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Overview of gingivitis and periodontitis in adults

Overview of gingivitis and periodontitis in adults
Literature review current through: Jan 2024.
This topic last updated: May 10, 2023.

INTRODUCTION — Periodontal diseases (mostly gingivitis and periodontitis) are common conditions that affect the dental supporting structures including the gingiva, cementum, periodontal ligament, and the alveolar bone (figure 1).

This topic will review gingivitis, periodontitis, and associated conditions including those that affect dental implants. The pathogenesis, clinical manifestations, and antibiotic treatment of odontogenic infections are discussed in detail separately. (See "Epidemiology, pathogenesis, and clinical manifestations of odontogenic infections" and "Complications, diagnosis, and treatment of odontogenic infections".)

DEFINITIONS — Periodontal disease, which includes gingivitis and periodontitis, is classified according to the presence or absence of periodontal ligament and/or alveolar bone involvement (figure 1) [1,2].

Gingivitis – Gingivitis involves only the gums (picture 1); it is an inflammatory process characterized by gingival redness, swelling, and bleeding that is provoked by routine brushing or flossing or by the use of a periodontal probe. Healthy gingival tissues are pink, stippled (similar to an orange peel), and firm (picture 2). Noninflamed gingival tissue should not bleed or suppurate during routine flossing and/or brushing, or when professionally probed.

Periodontitis – Periodontitis is characterized by gingival inflammation accompanied by the loss of supportive connective tissues including the periodontal ligament and alveolar bone (figure 1). Clinical findings include gingival bleeding on probing, increased probing depth, and increased tooth mobility (picture 3). Bone loss is seen on radiographs (picture 4). Progression of periodontitis will cause accelerated tooth mobility and eventual tooth loss.

Gingival health is evaluated in relationship to overall periodontal health [3]. The periodontium is classified as either intact or reduced. If reduced (eg, gingival recession, alveolar bone loss), it is further classified according to the status of overall periodontal disease (absence of periodontal disease, stable periodontal disease, or recurrent periodontitis).

EPIDEMIOLOGY AND ASSOCIATION WITH OTHER MEDICAL CONDITIONS — Gingivitis is the most common form of periodontal disease, and the majority of adults have signs of gingival inflammation in one or more sites. Globally, periodontitis is a major cause of tooth loss [4,5]. In the United States, the majority of adults have slight to moderate periodontitis, and 5 to 15 percent of the entire United States population suffers from severe forms of periodontitis [6,7].

Periodontal disease may be a risk factor for a number of conditions [8-10], including dementia [11], cardiovascular disease, and cancer [12], and negative pregnancy outcomes. (See "Epidemiology, pathogenesis, and clinical manifestations of odontogenic infections", section on 'Association with cardiovascular risk' and "Spontaneous preterm birth: Overview of risk factors and prognosis", section on 'Infection'.)

There may be a bidirectional association between periodontal disease and diabetes. Specifically, poorly controlled diabetes may be a risk factor for increased severity of periodontitis and poor response to periodontal treatment [13]. In addition, among patients with diabetes, treatment of periodontal disease may slightly improve glycemic control [14].

CLINICAL PRESENTATION — In the majority of cases, primary care providers are alerted to the presence of periodontitis or gingivitis in their patients after a diagnosis is made by a dental professional. Alternatively, primary care providers may notice the presence of periodontitis or gingivitis (ie, gum swelling and/or bleeding, bad breath) on routine physical exam, at which point the patient should be directed to seek care from a dental professional for further evaluation and management.

PLAQUE-ASSOCIATED (MOST COMMON TYPE) GINGIVITIS AND PERIODONTITIS — Bacterial biofilm (also known as dental plaque, or dental plaque biofilm) is the most common cause of both gingivitis and periodontitis.

However, other causes of gingival and periodontal disease (ie, peri-implant disease, necrotizing periodontal disease, pregnancy gingivitis, linear gingival erythema, vitamin C deficiency, drug-induced gingival overgrowth, gingival recession, and abscesses) may be encountered. (See 'Other causes of gingivitis and periodontitis' below and 'Other periodontal conditions' below.)

Pathogenesis — The most common form of gingivitis is bacterial biofilm-induced gingivitis, which affects only the gingival tissue and is reversible if treated. If untreated, gingivitis will likely develop into periodontitis, although the time to transition may vary from weeks to years. Periodontitis is associated with attachment loss or alveolar bone loss, and, more importantly, treatment for gingivitis can prevent such loss. When the bacterial biofilm is removed on a daily basis, the gingiva returns to health in approximately two weeks [5,15].

Dental plaque is a dense, non-mineralized, complex mass of bacterial colonies living in a gel-like intermicrobial matrix that forms around the gingival margin (gum line) and can be found both supra- and subgingivally [4,16]. Plaque begins to accumulate within 24 hours if not removed with brushing and flossing. The amount of tissue damage related to plaque accumulation is dependent upon the interaction between plaque and host defense mechanisms. Calculus ("tartar") is mineralized plaque which promotes the retention of bacterial biofilm.

Plaque buildup may also be promoted by dental restorations (eg, fillings, crowns, bridges, veneers) that are ill-fitting (eg, have overhanging or open margins). Such conditions increase inflammation and may lead to loss of both gingival attachment and alveolar bone [17].

Periodontitis usually develops as a slowly progressive condition, with unpredictable brief episodic periods of rapid progression and attachment loss [18-24]. The triggering mechanism for active bone loss has not been precisely determined but appears to be associated with a shift in bacterial microbiota from predominantly gram-positive to anaerobic gram-negative rods. Supragingival plaque may serve as a reservoir for pathogenic gram-negative bacteria, and, episodically, the pathogenic bacteria may migrate subgingivally to form a biofilm that can be detrimental to surrounding periodontal structures [25-27].

Host response to the pathogenic microbiota is variable and may contribute to the rate at which gingivitis progresses to periodontitis and the rate of periodontitis progression. Additional factors contributing to periodontitis progression include cigarette smoking, diabetes mellitus, and emotional stress [28-31]. The role of diet is unclear, although in observational data, a diet higher in fruit, vegetables, poultry, seafood, and plain water or tea was associated with less prevalent higher-grade periodontitis [32].

At the cellular level, disease activity and tissue destruction are modulated through production of inflammatory factors, including interleukins, prostaglandins, and matrix metalloproteinases [33,34].

Periodontitis is classified by stage and grade, according to severity and rate of progression (table 1A-B). Untreated disease causes irreversible bone loss and architectural defects (craters) in the alveolar bone as well as increased periodontal pocket (probing) depth.

Prevention of plaque-associated gingivitis and periodontitis — Mechanical debridement (regular brushing and flossing, supplemented by periodic instrumentation by a dental professional) is the most effective way to remove dental biofilms. The goal of daily dental hygiene is to reduce both supra- and subgingival bacteria to below the threshold level capable of initiating or perpetuating inflammation.

Personal plaque control is an essential component of gingivitis prevention and management. The goal is to reduce dental bacterial load; toothbrushing (via manual or powered toothbrush) twice daily, flossing once daily, and rinsing with an antimicrobial/antiseptic mouthrinse. Use of a dentifrice (eg toothpaste, powder, or gel) twice daily is part of an oral hygiene program recommended by most dental professionals. However, compared with toothbrushing alone, studies examining the addition of flossing and other supplemental biofilm reduction techniques on gingivitis are mixed. Representative studies include:

In a 2019 meta-analysis of 35 randomized trials, among participants with mild baseline gingival inflammation, the addition of floss or interdental brushes to toothbrushing minimally reduced gingivitis compared with brushing alone [35].

In a 2014 meta-analysis of 56 randomized trials comparing powered toothbrushes with manual brushing, the use of powered toothbrushes decreased plaque and gingivitis at both one and three months [36].

In a 2017 systematic review, chlorhexidine mouthrinse used as an adjunct to usual brushing for the control of gingivitis and plaque was evaluated [37]. Among those with mild gingivitis, there was no evidence of clinically relevant reduction in gingival inflammation with the use of chlorhexidine, although there was a large reduction in dental plaque development. However, there was also an increase in tooth staining among those who used the mouthrinse for four weeks or longer.

Despite the lack of high-quality data, we encourage the regular use of floss (or other interdental cleaning device) to reduce interdental bacterial biofilm, where the majority of caries and periodontal disease occurs.

Calculus (tartar buildup) must be professionally removed to promote resolution of inflammation; calculus cannot be removed by tooth brushing, flossing, or polishing. Calculus removal requires scaling and root planing procedures by a dental professional using special instrumentation and skills.

Treatment of plaque-associated gingivitis and periodontitis — The primary treatment of plaque-associated periodontitis includes debridement (scaling and root planing of subgingival biofilm and calculus) by a dental professional. This should be accompanied by an attentive home oral hygiene routine, which includes chlorhexidine rinses twice daily until regular tooth brushing can be safely resumed (typically two weeks following scaling or surgical procedures), then brushing (manual or power brush) twice daily, flossing once daily, and, when applicable, smoking cessation [28,31].

For patients with less severe disease, in addition to the treatments discussed above, topical antibiotics (including doxycycline or minocycline) may be applied to periodontal pockets by a dental professional (table 2). There is a lack of high-quality data supporting the efficacy of the use of topical antimicrobial drugs in combination with scaling and root planing. However, the overall consensus it that application of these drugs provides a limited, beneficial response on periodontal pockets [38].

For patients with more severe disease (eg, periodontitis with ≥5 mm pockets accompanied by gingival inflammation with swelling and bleeding of the gums), scaling and root planing alone may not be adequate [39,40]. Surgical intervention, such as gingival flap (pocket reduction) surgery, may be needed to optimize access to root surfaces to allow for more complete debridement.

In addition to mechanical debridement of plaque biofilm and calculus, patients with more severe periodontitis are treated with systemic antibiotics (table 2) [41,42]. The details of antibiotic therapy are discussed in detail elsewhere. (See "Complications, diagnosis, and treatment of odontogenic infections", section on 'Plaque-associated periodontitis'.)  

Following acute treatment, some dental professionals also prescribe low-dose oral doxycycline (20 mg twice daily) for up to nine months as an anti-collagenolytic agent. There are few data to support this approach [43], but at this low dose, although systemic levels do not reach bacterial inhibitory concentrations, the drug inhibits collagenase activity in vitro and may prevent further breakdown of connective tissue and alveolar bone [44,45].

OTHER CAUSES OF GINGIVITIS AND PERIODONTITIS

Peri-implant disease (mucositis and peri-implantitis) — Patients with dental implants (in which a replacement tooth is mounted upon a metal post that is surgically implanted in the jaw bone) may be affected by conditions similar to plaque-associated gingivitis and periodontitis.

Peri-implant mucositis – Peri-implant mucositis is the equivalent of gingivitis (which affects the natural teeth). In peri-implant mucositis, the inflammatory infiltrate remains in the soft tissue only and it does not lead to alveolar bone loss. As in gingivitis, it is a reversible condition if one implements effective methods for biofilm (dental plaque) removal [46]. If left untreated, this condition will develop into peri-implantitis.

Peri-implantitis – Peri-implantitis is a more serious disease causing the irreversible loss of alveolar bone and, if untreated, may lead to implant loss [47]. In a systematic review, peri-implantitis occurs in 19 percent of patients with implants [48].

In peri-implantitis, the tissues surrounding the implant may become inflamed and the implant itself may loosen. Peri-implant radiolucency (bone destruction) is seen on dental radiography (image 1). The bacteria associated with peri-implantitis are similar to those in chronic periodontitis. (See 'Pathogenesis' above.)

High-quality data on the optimal protocol for the management of peri-implant disease are lacking, but the majority of dental professionals treat peri-implantitis in the same manner as periodontitis. In severe cases, bone grafting, and even surgical removal of the implant may be necessary [49-52]. (See 'Treatment of plaque-associated gingivitis and periodontitis' above.)

Necrotizing periodontal disease — Necrotizing periodontal disease (NPD) includes both necrotizing ulcerative gingivitis (NUG) and necrotizing ulcerative periodontitis (NUP) [53].

Although both of these conditions are associated with bacterial infections of the gingiva and periodontium, the pathophysiology of these infections are distinct from plaque-associated gingivitis and periodontitis in their exuberant, necrotizing effect on periodontal tissues.

Necrotizing ulcerative gingivitis – NUG, also called Vincent's angina or "trench mouth," is characterized by the acute onset of fetid breath, severe oral pain, blunting of the interdental papilla, and an ulcerative necrotic slough of the gingiva. The sloughed material, or film, consists of fibrin, necrotic tissue, leukocytes, erythrocytes, and bacteria. Removal of this film causes bleeding and exposure of ulcerated and erythematous tissue.

The patient with NUG may be febrile and have associated anterior submandibular and submental lymphadenopathy. The disease typically occurs in individuals in their 20s, and risk factors include poor oral hygiene, existing gingivitis, stress, smoking, impaired host immune response, and malnutrition [54-58].

In addition to treatment with debridement and antimicrobial rinses (eg, 0.12 percent chlorhexidine gluconate twice daily for two weeks), we treat all of these patients with systemic antibiotics (table 2) [59,60]. Treatment details are discussed in detail elsewhere. (See "Complications, diagnosis, and treatment of odontogenic infections", section on 'Plaque-associated acute gingivitis'.)

Necrotizing ulcerative periodontitis – NUP, once termed "HIV periodontitis," involves severe loss of periodontal attachment and alveolar bone. It is not limited to patients with HIV infection, however; it can affect people with HIV infection and CD4 counts less than 400, as well as patients with severe immunosuppression related to cancer chemotherapy or advanced protein-energy malnutrition [61,62].

NUP manifests as acute-onset, painful, necrotizing ulceration of the gingiva, which causes rapid attachment loss and alveolar bone loss. Necrotic clefts in the affected gingiva may be seen, and tissue destruction is so rapid that denuded bone is visible, in some cases followed by bone sequestration (picture 5).

The microbiota in NUP is unique; in addition to the gram-negative rods typically associated with chronic periodontitis, enteric organisms and fungi are often identified in these infections.

Treatment for NUP consists of debridement (scaling and root planing) along with systemic antibiotics and topical chlorhexidine rinses (picture 6). We use metronidazole 250 to 500 mg orally three times daily for at least seven days as well as chlorhexidine rinses (0.12 percent chlorhexidine gluconate twice daily for two weeks) (table 2) [63]. Proper treatment can result in successful outcomes (picture 7).

Non-plaque-associated gingivitis and gingival disease — Non-plaque-induced gingivitis represents a small percentage of gingivitis cases. In such cases, gingival inflammation may be due to one or more factors, including hormonal changes (eg, pregnancy, menarche, or ovulation), systemic infection (HIV), gingival fungal infection, connective tissue disorders, medication effect, and metabolic and endocrine diseases [3,64].

Pregnancy gingivitis and gingival conditions — Hormonal shifts that occur during pregnancy may cause the gingiva to become inflamed and overgrown (picture 8). When present, gingival inflammation tends to increase during the pregnancy and then diminishes postpartum. Pregnancy-related gingivitis may be unrelated to the amount of plaque biofilm and usually does not increase rates of attachment loss or bone loss (periodontitis) [65].

Affected patients are instructed to perform meticulous oral hygiene procedures to minimize plaque biofilm levels [66]. Additional therapy for more severe pregnancy gingivitis may consist of debridement and adjunctive local antimicrobial therapy, such as chlorhexidine rinses. Dental professionals commonly schedule periodontal treatments for the early part of the second trimester [67] and defer additional treatment of non-urgent periodontal needs until the postpartum period, although there is no high-quality evidence to support this practice. Acute infection, abscess, or potential sources of sepsis require urgent intervention, regardless of the pregnancy stage. (See "Spontaneous preterm birth: Overview of risk factors and prognosis".)

Another gingival condition, pregnancy-associated pyogenic granuloma, occurs in approximately 0.5 to 5 percent of pregnant women (picture 9) [68]. This is an exaggerated inflammatory response to local irritants (plaque and calculus) that occur during pregnancy [4]. Pyogenic granuloma is painless and usually occurs in the anterior mandibular or maxillary gingiva [69,70]. Plaque and calculus should be removed, but the pregnancy granuloma should not be excised during pregnancy, as it may resolve spontaneously after parturition; excision is necessary if it does not resolve [71]. (See "Maternal adaptations to pregnancy: Skin and related structures", section on 'Mucosa and nonkeratinized epithelium'.)

Hormonal changes outside of pregnancy may also influence gingival health. Some women experience an increase in gingival inflammation with ovulation (menstrual cycle-associated gingivitis) [68]. Gingival inflammation also increases with puberty-related hormonal changes [72].

Linear gingival erythema — Linear gingival erythema (previously called HIV-related gingivitis) presents as a brightly inflamed and well-defined band of marginal gingiva (picture 10). The gums are painful and bleed easily, and there may be rapid periodontal destruction. The microbiologic pattern is dominated by yeast (Candida albicans), gram-negative anaerobes, and enteric organisms not found in routine cases of gingivitis. (See "Epidemiology, pathogenesis, and clinical manifestations of odontogenic infections".)

Treatment consists of debridement and topical antifungals such as nystatin rinses or clotrimazole troches. In addition, topical antibacterial treatment (eg, chlorhexidine rinses) may be used as adjunctive therapy to reduce the burden of contributing oral pathogens.

Patients presenting with linear gingival erythema should be evaluated for the presence of underlying immunocompromised conditions.

Vitamin C deficiency — Gingival diseases associated with malnutrition are rare in regions with adequate food supply, but vitamin deficiencies may still occur. Vitamin C deficiency may cause scurvy, a disease characterized by impaired collagen synthesis, which may become symptomatic as early as three months after deficient intake begins. Scurvy-associated gingival abnormalities may be difficult to distinguish from bacterial biofilm-induced gingivitis (picture 11). However, scurvy is associated with other symptoms, including ecchymoses, petechiae, coiled hairs, and hyperkeratosis. Treatment of vitamin C deficiency is discussed elsewhere. (See "Overview of water-soluble vitamins", section on 'Vitamin C (ascorbic acid)'.)

Other than vitamin C deficiency, the precise role of nutrition in the initiation or progression of periodontal diseases remains unclear.

Drug-induced gingival overgrowth — Certain medications may affect the periodontium by causing gingival overgrowth or enlargement (picture 12). Drugs that cause this reaction include phenytoin, cyclosporine, and calcium channel blockers (most commonly nifedipine, diltiazem, verapamil, and amlodipine, although in case reports, felodipine, nitrendipine and nicardipine have also been implicated) [73,74].

The term "gingival hyperplasia" is still used by some clinicians, but this describes a histologic rather than a clinical presentation. The gingival overgrowth caused by these drugs may be due to hyperplasia and/or hypertrophy, and the preferred clinical terminologies are either drug-induced "gingival overgrowth" or drug-induced "gingival enlargement."

The clinical manifestations of gingival overgrowth are the same, regardless of which drug caused the reaction. The gingival tissues can grow disproportionally by several millimeters, covering one-third or more of the teeth crowns. The overgrown tissues form pseudo-gum pockets which interfere with appropriate oral hygiene, easily harboring bacterial biofilm. As a result, gingival inflammation develops, causing bleeding and discomfort when chewing, brushing, and flossing. These subsequent inflammatory changes potentiate further tissue overgrowth. In addition to the discomfort caused by the inflammation, gingival overgrowth may also become an aesthetic problem for the patient.

The severity and distribution of the overgrowth is variable and, for some drugs, may be reversible upon discontinuation of the causative drug. As an example, in a case report of cyclosporine-induced gingival overgrowth, regression of gingival overgrowth occurred upon interruption of drug therapy within several months [75].

Management of gingival overgrowth includes aggressive plaque (bacterial biofilm) control (eg, brushing and flossing and the use of antimicrobial dentifrices and rinses). Even with excellent oral hygiene, surgical removal of the overgrown tissue (gingivectomy) is likely inevitable. Excision of excessive gingival tissue is indicated for severe cases that affect oral hygiene or function (chewing) or for esthetic issues. Gingivectomy can be performed by scalpel, electrosurgery, high-speed dental handpiece with a diamond burr, or laser therapy. Successful outcome depends upon restoration of normal gingival contours and careful postoperative care (picture 13).

If medically possible, the drug responsible for gingival overgrowth should be discontinued; recurrence of overgrowth is likely if the medication cannot be eliminated. If these drugs cannot safely be replaced, dental prophylaxis (dental cleaning) at three-month intervals is advised.

OTHER PERIODONTAL CONDITIONS — As in non-plaque-associated gingivitis, a variety of systemic conditions can affect the course of periodontitis or impact the periodontal attachment apparatus [76]. Other systemic conditions that are associated with periodontal diseases include emotional stress and depression, smoking, and medications. Finally, there are systemic disorders that may result in loss of periodontal tissue independent of periodontitis, including primary neoplasms of the periodontal tissue and metastatic disease to the periodontium from other sites.

Gingival recession — Gingival recession is extremely common and can occur in patients with or without other forms of periodontal disease. The etiology may include severe chronic periodontitis, genetic predisposition (ie, larger teeth in smaller dental arches), and/or excessive and overly vigorous toothbrushing.

Gingival recession may cause hypersensitivity to cold and sweets, root caries, discomfort with chewing and/or brushing (and as a result interfere with good oral hygiene), or unacceptable cosmetic appearance. For such patients, gum grafting surgery is offered as a primary treatment (picture 14). In addition, patients with thin alveolar bone and gum tissue may benefit from preventative gum grafting prior to orthodontic therapy to prevent gum recession. However, there is no evidence that prophylactic gum grafting surgery will prevent alveolar bone loss.

Periodontal and gingival abscesses — Periodontal and gingival abscess are common acute infections of the periodontal supporting structures. Risk factors for abscess formation include:

Deep periodontal pockets [77,78]

Incomplete removal of subgingival calculus after a professional scaling and root planing [78,79]

Occlusion of the pocket orifice by foreign bodies (ie, popcorn kernel) [78,80]

Inadequate treatment of periodontitis (eg, administration of antibiotics in the absence of scaling or planing mechanical therapy) [81]

Poorly controlled diabetes

An abscess usually presents as a painful swelling of the buccal or lingual/palatal gingiva but can also be asymptomatic. The patient may complain of fever, a painful tooth/teeth in the affected region, and discomfort with chewing; local lymphadenopathy can develop. When palpating the abscess, a sinus tract fistula may become evident with production of purulent material. (See "Epidemiology, pathogenesis, and clinical manifestations of odontogenic infections", section on 'Clinical manifestations'.)

A periodontal abscess can cause rapid alveolar bone resorption, which can be confirmed radiographically. However, prompt treatment often leads to bone repair. The prognosis is dependent upon the presence of other endodontic complications. Treatment of the abscess consists of incision and drainage followed by antibiotic therapy. (See "Complications, diagnosis, and treatment of odontogenic infections".)

Odontogenic infections, including periodontal abscesses, may spread hematogenously to seed heart valves (native, mechanical, or bioprosthetic), joint replacements, or other prosthetic devices. (See "Native valve endocarditis: Epidemiology, risk factors, and microbiology", section on 'Poor dentition or dental infection' and "Prosthetic joint infection: Epidemiology, microbiology, clinical manifestations, and diagnosis", section on 'Risk factors'.)

SUMMARY AND RECOMMENDATIONS

Definitions – Periodontal disease, which includes gingivitis and periodontitis, is classified according to the presence or absence of alveolar bone involvement (figure 1). (See 'Definitions' above.)

Gingivitis involves only the gums (picture 1); it is an inflammatory process characterized by gingival redness, swelling, and bleeding that is provoked by routine brushing or flossing or by a use of a periodontal probe. Healthy gingival tissues are pink, stippled (similar to an orange peel), and firm (picture 2).

Periodontitis is characterized by gingival inflammation accompanied by the loss of supportive connective tissues including the periodontal ligament and alveolar bone (figure 1). Clinical findings include gingival bleeding on probing, increased probing depth, and increased tooth mobility.

Clinical presentation – In the majority of cases, primary care providers are alerted to the presence of periodontitis or gingivitis in their patients after a diagnosis is made by a dental professional. Alternatively, primary care providers may notice the presence of gingival or periodontal disease on routine physical exam, at which point the patient should be directed to seek care from a dental professional for further evaluation and management. (See 'Clinical presentation' above.)

Plaque-associated gingivitis and periodontitis: Disease course and management – The most common form of gingivitis is bacterial biofilm-induced gingivitis, which affects only the gingival tissue and is reversible if treated. If untreated, gingivitis will likely develop into periodontitis, although the time to transition may vary from weeks to years. Periodontitis usually develops as a slowly progressive condition, with unpredictable brief episodic periods of rapid progression and attachment loss. The triggering mechanism for active bone loss has not been precisely determined but appears to be associated with a shift in bacterial flora from predominantly gram-positive to anaerobic gram-negative rods. (See 'Pathogenesis' above.)

To prevent plaque-associated gingivitis and periodontitis, we suggest mechanical debridement (the addition of flossing to routine toothbrushing, supplemented by periodic instrumentation by a dental professional) (Grade 2C). The goal of daily dental hygiene is to reduce both supra- and subgingival bacteria to below the threshold level capable of initiating or perpetuating inflammation. (See 'Prevention of plaque-associated gingivitis and periodontitis' above.)

Calculus must be professionally removed to promote resolution of inflammation. (See 'Prevention of plaque-associated gingivitis and periodontitis' above.)

The primary treatment of plaque-associated periodontitis includes debridement (scaling and root planing of subgingival biofilm and calculus) by a dental professional. This should be accompanied by an attentive home oral hygiene routine, which includes chlorhexidine rinses twice daily until regular tooth brushing can be safely resumed (typically two weeks following scaling or surgical procedures), then brushing (manual or power brush) twice daily, flossing once daily, and, when applicable, smoking cessation. (See 'Treatment of plaque-associated gingivitis and periodontitis' above.)

-For patients with less severe disease, in addition to the treatments discussed above, topical antibiotics (including doxycycline or minocycline) may be applied to periodontal pockets by a dental professional (table 2).

-Patients with more severe disease may also require surgical intervention such as flap surgery (pocket reduction surgery) for greater access to root surfaces to allow for more complete debridement. In addition to mechanical debridement and local antimicrobial therapy, these patients are treated with systemic antibiotics (table 2).

Necrotizing periodontal disease – Necrotizing periodontal disease (NPD) includes both necrotizing ulcerative gingivitis (NUG) and necrotizing ulcerative periodontitis (NUP). Although both of these conditions are associated with bacterial infections of the gingiva and periodontium, the pathophysiology of these infections are distinct from plaque-associated gingivitis and periodontitis in their exuberant, necrotizing effect on periodontal tissues. Treatment for each condition includes plaque debridement, local antimicrobial therapy (chlorhexidine 0.12% mouth rinses), and systemic antibiotics. (See "Complications, diagnosis, and treatment of odontogenic infections", section on 'Plaque-associated acute gingivitis' and 'Necrotizing periodontal disease' above.)

Non-plaque-associated gingival disease – Non-plaque-associated gingival disease represents a small percentage of gingivitis cases. In such cases, gingival inflammation may be due to one or more factors, including hormonal changes (eg, pregnancy, menarche, or ovulation) (picture 8), systemic infection (HIV), gingival fungal infection, connective tissue disorders, medication effect (eg, gingival overgrowth) (picture 12), and metabolic and endocrine diseases. (See 'Non-plaque-associated gingivitis and gingival disease' above.)

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Topic 6858 Version 51.0

References

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