Interventions for the prevention of dry socket: an evidence-based update (2024)

Alveolar osteitis is a relatively common complication following dental extractions. General dental practitioners (GDPs)²⁴ should therefore be aware of the effectiveness of available local and systemic interventions for the prevention and treatment this painful and often distressing complication. As outlined in this report, the evidence available in the form of two Cochrane systematic reviews suggests that in terms of prevention: the use of chlorhexidine gel (0.2%) placed into extraction sockets immediately post treatment could help to prevent approximately 60% AO.¹⁰ Furthermore, the authors concluded that there is some evidence that rinsing with chlorhexidine (0.12% and 0.2%) also provides some benefit in preventing dry socket. In terms of treatment for AO: the use of systemic therapy showed that antibiotics might reduce the risk of AO by 38%.¹³

Normal healing socket

It is prudent for the clinician to identify what the appearance of a normal healing socket is in order to realise when healing has become impaired. A significant clinical and histological change occurs following an extraction. Distinctive stages occur between the healing stages, which can be observed both clinically and histologically. It is important to remember that the speed of healing is variable between individuals with significant factors impairing the speed regeneration such as older age,²⁵ compromised medical status (such as diabetes, anaemia)²⁵ or in smokers.²⁶

Figures 2,3,4,5,6,7,8 show the clinical stages of a healing socket. The procedure of extraction inadvertently damages local blood capillaries surrounding the tooth, following which blood fills the socket.²⁷ Furthermore the normal clotting mechanisms of the intrinsic and extrinsic clotting pathways as part of the coagulation cascade²⁸ produces a loose clot (Fig. 3) that fills the socket. Initially platelets are activated and adhere to the site of insult forming a platelet plug; this aims to reduce the blood loss.²⁸ The platelets then retract the clot so that it gradually becomes harder and subsequently shrinks below the level of the soft tissues; this contraction pulls the soft tissue inwards reducing the socket size. This is usually complete within 4 hours and the clot stabilises by fibrin crosslinking.²⁹ This is why avoiding rinsing is essential within the first 24 hours post-extraction as this could destabilise the clot and ultimately expose the socket and impair healing.

Two days later lysis of the clot begins by activation of the fibrinolytic enzyme plasmin. This is done by the conversion of plasminogen to plasmin via the plasminogen activator (PA) system.³⁰ Plasminogen is found primarily within the plasma and is synthesised within the liver.³⁰ This pro-enzyme is activated by the release of tissue-type PA (t-PA), which is found within the walls of the endothelium that lines the blood vessels. This then cleaves a specific peptide bond located within plasminogen pro-enzyme, converting it to the active plasmin.

Within 4 days' time, fibroblasts begin migrating into the blood clot from the socket wall.²⁹ The growth of new capillaries with the migration of fibroblasts into the socket begins the synthesis of granulation tissue depicted in Figure 4. Granulation tissue is a connective tissue matrix comprising mesenchymal cells and infiltrates of leucocytes (macrophages, lymphocytes and neutrophils).³ Phagocytosis of the remnants of the clot by leucocytes (predominantly by macrophages) allows for replacement by granulation tissue. As is seen in Figure 4 the superficial layer of the clot appears white and is in fact porous histologically. This surface layer contains high levels of bacteria such as Staphylococcus aureus, which act like t-PA and activate plasmin, leading to further clot destruction and degradation of the surface fibrin.³¹

A week post-extraction the socket now almost entirely filled with granulation tissue synthesised by fibroblasts as shown in Figure 5. This tissue is soft and has a swollen appearance to it as it contains little collagen. The superficial layers also contain a dense layer of inflammatory cells; as shown in by the slight erythema of the regenerated gingival tissue seen clinically.²⁹ Furthermore early resorption is taking place at the lamina dura by osteoclasts. Between 7 and 10 days early epithelial migration occurs, as can be seen in Figure 5, there is slight contact between the regenerated gingival tissues across the socket.

Figure 6 shows the socket 2 weeks post-operatively. At this stage the socket is now entirely filled by granulation tissue and osteoid, a pre-ossified bone matrix.³ The earliest woven bone trabeculae form on the periphery of the socket^27,32 and also at the apical portion of the socket.³ This can be seen clinically (Fig. 7), with the base of the socket appearing less hollow as these early depositions form much of the contents. However, at this early stage the majority of healing involves the rejection of the original socket wall and the exfoliation of bony fragments.^27,32

Figure 7 shows healing at 1month as the extraction site enters the early intermediate phase. The majority of the socket is now filled with early woven bone,²⁹ however, there is still some fibrous connective tissue with some, albeit very few, inflammatory cells.³³ As can be seen clinically, the regenerated gingival tissue overlying the socket appears far less erythematous than before.

Figure 8 shows healing stage at 6 weeks. Amler's study on clinical and histological stages of the healing socket states that it normally takes 24 to 35 days for total epithelial coverage of the socket.³⁴ The majority of healing now takes place beneath the epithelial surface; with histological samples at this stage showing that the number of osteoblasts reach a peak at this stage.³ The emphasis shifts from bone resorption and epithelial regeneration to bone deposition; usually reaching a peak of bone deposition by 3 months.³⁵

Implications for current practice

The Cochrane reviews reporting on local measures to prevent AO found that 232 patients would have to be treated with a preventive intervention to stop one patient developing AO.¹⁰ Furthermore the Cochrane review on systemic measures (antibiotics) indicated that to prevent one case of AO, between 24 and 250 people would need to receive prophylactic antibiotics.¹³ In addition, the review concluded, 'the size of the benefit is not enough to recommend a routine use of this practice'.¹³

There are measures GDPs can take as an alternative to anti-bacterial prophylaxis to reduce the risk of AO. These include reducing the amount of vaso-constrictive local anaesthetic used, carrying out the extraction with minimal trauma as possible, or advising on smoking cessation.²⁹ Furthermore, identifying patients that are at high risk of developing AO is important. Risk factors include:^29,36,37,38

• Oral contraceptives

• Radiotherapy

• Previous history of AO

• Lower molar extractions

• Smokers

• Female gender

• Osteosclerotic disease (Paget's disease)

• Older age group (above 26)

• Experience of surgeon.

It would be wise for the GDP to take precautions to reduce the risk of AO in this cohort of high-risk patients. As outlined above, simple clinical measures to reduce the risk can be taken, and in those patients who have osteosclerotic disease or are undergoing radiotherapy it is advised these patients are referred to secondary care for treatment under the supervision of a specialist. It is important to remember that if there is any doubt with regards to a patients' medical/dental/drug/social background, then liaising with either the patients' general medical practitioner (GP) or a specialist in secondary care would be a useful source of guidance.

Another consideration when deciding on how to manage AO should be that of antibiotic resistance. Due to the increasing prevalence of bacterial resistance to many common antibiotics, including those used routinely in dentistry, clinicians should think carefully as to whether the risk outweighs the potential benefit. Additionally, thought should be given to the potential for hypersensitivity reactions that can be associated with chlorhexidine and antibiotic prophylaxis. Recent reports have highlighted two cases of death due to anaphylaxis following the use of chlorhexidine in post-extraction tooth sockets.³⁹ The case report concluded that there needs to be an increased awareness of the possibility of anaphylaxis to chlorhexidine-based products; with dentists playing an active role in reporting adverse drug reactions to the British National Formulary (BNF). Furthermore following their analysis of the case reports it was postulated that 'open wounds'³⁹ might increase the likelihood of allergic reactions occurring. Nevertheless, chlorhexidine-based products are widely used in routine dentistry. In fact chlorhexidine gluconate 0.2% accounts for 10.2% of all prescribed drugs by the GDP.⁴⁰ However, considering how routinely chlorhexidine is used in both primary and secondary care, the incidences of hypersensitivity are contextually still very low. Although mounting evidence of hypersensitivity reactions to chlorhexidine will place its routine use into question.

Implications for future research

Currently the majority of studies focus on the development of AO following the removal of third molars, therefore, there is a need for future research into prophylactic interventions for other high risk patients. In addition, all of the studies identified by the Cochrane reviews were conducted in a hospital setting and this is in contrast to the fact that the majority of extractions in the UK are performed in primary and specialist settings. The robustness and applicability of future research would be improved if large studies (prospective randomised controlled trials) were conducted in primary/specialist practice settings. Furthermore, in order to ascertain the most recent trials on the effectiveness of antibiotics or chlorhexidine (CHX) prophylaxis to alveolar osteitis, the search terms used in the Cochrane reviews were re-run. This enabled any recent studies to be highlighted and also analysed. The results showed that no new studies had been published examining the benefits of systemic antibiotic prophylaxis to AO, while only one study had been published on the effectiveness of CHX. This was a double blind split mouth randomised controlled clinical trial, which concluded that 0.2% CHX gel postoperatively can significantly reduce the incidence of AO following third molar extraction.⁴¹