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Dentistry

Cite as: Archiv EuroMedica. 2026. 16; 4. DOI 10.35630/2026/16/Iss.4.29

Received 12 May 2026;
Accepted 15 July 2026;
Published 2 August 2026

THE ROLE OF THE ORAL MICROBIOME IN POST-EXTRACTION SOCKET HEALING AND THE RISK OF ALVEOLITIS SICCA: A NARRATIVE REVIEW

Katarzyna Raczek1 orcid id logo, Justyna Polko2 orcid id logo,
Zuzanna Jeziorska2 orcid id logo, Izabela Migdał2 email orcid id logo,
Bartosz Szymajda2 orcid id logo, Maja Witek3 orcid id logo,
Zuzanna Galicka2 orcid id logo, Jakub Artur Czapkiewicz2 orcid id logo,
Weronika Kwaśnica4 orcid id logo, Tomasz Horodniczy5 orcid id logo

1 Wroclaw Medical University, Wroclaw, Poland
2 Medical University of Silesia in Katowice, Poland
3 Medical University of Warsaw, Poland
4 Poznan University of Medical Sciences, Poznan, Poland
5 Ortho.pl Dental Office, Wroclaw, Poland

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  izabela.migdal14@gmail.com

ABSTRACT

Background

Post-extraction socket healing occurs in a wound that is continuously exposed to saliva, dental plaque and periodontal biofilms. Although alveolitis sicca has traditionally been interpreted mainly as premature clot loss, recent culture-independent studies indicate that the preoperative and early postoperative oral microbiome may influence clot stability, local inflammation and symptom persistence.

Aims

This narrative review aimed to synthesize current evidence on the relationship between oral microbiota composition, socket healing and alveolitis sicca, with emphasis on bacterial taxa, modifiable risk factors and clinically relevant preventive strategies.

Methods

PubMed, Scopus and Web of Science were searched, with the last literature search conducted on 8 July 2026, for studies on oral microbiome, alveolar osteitis, dry socket, tooth extraction, third molar surgery, biofilm, 16S rRNA sequencing, antiseptics and antibiotics. Forty sources were included after thematic selection.

Results

Uneventful healing was consistently associated with a commensal-rich profile dominated by Streptococcus, Actinomyces, Veillonella, Neisseria and Rothia. In contrast, dry socket and high-risk states were associated with enrichment of anaerobic and periodontal taxa, particularly Prevotella, Fusobacterium, Treponema and Fretibacterium, together with a relative reduction of Neisseria and Rothia. Newer evidence supports microbiome-informed risk assessment but does not justify routine antibiotic prophylaxis in healthy patients.

Conclusions

Alveolitis sicca should be considered a biofilm-modulated postoperative complication in which surgical trauma, clot instability, host response and oral dysbiosis interact. Prevention should combine atraumatic surgery, periodontal optimization, selective antiseptic use, irrigation and antibiotic stewardship.

Keywords: oral microbiome; oral microbiota; alveolar osteitis; dry socket; alveolitis sicca; extraction socket; biofilm; third molars; 16S rRNA sequencing; antibiotic stewardship.

INTRODUCTION

The oral cavity is one of the most densely colonized microbial ecosystems of the human body. Molecular surveys and curated oral microbiome databases show that hundreds of bacterial taxa inhabit tooth surfaces, gingival crevices, the tongue, mucosal surfaces and saliva, and that each habitat maintains a partly distinct microbial community [1,2,22-25]. In health, this ecosystem is not sterile, but stable. Early colonizers such as streptococci and Actinomyces spp. support biofilm maturation, while commensal Neisseria, Rothia and Veillonella participate in metabolic cross-feeding and ecological resistance against pathogens [1,2,22-25].

This ecological perspective is clinically important because post-extraction healing does not occur in a microbially neutral field. Saliva carries organisms from supragingival plaque, periodontal pockets, the tongue and mucosal surfaces into the socket, whereas the remaining tooth surfaces may act as reservoirs for recolonization. Therefore, the microbiological status before surgery may partly determine the early wound environment. A commensal-rich community may support ecological stability, while a community dominated by anaerobic proteolytic organisms may increase exposure to enzymes, volatile metabolites and inflammatory stimuli. For this reason, oral hygiene, periodontal inflammation and local plaque control should be considered not merely general dental variables, but biologically plausible determinants of the extraction wound microbiome [1,2,22-25].

Tooth extraction abruptly converts a protected tooth-bearing site into an open osteomucosal wound. The extraction socket is filled by a blood clot, then infiltrated by inflammatory cells, fibroblasts, endothelial cells and osteogenic precursors before being remodeled into woven and then lamellar bone [3,21]. This sequence depends on clot stability, adequate vascularization and controlled inflammation. However, the socket is never isolated from the oral environment. It is continuously bathed in saliva and exposed to plaque-derived biofilm, gingival crevicular fluid, food debris and bacterial metabolites. The microbial community that contacts the clot and socket wall can therefore influence fibrinolysis, inflammatory tone, epithelial closure and early bone remodeling [3,18,21].

The blood clot has a dual function in this setting. Mechanically, it covers the socket wall and provides a provisional matrix for cellular migration. Biologically, it concentrates platelets, fibrin, inflammatory mediators and serum proteins that regulate early repair. If the clot is prematurely degraded or persistently colonized by a dysbiotic biofilm, the socket may remain in a prolonged inflammatory phase. This does not mean that bacteria alone cause AO, but it supports a model in which microbial products intensify fibrinolysis, nociception and delayed granulation tissue formation in susceptible patients. Such a model helps reconcile the traditional fibrinolytic theory with newer microbiome findings [3,4,6,18,21].

Alveolitis sicca, also termed dry socket or alveolar osteitis (AO), is one of the most painful early complications of extraction. It is typically characterized by severe postoperative pain, partial or complete disintegration of the clot, exposed alveolar bone and delayed socket healing [4,7,26]. Reported incidence varies widely because case definitions, extraction types and follow-up periods differ. In routine extractions, newer observational data confirm a generally low frequency, whereas systematic reviews of impacted mandibular third molar surgery show substantially higher rates [26,28,29]. Smoking, traumatic extraction, mandibular molars, pericoronitis, poor oral hygiene and active periodontal disease are repeatedly identified as clinically relevant risk factors [7,8,26,28,29].

For many years, AO was explained primarily by local fibrinolysis and mechanical clot loss. This explanation remains important, but it is incomplete. Culture-based and molecular studies have repeatedly identified anaerobic periodontal bacteria in dry sockets, while high-throughput 16S rRNA sequencing has shown that patients who develop AO may already have a dysbiotic salivary profile before extraction [4-6]. This observation reframes AO as a complication in which surgical trauma, host immune response and microbiological ecology interact. The scientific gap is therefore not whether bacteria are present, but which microbial patterns are most relevant, how they change during healing, and how this knowledge should guide prevention without encouraging unnecessary antimicrobial use.

The clinical significance of this gap is substantial. AO is usually not life-threatening, but it causes severe pain, repeated postoperative visits, additional irrigation or dressing procedures, delayed recovery and patient dissatisfaction. Because its pathogenesis is multifactorial, prevention based on one isolated measure is unlikely to be universally effective. A narrative synthesis is therefore appropriate for integrating mechanistic microbiology, clinical epidemiology and pragmatic oral surgery measures. The central question is how to reduce the dysbiotic burden around the socket while avoiding unnecessary systemic antibiotic exposure.

The aim of this narrative review is to critically synthesize current evidence on the role of the oral microbiome in post-extraction socket healing and the risk of alveolitis sicca. The review addresses four research questions: (1) which microbial communities are associated with uncomplicated socket healing; (2) which bacterial taxa and ecological shifts are associated with AO; (3) how patient-related and procedure-related risk factors may act through oral dysbiosis; and (4) which preventive interventions can modulate the socket microenvironment while preserving antibiotic stewardship.

METHODS

This article is a narrative review designed to provide an analytical synthesis of published evidence rather than to estimate a pooled effect size. PubMed, Scopus and Web of Science were searched from database inception to the last literature search date, 8 July 2026. The search strategy, eligibility criteria and thematic selection process were defined to improve transparency, while interpretation focused on biologically and clinically coherent patterns across microbiological, surgical and preventive literature.

The exact final search strings were as follows. PubMed: (("oral microbiome"[Title/Abstract] OR "oral microbiota"[Title/Abstract] OR "salivary microbiota"[Title/Abstract] OR biofilm[Title/Abstract] OR "16S rRNA"[Title/Abstract]) AND ("alveolar osteitis"[Title/Abstract] OR "dry socket"[Title/Abstract] OR "alveolitis sicca"[Title/Abstract] OR "tooth extraction"[Title/Abstract] OR "third molar surgery"[Title/Abstract] OR "extraction socket healing"[Title/Abstract])) OR (("alveolar osteitis"[Title/Abstract] OR "dry socket"[Title/Abstract]) AND (chlorhexidine[Title/Abstract] OR amoxicillin[Title/Abstract] OR "antibiotic prophylaxis"[Title/Abstract] OR "socket irrigation"[Title/Abstract] OR periodontitis[Title/Abstract] OR pericoronitis[Title/Abstract] OR Prevotella[Title/Abstract] OR Fusobacterium[Title/Abstract] OR Treponema[Title/Abstract] OR Fretibacterium[Title/Abstract])).

Scopus: TITLE-ABS-KEY((("oral microbiome" OR "oral microbiota" OR "salivary microbiota" OR biofilm OR "16S rRNA") AND ("alveolar osteitis" OR "dry socket" OR "alveolitis sicca" OR "tooth extraction" OR "third molar surgery" OR "extraction socket healing")) OR (("alveolar osteitis" OR "dry socket") AND (chlorhexidine OR amoxicillin OR "antibiotic prophylaxis" OR "socket irrigation" OR periodontitis OR pericoronitis OR Prevotella OR Fusobacterium OR Treponema OR Fretibacterium))). Web of Science: TS=((("oral microbiome" OR "oral microbiota" OR "salivary microbiota" OR biofilm OR "16S rRNA") AND ("alveolar osteitis" OR "dry socket" OR "alveolitis sicca" OR "tooth extraction" OR "third molar surgery" OR "extraction socket healing")) OR (("alveolar osteitis" OR "dry socket") AND (chlorhexidine OR amoxicillin OR "antibiotic prophylaxis" OR "socket irrigation" OR periodontitis OR pericoronitis OR Prevotella OR Fusobacterium OR Treponema OR Fretibacterium))).

The search emphasized recent publications where available, especially studies published after 2019, but older foundational studies were retained when they provided essential microbiological definitions, classical periodontal complexes or long-term observations not replaced by newer work. Records were screened thematically in three stages: first for relevance to oral microbial ecology and biofilm behavior; second for direct relevance to extraction wounds, third molar surgery, AO or postoperative infection; and third for clinical applicability of prevention studies, including whether the intervention targeted local biofilm control, systemic antibiotics or postoperative socket care.

Studies were eligible for inclusion when they were reviews, systematic or scoping reviews, observational studies, randomized or interventional clinical studies, culture-based or sequencing-based microbiological studies, or mechanistic studies with clear relevance to human oral wound healing, and when they addressed at least one of the following: oral microbial ecology, biofilm biology, extraction socket healing, microbiology of AO, clinical risk factors for AO, microbiota changes after oral surgery, antiseptic or antibiotic effects on oral microbiota, or interventions relevant to socket healing. Exclusion criteria were: lack of direct relevance to extraction wounds, AO or oral microbial ecology; non-human experimental work not interpretable for oral healing mechanisms; papers focused on unrelated oral or systemic diseases without extraction-related outcomes; duplicate publications; inaccessible bibliographic data or full text; and sources without sufficient methodological or clinical value for the aims of the review. Forty sources were included in the final synthesis. The reference list was checked to remove duplicates and to provide DOI links wherever available.

RESULTS

Evidence base

The final synthesis included 40 sources selected for direct relevance to oral microbial ecology, extraction socket healing, alveolitis sicca, risk factors, preventive interventions and antibiotic stewardship. The evidence base combined narrative and systematic reviews, observational clinical studies, microbiome sequencing studies, randomized or interventional trials, and mechanistic studies relevant to host-biofilm interactions. The selected literature allowed the topic to be analyzed at three complementary levels: microbial community composition, clinical risk stratification and practical prevention in oral surgery.

The included studies were heterogeneous in design and methodology, which is expected in a narrative review of a clinically complex complication. Culture-based studies were useful for identifying anaerobic organisms historically associated with dry socket, whereas sequencing studies provided broader community-level profiles. Clinical studies supplied data on incidence and risk factors, but often differed in diagnostic criteria, extraction difficulty, smoking definitions and postoperative follow-up. Preventive studies evaluated local antiseptics, irrigation, dressings or antibiotics and therefore addressed different points in the causal pathway. For this reason, results are presented by thematic domain rather than as a pooled quantitative estimate.

Microbiota in health and uncomplicated socket healing

Healthy oral communities are site-specific and functionally organized. Tooth-associated biofilms and gingival habitats are enriched in organisms adapted to adhesion and coaggregation, whereas saliva functions as a transport medium that reflects multiple oral niches [22-25]. In the context of extraction, a commensal-rich environment is characterized by Streptococcus sanguinis, S. mitis, S. gordonii, Actinomyces naeslundii, Veillonella parvula, Neisseria spp. and Rothia spp. [1,2,22-25]. These taxa are not necessarily "protective" as isolated organisms, but in ecological context they indicate a balanced community with lower anaerobic inflammatory burden.

A commensal-dominated profile should not be interpreted as the absence of bacteria. Rather, it reflects an ecological balance in which early colonizers and health-associated taxa limit overgrowth of proteolytic anaerobes. Streptococci and Actinomyces participate in early adhesion and matrix formation, Veillonella uses lactate produced by other organisms, and Neisseria and Rothia are often associated with nitrate reduction and metabolic functions considered compatible with oral health. In a healing socket, this type of community may reduce the probability of sustained anaerobic inflammation and may facilitate the transition from the initial inflammatory phase to granulation tissue formation [1,2,22-25,36].

The biological sequence of healing supports this interpretation. In the first hours and days after extraction, the clot provides a provisional matrix. Neutrophils and macrophages remove tissue debris and bacterial products; fibroblasts, endothelial cells and osteogenic progenitors subsequently organize granulation tissue and vascular ingrowth [3,21]. Excessive bacterial challenge may amplify the early inflammatory phase, whereas a stable commensal-dominated biofilm may allow inflammation to remain self-limited. This is clinically important because AO usually becomes symptomatic during the period in which clot organization and early granulation tissue formation should be progressing.

Dysbiosis and microbial signatures of alveolitis sicca

Culture-based studies and systematic reviews show that dry sockets are frequently colonized by anaerobic organisms associated with periodontal disease, including Prevotella, Fusobacterium, Porphyromonas, Actinomyces and Treponema [4]. No single organism is sufficient to explain AO; instead, the evidence supports a polymicrobial biofilm model. In sequencing-based work, Shen et al. found that dry sockets displayed greater microbial diversity and a stronger anaerobic signature than normally healing sockets. Prevotella, Fusobacterium, Treponema and Fretibacterium were enriched in AO, whereas Streptococcus, Rothia and Neisseria were more prominent in uncomplicated healing [6].

The taxa repeatedly associated with AO have biological properties that make their presence plausible rather than incidental. Prevotella and Fusobacterium species are common in periodontal and odontogenic infections and are adapted to anaerobic, protein-rich environments. Fusobacterium nucleatum also acts as a bridging organism in complex biofilms, helping connect early and late colonizers. Treponema and Fretibacterium are frequently linked with deeper dysbiotic periodontal communities and inflammatory tissue destruction. Their enrichment in painful sockets is therefore consistent with a shift toward a mature anaerobic biofilm rather than a simple contamination of the wound surface [2,4,6,34-38].

The prospective study by Wu et al. is particularly important because it examined saliva and socket samples over time. Patients who later developed dry socket already showed higher salivary proportions of Prevotella and Fusobacterium before extraction, while controls had greater relative abundance of Neisseria and Rothia [5]. Around postoperative day 3, the period that typically corresponds to peak pain, AO was associated with increased Treponema and Fretibacterium. By approximately day 7, Haemophilus and Megasphaera were more strongly associated with uneventful healing, whereas the dysbiotic profile persisted in AO [5]. A predictive model based on preoperative salivary microbiota achieved approximately 75% accuracy for predicting uncomplicated healing [5].

Table 1 summarizes the main microbial patterns described across the reviewed evidence and places them in the clinical sequence of extraction healing.

Table 1. Microbial patterns associated with uneventful healing and alveolitis sicca as reported in the reviewed literature.

Clinical context Dominant/enriched taxa Reduced taxa or missing balance Interpretive significance
Commensal-rich oral state Streptococcus, Actinomyces, Veillonella, Neisseria, Rothia Lower burden of anaerobic periodontal taxa Ecological profile compatible with controlled early inflammation and uncomplicated clot organization in health-associated oral communities [1,2,22-25,36].
Preoperative high-risk salivary profile Prevotella, Fusobacterium Neisseria, Rothia Dysbiotic signature detectable before extraction in patients who subsequently develop AO [5].
Symptomatic dry socket around day 3 Treponema, Fretibacterium, Prevotella, Fusobacterium Commensal Neisseria and Rothia Profile corresponds to peak pain and persistent inflammatory biofilm described in AO-associated observational and sequencing studies [4-6].
Late uncomplicated healing around day 7 Haemophilus, Megasphaera, commensal streptococci Periodontal pathogens Suggests transition toward ecological recovery and wound stabilization during uneventful healing [5].

Note: The microbial profiles shown in the table represent associations reported in the reviewed literature and should not be interpreted as proven causal markers or validated diagnostic biomarkers of alveolitis sicca. Because most available data are observational and based on relative abundance, the taxa should be interpreted in ecological and clinical context rather than as isolated causal agents [4-6].

Relationship with periodontal and odontogenic reservoirs

Periodontal pockets, pericoronal tissues and odontogenic inflammatory lesions are plausible reservoirs of the anaerobic taxa repeatedly associated with AO. Advanced periodontitis is characterized by enrichment of Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola, Fusobacterium nucleatum, Prevotella intermedia and Aggregatibacter actinomycetemcomitans [2,9,10]. De Waal et al. demonstrated that full-mouth extraction and prosthetic rehabilitation led to disappearance or major reduction of A. actinomycetemcomitans and P. gingivalis, emphasizing that teeth with diseased periodontal tissues can maintain pathogens in the oral cavity [9].

The reservoir concept has practical consequences. A patient with untreated periodontitis or pericoronitis may carry a high microbial load before the surgical trauma occurs. Once the tooth is removed, the socket receives bacteria from adjacent plaque, inflamed soft tissues and saliva. The study showing marked reduction of P. gingivalis and A. actinomycetemcomitans after full-mouth extraction supports the idea that diseased teeth and periodontal pockets can sustain pathogens within the mouth [9]. Similarly, odontogenic lesions and pericoronal pockets contain mixed anaerobic communities that can influence early postoperative symptoms [10,19,20].

Pericoronitis and partially erupted third molars are especially relevant for AO risk because they create sheltered niches that retain biofilm near the surgical field. Todorić et al. showed that pericoronary microbiota composition was associated with postoperative recovery after third molar alveotomy, including pain and swelling [19]. Older microbiological work on partly erupted third molars also supports the concept that removing such teeth changes subgingival microbial reservoirs [20]. These findings justify preoperative evaluation of periodontal and pericoronal inflammation as part of AO risk assessment, rather than treating dry socket as an entirely unpredictable postoperative event.

Patient and surgical risk factors interpreted through the microbiome

Smoking is one of the most consistent clinical risk factors for AO. It can impair tissue perfusion, alter neutrophil function, increase local fibrinolysis and promote anaerobic ecological shifts in oral biofilm [7,26]. Traumatic extraction and mandibular third molar surgery increase tissue injury and may expose more bone marrow activators, while also creating larger surfaces for microbial colonization [7,26,29]. Medically complex patients may have altered immune responses and higher baseline inflammatory burden; Boyer et al. showed that post-extraction infection and dry socket in medically complex patients were associated with both patient factors and features of the procedure in the absence of routine antibiotic prophylaxis [8].

Risk factors should be interpreted as interacting variables rather than as independent isolated causes. Smoking may reduce tissue oxygenation and impair neutrophil function while also favoring anaerobic ecological conditions. Difficult mandibular third molar surgery increases tissue trauma, operative time and inflammatory burden, which may amplify the effect of dysbiotic biofilm. Poor oral hygiene increases plaque reservoirs, while pericoronitis provides a local anaerobic niche before extraction. Systemic diseases may influence wound vascularity, immune regulation and microbial resilience. These mechanisms explain why AO risk is highest when several factors coincide in the same patient [7,8,19,26,28,29,33].

Contemporary epidemiological studies reinforce this multifactorial model. Cardoso et al. reported risk factors for dry socket after routine dental extraction, while Kostares et al. quantified fibrinolytic alveolitis after impacted mandibular third molar extraction in a systematic review and meta-analysis [28,29]. These studies do not replace microbiome data, but they help identify where microbiome-mediated mechanisms are most likely to matter: high-risk sockets, high-risk patients, inflamed periodontal/pericoronal tissues and procedures with greater tissue trauma.

Preventive interventions and microbiota modulation

Chlorhexidine remains the most studied antiseptic for AO prevention. Systematic reviews and meta-analyses indicate that chlorhexidine, particularly gel formulations placed after third molar extraction, can reduce the incidence of AO [7,27,31,32]. However, antisepsis is not biologically neutral. Das Neves et al. observed Firmicutes dysbiosis after chlorhexidine prophylaxis in healthy patients undergoing impacted lower third molar extraction, and Menon et al. showed that oral surgery with or without amoxicillin can have measurable longer-term effects on the oral microbiome [11,12]. Therefore, chlorhexidine should be used selectively, for a defined short period, and preferably in patients whose risk profile justifies it.

Local interventions are attractive because they address the socket environment without exposing the whole oral and gut microbiome to systemic antibiotics. Chlorhexidine can reduce bacterial load and has evidence of benefit in third molar surgery, but repeated or indiscriminate use may disturb health-associated taxa and should be limited to defined clinical indications. Socket irrigation removes loose debris and disrupts early biofilm accumulation mechanically. In contrast, systemic antibiotic prophylaxis may reduce selected postoperative complications in some high-risk surgical settings, but the absolute benefit in healthy patients must be weighed against adverse reactions, selection of resistance and disruption of commensal communities [10-13,27,30-32,39,40].

Antibiotic prophylaxis is more controversial. Network meta-analysis suggests that antibiotics may reduce dry socket and surgical site infection after lower third molar extraction, but this benefit must be balanced against adverse effects, antimicrobial resistance and microbiome disruption [30,39,40]. In otherwise healthy patients, routine systemic antibiotics solely to prevent AO are difficult to justify. Antibiotics are more defensible when systemic risk, spreading infection, immunosuppression or a clear surgical indication exists. Socket irrigation provides a low-risk mechanical strategy. Ghaeminia et al. demonstrated that postoperative irrigation with drinking tap water reduced inflammatory complications after third molar removal [13]. Mechanistically, irrigation reduces food debris and loose biofilm accumulation without imposing strong antimicrobial selection pressure.

DISCUSSION

The revised evidence supports a shift from a purely mechanical model of AO toward an integrated host-wound-microbiome model. Mechanical clot loss remains clinically visible, but it may be the downstream manifestation of local fibrinolysis, tissue trauma, inflammation and microbial enzymatic activity. The repeated enrichment of anaerobic periodontal taxa in AO suggests that the socket environment can be pushed toward a community capable of sustaining inflammation, producing proteolytic enzymes and interfering with normal clot organization [4-6].

This integrated model is compatible with everyday clinical observations. Many sockets heal normally despite bacterial exposure, indicating that bacterial presence alone is insufficient. Conversely, some sockets develop severe pain despite apparently adequate clot formation immediately after surgery, suggesting that later biological events, including microbial succession and host inflammatory response, are relevant. The most reasonable interpretation is that AO develops when clot instability, local trauma, anaerobic biofilm and an unfavorable host response reinforce each other. This interpretation avoids replacing a mechanical theory with a purely microbiological theory and instead treats AO as a wound ecology disorder.

The most clinically useful insight is that microbial risk is not confined to the socket after the clot has been lost. Wu et al. showed that salivary differences were present before extraction [5]. This implies that saliva may function as an accessible proxy for oral ecological risk. Although a 75% predictive accuracy is not sufficient for clinical decision-making on its own, it supports future development of risk scores combining microbiological, periodontal, smoking and surgical variables. Such models could help identify patients who would benefit from intensified preoperative hygiene, periodontal stabilization, targeted antisepsis or structured postoperative irrigation.

The role of periodontal reservoirs is particularly important. The same organisms implicated in periodontitis and odontogenic infections recur in AO-related studies. Fusobacterium nucleatum is a bridging organism that supports biofilm maturation and coaggregation, Prevotella and Porphyromonas spp. contribute proteolytic and inflammatory capacity, and spirochetes such as Treponema denticola are markers of deeper anaerobic dysbiosis [2,4-6,9,10]. Fretibacterium, repeatedly detected in molecular periodontal studies, may be a useful marker of advanced dysbiotic communities, although its direct causal contribution to AO remains unclear [5,6].

The therapeutic implications must be interpreted cautiously. Chlorhexidine has evidence of effectiveness, but broad suppression of oral flora may also disturb commensal communities [12,31,32]. Antibiotics may reduce postoperative complications in selected lower third molar settings, but antimicrobial stewardship requires avoiding routine use in low-risk healthy patients [30,39,40]. The microbiome perspective therefore does not support more indiscriminate antimicrobial therapy. On the contrary, it supports more precise preventive care: reduce modifiable dysbiosis before surgery, minimize tissue trauma, mechanically control debris and biofilm after surgery, and reserve systemic antimicrobials for clearly defined indications.

Antibiotic stewardship is particularly important in dentistry because prophylactic prescriptions are common and not always supported by patient-specific risk assessment. The reviewed literature supports selective prescribing for medically compromised patients, spreading infection, or clearly elevated surgical risk, rather than routine antibiotics for all extractions. For many patients, the safer preventive emphasis is local: preoperative plaque control, management of pericoronitis or periodontal inflammation when feasible, atraumatic surgical technique, avoidance of smoking, patient education and gentle socket irrigation when indicated. This strategy is consistent with microbiome preservation and with the principle that commensal communities may contribute to healing.

A practical preventive pathway can be proposed. Before extraction, clinicians should document smoking, oral hygiene, periodontal status, active pericoronitis, history of AO, systemic disease and expected surgical difficulty. When feasible, acute periodontal or pericoronal inflammation should be controlled before elective extraction. During surgery, atraumatic technique, adequate irrigation and careful debridement reduce the biological burden placed on the clot. After surgery, patient instructions should emphasize smoking cessation, gentle hygiene, avoidance of vigorous early rinsing and, in selected cases, controlled socket irrigation from the appropriate postoperative time point. Short-term chlorhexidine may be considered in high-risk third molar cases, whereas systemic antibiotics should be individualized rather than routine.

After surgery, follow-up should distinguish expected postoperative discomfort from the characteristic pattern of AO: pain that intensifies after an initial interval, exposed bone or disintegrated clot, malodor and delayed granulation. Treatment remains primarily local and symptomatic. Irrigation, removal of debris, analgesia and temporary medicated dressings may reduce pain, but repeated aggressive curettage can further traumatize the socket. From a microbiome perspective, the goal is not sterilization of the wound, which is impossible in the mouth, but reduction of excessive anaerobic biofilm and restoration of conditions compatible with granulation tissue and epithelial coverage [3,7,27,32].

Limitations

This narrative review has several limitations. The evidence base is heterogeneous, and most microbiome studies are observational, use small samples and report relative rather than absolute microbial abundance. Sequencing identifies microbial DNA but does not always prove viability, metabolic activity or causality. Therefore, microbial profiles associated with AO should be interpreted as ecological associations and hypothesis-generating signals, not as validated causal biomarkers or diagnostic markers.

Different sampling sites, extraction types, diagnostic criteria and postoperative time points reduce comparability across studies. Many clinical trials of prevention focus on clinical AO incidence without microbiome endpoints, while microbiome studies often lack standardized pain, clot and healing assessments. In addition, because this was a narrative review, no formal risk-of-bias assessment or meta-analysis was performed. Future studies should integrate longitudinal 16S rRNA or metagenomic sequencing with clinical scoring, smoking status, periodontal indices, extraction difficulty and standardized definitions of AO. Ideally, future trials should test whether microbiome-informed prevention improves outcomes compared with conventional risk-factor-based care.

CONCLUSIONS

Alveolitis sicca is best understood as a multifactorial postoperative complication in which clot instability, surgical trauma, host inflammatory response and oral dysbiosis interact. The microbial pattern most consistently associated with increased risk involves enrichment of anaerobic periodontal taxa, particularly Prevotella, Fusobacterium, Treponema and Fretibacterium, together with reduced relative abundance of commensal Neisseria and Rothia. This pattern may be detectable before extraction and may persist during the symptomatic phase of AO.

Clinical prevention should therefore move beyond clot preservation alone. The most coherent strategy is to optimize periodontal and pericoronal health before elective extraction, reduce surgical trauma, control local debris and biofilm mechanically, use chlorhexidine selectively and briefly, and prescribe antibiotics only when patient risk or infection-related indications justify them. Microbiome-based risk prediction is promising but not yet ready to replace clinical judgment. Further prospective studies combining microbiome analysis with standardized clinical endpoints are needed to convert microbial signatures into practical protocols for preventing and managing dry socket.

DISCLOSURE

Author Contributions

Conceptualization: Katarzyna Raczek, Izabela Migdał, Maja Witek.

Methodology: Katarzyna Raczek, Izabela Migdał, Justyna Polko, Zuzanna Jeziorska.

Data collection and literature selection: all authors.

Analysis and interpretation: Katarzyna Raczek, Bartosz Szymajda, Jakub Artur Czapkiewicz.

Writing original draft: Katarzyna Raczek, Jakub Artur Czapkiewicz, Maja Witek, Zuzanna Galicka.

Writing review and editing: Jakub Artur Czapkiewicz, Zuzanna Galicka, Maja Witek.

Supervision: Katarzyna Raczek, Weronika Kwaśnica, Tomasz Horodniczy.

Final approval of the manuscript: Weronika Kwaśnica, Tomasz Horodniczy, Maja Witek, Izabela Migdał.

Funding

No external funding was received for this manuscript.

Conflict of Interest

The authors declare no conflict of interest.

Use of Artificial Intelligence

AI was used only as an auxiliary tool to support literature search and language editing. All references, scientific interpretation, conclusions and the final version of the manuscript were independently checked and approved by the authors. The authors independently verified the scientific content, references, interpretation of evidence and final wording, and accept full responsibility for the submitted manuscript.

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