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Necrotizing Periodontitis


Necrotizing Periodontitis

Article Author:
Noah Gasner
Article Editor:
Ryan Schure
Updated:
5/31/2020 4:16:13 PM
For CME on this topic:
Necrotizing Periodontitis CME
PubMed Link:
Necrotizing Periodontitis

Introduction

Necrotizing periodontitis (NP), previously referred to as necrotizing ulcerative periodontitis, is a specific subset of necrotizing periodontal diseases (NPD). In general, NP is a reactive, destructive inflammatory process in response to bacterial inflammation, and represents the most severe form of the biofilm-related diseases.[1] Although rare in modern industrialized society, this disease process can progress through various stages that are considered to be of the same disease due to their shared etiology and clinical presentation.[2] These stages are necrotizing gingivitis (NG), NP, and necrotizing stomatitis (NS).[3] NG is the most common form and is seen to progress to NP in susceptible populations, such as in immunosuppressed patients. The classification and staging of NPDs are further discussed in the 'staging' subsection.

Etiology

Although necrotizing periodontal diseases are infectious conditions, the most critical predisposing factor is immunosuppression. Cases of NG and NP are almost always found in patients who have an immunosuppressed condition, most notably HIV, but other conditions such as leukemia, neutropenia, diabetes mellitus, and long-term immunosuppressant therapy have also been noted.[4][5][6][7]

Other etiological factors include tobacco smoking, psychological stress, malnutrition, poor sleeping habits, poor oral hygiene, and a possible genetic predisposition. Most cases of NPDs are seen in patients that are tobacco smokers. Additionally, malnutrition has been shown to be a causative factor as in industrialized countries, NPDs are associated with populations who display poor eating habits, such as college students, whereas, in developing countries, they are associated with young children who have been found to have deficient protein intake.[8]

Virulent bacteria, specifically Fusobacteria and spirochete species, have been identified in the necrotizing lesions associated with NP. Additionally, antibiotics have been shown to alleviate symptoms in the acute phase, indicating a bacterial involvement in the NP disease process. However, it is unclear whether these organisms are the causative agent in the disease process, or if they represent a secondary overgrowth due to the immunosuppressed condition. Furthermore, the disease is not known to be transmissible, indicating that the etiology is not due to exogenous factors, but rather due to preexisting host factors.[7]

A limited understanding exists surrounding the actual cause of NP; however, evidence points to an existing periodontal condition that is given the opportunity to proliferate into a more rapid and destructive state.[9]

Epidemiology

In general, necrotizing periodontal diseases, including necrotizing periodontitis, are more commonly found in developing countries with lower socioeconomic status. A major correlative epidemiologic risk factor is malnutrition, and an age difference is seen between developed and developing countries. In developing countries, NP is most commonly associated with very young children and is related to poor nutrition, specifically a low protein intake.[10] Contrarily, in developed countries, NP is commonly found in people aged 15 to 30 and is seen as related to poor nutritional habits, such as those of college students. Additional risk factors more commonly associated with lower socioeconomic status countries include tobacco smoking and poor oral hygiene.[11]

Pathophysiology

The exact pathogenesis of necrotizing periodontal diseases is not fully known; however, the initial stage of NG is believed to be caused by commensal oral organisms, which become pathogenic in the presence of a reduced host response. Fusobacteria and spirochete species have commonly been implicated in NPD; however, it is unclear whether these are causative organisms, or if they represent a secondary or opportunistic infection, due to the patient's immunosuppressed condition.[12] These bacteroids, in addition to other primarily gram-negative species, produce a vast array of metabolites that produce the destruction seen in NP. These metabolites include collagenases, endotoxins, hydrogen sulfide, and fibrinolysin. The destructive actions of these metabolites result in the rapid destruction of the periodontium, including the gingiva, periodontal ligament, and alveolar bone, as is characteristic of NP.[7][13]

Histopathology

The histopathology of necrotizing periodontitis is identical to that of NG; however, in NP the destructive metabolites have been present for a longer time, resulting in the destruction of the underlying periodontium.

In 1965, Listgarten provided electron microscopy (EM) data of the invasion of spirochetes in what was previously referred to as necrotizing ulcerative gingivitis (NUG) and differentiated between various zones within NUG. The zones are listed in order of increasing depth.

  1. Bacterial zone
  2. Neutrophil-rich zone
  3. Necrotic zone
  4. Zone of spirochete infiltration

The most superficial bacterial zone contains a variety of bacterial species. The neutrophil-rich zone contains various leukocytes, with the most prominent cell type being the neutrophil. In the next deeper zone, the necrotic zone, an abundance of dead cells, and fragmented connective tissue can be found. Up until this final zone, a variety of bacteria species could be found, including spirochetes, however in the zone of spirochete infiltration, spirochetes are the sole organism present and can be found in the deep, preserved tissue.[14]

History and Physical

The history of a patient presenting with suspected NP should include some of the noted etiological factors such as immunosuppression, psychological stress, and smoking. Additionally, patient history should include a rapid onset of the condition as is characteristic of necrotizing periodontal diseases. NP is an extremely rapid and destructive disease process and can produce a loss of periodontal attachment in as short as a few days.[1]

The three characteristic features of all necrotizing periodontal diseases are tissue necrosis, spontaneous bleeding, and pain.[8] Other common clinical features include halitosis or fetid oral odor, sloughing off of dead epithelial tissue, and the presence of a pseudomembrane. Tissue necrosis in NPD manifests as ulcerated and necrotic gingiva, producing a “punched-out” or “cratered” appearance.[13][15] These necrotic areas are covered by a pseudomembrane, which is a yellowish slough of tissue containing plasma proteins, and white blood cells. In some cases of NPDs, systemic involvement can be seen via swelling of regional lymph nodes. Fever and malaise are generally only seen in more severe cases of NPDs.[1]

NPD lesions are generally very painful, which provides a good differentiating feature from normal periodontal diseases, such as gingivitis and periodontitis, which are not normally painful. As a result of the pain, patients tend to stop their oral hygiene practices, which can manifest as fetid oral odor or halitosis. Additionally, patients may decrease the amount they eat or drink, potentially leading to them becoming malnourished, which can exacerbate symptoms of fever or malaise.[15]

NP is a definitive stage of the disease process with the initiation of the destruction of the periodontium resulting in alveolar bone loss and periodontal ligament destruction, in addition to gingival necrosis. As necrosis progresses, interproximal craters begin to form between the facial and lingual papillae, creating a depression between teeth. With the production of the interproximal craters, periodontal tissues, including the periodontal ligament and alveolar bone are generally altered, producing loss of attachment, the key feature of NP. Deep periodontal pockets are uncommon in NP since the disease progresses so rapidly that there is little time for pocket formation.[9][13]

Evaluation

Necrotizing periodontitis is a clinical diagnosis and biopsy has been shown to be unhelpful, as it will present as non-specific inflammation. The clinical findings will include a history of rapid onset tissue necrosis, spontaneous bleeding, and pain. In cases of NP, the rapid loss of periodontium will also be noted, including attachment loss, periodontal ligament destruction, and alveolar bone loss producing interproximal cratering. Radiographs can be used to demonstrate the extent of alveolar bone loss.

An additional important step in the evaluation of NPDs is the administration of appropriate blood tests to rule out predisposing illnesses such as leukemia, neutropenia, and agranulocytosis.[15][8]

Treatment / Management

The treatment of necrotizing periodontitis depends on the extent and severity of the disease state. In the case of localized lesions, daily professional mechanical debridement of the lesions and adjacent structures with the use of topical antiseptics (e.g., hydrogen peroxide) are indicated. Additionally, 0.2% chlorhexidine gluconate (CHX) has been demonstrated to be useful in a patient that struggles in maintaining adequate oral hygiene.[2][16]

In cases of more generalized, painful lesions, systemic antibiotics may be used. Metronidazole, penicillin, and tetracycline have all been shown to be effective in this case, with metronidazole being the most commonly prescribed antibiotic agent. However, these antibiotic regimens are most effective when used in combination with regular mechanical debridement.[17]

NP is a disease of tissue destruction of both soft tissue (gums) and hard tissue (alveolar bone). As a result of the disease, both soft and hard tissue defects can be created that make oral hygiene difficult. Following the completion of the acute treatment phase, patients may undergo treatments to surgically correct any defects, such as a gingivoplasty for smaller soft tissue defects, or osteoplasty to repair larger, bony defects.[16]

The management of patients with NP should be based on the modification of risk factors and the treatment of underlying etiologies. Patients with NP may require a medical consultation as the patient may have a serious underlying immunocompromising condition (e.g., HIV). Clinicians should always be aware that the patient may be HIV positive, and all appropriate precautions should be taken for effective infection control. Additionally, etiologies such as tobacco smoking, psychological stress, and malnutrition should be managed to reduce the risk of future disease.[8][12] These underlying or concurrent conditions need to be treated simultaneously with the required dental therapy.

Differential Diagnosis

There are several similarly presenting conditions that must be ruled out in the diagnosis of NP.

  1. Oral mucositis 
  2. HIV-associate periodontitis
  3. Herpes simplex virus (HSV)
  4. Scurvy
  5. Gingivostomatitis
  6. Invasive fungal disease 
  7. Illicit-drug related gingival disease 

All of these conditions can involve the gingiva and periodontium, and the appropriate testing and history taking must be performed for an accurate diagnosis.[18][1]

Staging

According to the 2017 classification system put forth by the American Academy of Periodontology, necrotizing periodontal disease is a category of diseases that affects the periodontium through the extent of ulceration and necrosis. Within this group, there are three major subsets:

  1. Necrotizing (ulcerative) gingivitis
  2. Necrotizing (ulcerative) periodontitis
  3. Necrotizing stomatitis

The differences between these subsets are based on the extent and site of damage. Necrotizing gingivitis is the term used to describe necrosis and ulceration limited to the gingiva (gums). A progression of that condition is necrotizing periodontitis wherein there is damage to, and loss of the periodontium that surrounds each tooth which includes the gingival tissues, alveolar bone, and periodontal ligament. Lastly, necrotizing stomatitis is a term used to describe the destruction of the mucous membranes in the mouth, the areas beyond the mucogingival junction such as the cheek, tongue, and palate.[3]

Prognosis

Recurrence of necrotizing periodontal diseases is not uncommon, and therefore regular recalls are recommended to monitor for signs of future disease. Additionally, a key factor in the prognosis of NPDs is in the management of risk factors. If risk factor modification includes improving oral hygiene, nutrition, psychological stress, and smoking cessation, the patient has a much more favorable prognosis. Additionally, treatment of underlying conditions, such as therapy for HIV may reduce the patient's immunosuppressed state, thus also improving their prognosis.[6][1]

Complications

There are several noted complications of necrotizing periodontitis, most of which are related to the destructive nature of the disease. These complications include:

  • Tooth loss
  • Further loss of attachment
  • Extensive soft tissue necrosis
  • Exposure of alveolar bone
  • Sequestration of bone fragments
  • Bacteremia
  • Weight loss and dehydration[9][16][19]

Deterrence and Patient Education

Provide at-risk patients with education about how to modify risk factors such as oral hygiene and nutrition to prevent the occurrence of necrotizing periodontitis. Interdisciplinary healthcare professionals should work together to identify, monitor, treat, and manage patients with necrotizing periodontal diseases, and treat underlying conditions, including HIV. The importance of rapid identification of the signs and symptoms of necrotizing periodontitis to provide rapid and effective treatment and patient management to limit the extent of the destruction.

Enhancing Healthcare Team Outcomes

Necrotizing periodontitis is a rapidly destructive subcategory within necrotizing periodontal diseases. The most commonly noted predisposing factor of necrotizing ulcerative periodontitis (NUP) is an immunocompromised state, such as that found in patients with HIV. Additionally, other modifiable etiological factors have also been suggested, including tobacco smoking, poor oral hygiene, malnutrition, and psychological stress. Clinicians should understand and appreciate the interconnection between the systemic state and the oral cavity when assessing patients on their risk for developing NPD as a patient may present to them with a history of known risk factors requiring counseling and intervention. These clinicians can play an invaluable role by acting as counselors for smoking cessation, proper nutrition, and stress reduction practices.

Furthermore, clinicians should be able to identify when a patient should see their dentist or require referral to a periodontal specialist for them to receive rapid, appropriate care. A major complication of NP is tooth loss, which can greatly impact a patient's well-being. Therefore, an interprofessional approach will allow patients affected by NP to have improved outcomes.


References

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