.[30]

Differential Diagnosis

Gingivitis can be differentiated from periodontitis by the attachment loss undergone in the latter, which can be clinically noticed during periodontal probing.[31] The 2 conditions can also be differentiated histologically and radiographically.

Prognosis

The prognosis for plaque-induced gingivitis is excellent with appropriate treatment, as the inflammation is fully reversible with effective plaque control.[32] In a randomized clinical trial, 89% of patients with generalized gingivitis achieved complete resolution within 1 month of intensive oral hygiene instruction and electric toothbrush use, compared to only 7% in the control group. Gingivitis is fundamentally reversible because the inflammatory changes are confined to the gingival soft tissues without destruction of the underlying periodontal attachment apparatus.[6] Resolution of the inflammation is accompanied by a shift in the subgingival microbiota toward health-associated species, confirming the critical role of oral hygiene measures in restoring microbial eubiosis.[33]

Treatment response varies by disease extent:

• Localized gingivitis: 80% achieve periodontal health after single-session therapy (scaling, polishing, oral hygiene instruction).
• Generalized gingivitis: Only 30% resolve after single-session therapy, with 70% requiring multiple retreatments due to higher baseline inflammation.[34]

However, untreated gingivitis may progress to periodontitis, an irreversible condition with permanent loss of periodontal attachment and alveolar bone.[32] Although gingivitis precedes periodontitis, progression is not inevitable. The transition depends on host susceptibility, risk factors, and sustained microbial challenge. For patients who achieve gingival health, the prognosis remains favorable with sustained oral hygiene practices. However, a treated and stable patient with a history of periodontitis remains at increased risk of recurrent periodontitis and must be closely monitored, despite current gingival health.

Complications

The primary complication of untreated gingivitis is progression to periodontitis, an irreversible condition characterized by destruction of the periodontal ligament and alveolar bone, ultimately leading to tooth loss. Additionally, periodontal disease is associated with systemic complications, including cardiovascular disease, diabetes mellitus, adverse pregnancy outcomes, and aspiration pneumonia through shared inflammatory pathways.[35]

Gingivitis is a necessary precursor to periodontitis, though not all cases of gingivitis progress to periodontitis; the transition depends on host susceptibility and sustained microbial challenge. Key features of this progression are described below:

• Periodontitis-like microbiome dysbiosis can emerge as early as 24 to 72 hours after cessation of oral hygiene, defining an asymptomatic "suboptimal health" stage that links gingivitis to periodontitis.
• Gingivitis can accelerate aging of the oral microbiota by over 1 year within 28 days, underscoring the importance of early intervention.
• Once a periodontal pocket forms and becomes filled with bacteria, the situation becomes largely irreversible; even with treatment, complete restoration of lost tooth support is impossible.
• Destructive periodontitis lesions are dominated by B lymphocytes and plasma cells, whereas nonprogressive inflammatory foci (gingivitis) tend to be composed predominantly of T lymphocytes and macrophages.

Several factors increase the likelihood of gingivitis progressing to periodontitis:

• Smoking/tobacco use: Well-established independent risk factor
• Diabetes mellitus: Increases susceptibility approximately threefold
• Host immune dysregulation: Both hypo- and hyperresponsiveness can enhance tissue destruction
• Poor oral hygiene: Sustained plaque accumulation
• Genetic susceptibility: Influences inflammatory response [36]