Alveolar Osteitis

Etiology

Despite the longstanding awareness of this condition, the etiology of alveolar osteitis is not fully understood. It is most commonly noted as a premature fibrinolytic breakdown of the early platelet clot, exposing the underlying bone in the extraction socket.

Birn first hypothesized in 1973 that AO develops from a complete absence of a blood clot or development of an initial clot that is successively lysed soon after creation.[1] Breakdown of the clot results from the plasminogen pathway activation, but the trigger is unknown. Either physiologic or non-physiologic mediators produce the activator substance. Many specific factors have been investigated and debated. Although there is still a poor understanding, all have a promotor effect on clot lysis leading to fibrinolysis.[4]

The immune system's response to tooth extraction is comparable to any other tissue trauma. The inflammatory response in the alveolus involves pro-and anti-inflammatory cytokines. Studies have primarily focused on the effects of IL-6. IL-6 has a dual role in bone formation and bone resorption, which could contribute to the fibrinolysis in alveolar osteitis.[5] 

Investigating biomarkers such as tumor necrosis factor-alpha (TNF-a), osteocalcin, and runt-related transcription factor 2 has also been suggested. These physiologic mediators could help create an enhanced understanding of the pathologic process of alveolar osteitis.[6]

Focal fibrinolytic activity influenced by bacteria has also been investigated. The microbiota in alveolar osteitis was significantly different from the patients who presented without postoperative complications. Prevotella, Fusobacterium, Parvimonas, and Peptostreptococcus were the most common bacteria detected in patients with alveolar osteitis in one systematic review.[7] 

Another found Treponema denticola, a known red-complex periodontal pathogen, could be a likely culprit in the pathogenesis of AO. For a bacteria to be a causative agent of alveolar osteitis, it needs to be capable of fibrinolysis but must not induce swelling, purulence, or erythema. They must also be isolated from a post-extraction socket and conducive to proliferation. These bacteria thrive with poor oral hygiene. The bacteria are limited to the bone's surface, and thus alveolar osteitis is not categorized as a true infectious process.

Epidemiology

The incidence of alveolar osteitis varies significantly in current literature, reported between 0.5% and 68%. Studies with larger patient populations trend towards a lower incidence, commonly less than 5%.[1][2][5] Multiple systematic reviews found that around 30% of mandibular third molar extractions develop alveolar osteitis.[8]

There is a significantly higher incidence of alveolar osteitis in lower third molars than in all other dental extraction sites combined. The alveolus of posterior mandibular teeth, specifically the third molars, has greater vascularity when compared to the anterior teeth. This finding contradicts the belief that alveolar osteitis is triggered by a lack of blood supply, which is the most common hypothesis to explain why alveolar osteitis is much less common in the maxilla.[4]

Although there is conflicting data, many studies found that patient age and female gender increased the incidence of alveolar osteitis. The prevalence was similar worldwide, and there were no documented differences in ethnicity.[2][5][9] 

Many studies show a statistically significant increase in alveolar osteitis in female patients taking oral contraceptive pills or mid-menstrual cycle, explaining the higher incidence of alveolar osteitis in females. The increased incidence of alveolar osteitis in patients taking oral contraceptives is likely a result of decreased levels of plasminogen activator inhibitor and increased levels of plasminogen. This results in increased fibrinolysis and supports Birn’s fibrinolytic theory.[2]

Several other risk factors for developing AO have been investigated, including tobacco use, poor oral hygiene, lack of operator experience, flap design, and difficulty of extraction. These factors have support in multiple publications, but the role of most others has not been demonstrated.[2][4]

History and Physical

The cardinal symptom of alveolar osteitis is radiating pain that increases in intensity after tooth extraction. The pain is at, or near, the extraction socket in the trigeminal nerve distribution. It typically occurs between one and five days post-operatively and is unrelieved by analgesics.[4][3] Halitosis is also commonly reported.[1]

Physical examination is unremarkable mainly. Expected postoperative changes, such as erythema and edema, can be anticipated, but there should be no frank signs of infection. Rarely a low-grade fever or regional lymphadenopathy can be noted.[4] 

Vital signs are stable, and the patient is most commonly afebrile. The pain is accompanied by a totally or partially broken down blood clot in the alveolar socket. Exposed bone secondary to this fibrinolysis is the typical clinical presentation but may be difficult to visualize on examination.[3]

Evaluation

An increase in pain intensity a few days after a tooth extraction is the key feature. The absence of a blood clot and moderate to severe pain is pathognomonic of alveolar osteitis, and additional laboratory and radiographic studies are not required. As alveolar osteitis is not an infection but a delayed healing process, no leukocytosis would be expected.

Post-operative imaging, such as a panoramic radiograph, could rule out remaining tooth fragments or bony sequestra. Markers of fibrinolysis have been investigated for risk prediction in cardiovascular disease but are not helpful in a clinical setting with AO.[10]

Treatment / Management

Much of the current discussion regarding AO focuses on treatment strategies, but no consensus protocols have been developed. One systematic review concluded there was insufficient evidence to support any management strategies for established AO.[3] Management focuses on symptom relief rather than any particular disease process.(A1)

The initial management strategy for alveolar osteitis with the most support is intra-alveolar irrigation, which removes necrotic tissue and clot debris and reduces the bacterial load. Intra-alveolar irrigation alone may not relieve pain but should complement the other outlined strategies. It is commonly included in studies as an early measure, and curettage of the dry socket is not recommended as it will expose the bone further.

Topical local anesthetic gels can relieve pain shortly after irrigation, and long-acting local anesthetics can provide immediate symptom relief. Local anesthetics can be supplemented with oral analgesics, primarily non-steroidal anti-inflammatory drugs (NSAIDs). 

Multiple interventions include placing a medicated dressing into the extraction socket at the time of surgery or post-operatively. Some common options are zinc oxide eugenol or other obtundent dressings that include compounds with analgesic or antibacterial action. 

Multiple studies support the success of these interventions, but many dressings have to be removed from the alveolus to prevent foreign body reactions. They also slow the healing process.[8] Hyaluronic acid placement after irrigation has also shown success in reducing pain and inflammation.[2](A1)

Rinsing with chlorhexidine mouthwashes and placing chlorhexidine gels into the extraction socket have also shown treatment success. Many studies explore chlorhexidine as a preventive measure, but resolution after AO development has also been investigated.[8][11] (A1)

Although some studies show AO can be successfully managed by chlorhexidine, there is not as much support for treatment as there is for prevention. There is still insufficient evidence to recommend chlorhexidine as a treatment to relieve established AO.

Platelet-rich fibrin (PRF) has also been investigated. One study found that pain reduction was similar to irrigation alone, but the soft tissue healing was improved. PRF is more commonly used as a preventive measure, and the efficacy of using it as a treatment is debatable.

Recent evidence suggests that phototherapy, specifically low-level laser therapy (LLLT), has a role in symptom management. It is easy to use, quick, relatively safe, and financially advantageous. The results are comparable to all the alternative management strategies above, and many studies find the results superior. Photobiomodulation therapy has been shown to have a higher ability to decrease pain and is considered by some to be the most effective intervention available.[12] (A1)

Low-level laser therapy (LLLT) is a newer technology, and further evaluation is needed, but it could become a mainstay of treatment in the future.

Differential Diagnosis

Alveolar osteitis can be assumed when a patient presents within the first week after extractions with severe pain. Depending on the severity of the pain, it could be classified as normal post-operative discomfort or be a result of food debris impaction.

Treatment with intra-alveolar irrigation is indicated with any of the above diagnoses. Some sources contend that pain beyond a week from surgery is not consistent with alveolar osteitis, and others state that persistent pain longer than three weeks necessitates a different diagnosis.[4][1]

The primary differential diagnosis that needs to be considered is an infection, mainly if there are signs of disease beyond the extraction socket. Symptoms consistent with alveolar osteitis presenting or persisting weeks after surgery are concerning for acute osteomyelitis, subperiosteal infection, or bony sequestra formation. Based on the clinical evaluation of the patient, it may be appropriate to obtain a panoramic radiograph to evaluate healing.

Prognosis

Since alveolar osteitis is self-limiting, the prognosis is excellent. If the diagnosis is correct, it will resolve within days after initiating treatment.[4] Even without treatment, the course will be short, and it does not cause any long-term morbidity.[1]

Complications

There is no evidence that alveolar osteitis can result in additional complications. After resolution, the extraction socket heals as it does in patients who did not experience AO. There is no peer-reviewed literature correlating it with an increased risk of other complications associated with dental extractions.[1]

Chlorhexidine usage, the prevention strategy with the most support, does have some rare but serious adverse effects. The primary concern with chlorhexidine is hypersensitivity reactions, and there have been multiple documented cases of minor adverse reactions after irrigation of an AO socket with chlorhexidine mouthwash. 

There are two case reports from the United Kingdom of fatal adverse events related to chlorhexidine used in intra-alveolar irrigation secondary to hypersensitivity reactions. The dental practitioners who prescribe or administer this medication should be aware of potential hypersensitivity and educate their patients on minor and severe adverse side effects.[8]

Another known complication of alveolar osteitis treatment is possible foreign body reactions. The delivery vehicles of the intra-socket medicaments delay healing and can cause this reaction.[4] This results from granulomatous inflammation and the body's inability to phagocytose foreign materials. Therefore, obtundent dressings should be removed to prevent this from happening. Many authors will discourage the use of topical medicaments for this reason.[8]