A review of the literature (2024)

Update on dry socket: A review of the literature

TORRES-LAGARES D, SERRERA-FIGALLO MA, ROMERO-RUÍZ MM, INFANTE-COSSÍO P, GARCÍA-CALDERÓN M, GUTIÉRREZ-PÉREZ JL. UPDATE ON DRY SOCKET: A REVIEW OF THE LITERATURE. MED ORAL PATOL ORAL CIR BUCAL 2005;10:77-85.

SUMMARY

Dry socket is a postoperative complication that occurs after adental extraction and has been defined as an inflammation of thealveolus. If this inflammation should surpass the alveolar walls, itwould result in a located osteitis. The frequency of appearance ofdry socket has been reported in a very wide margin, from 1% until70%. It is generally accepted that most dry sockets appear afterextraction of third retained molars, in which the occurrence of thiscomplication is about 20-30% of dental extractions, ten times morethan in the rest of dental extractions.
In this work we review the forms of clinical appearance, the riskfactors related to this affection and the etiopathogenic theoriesthat try to explain its appearance. The treatment management is alsoexamined. Fibrinolitic agents, laundries, antiseptic, and antibioticshave been studied for its prevention, according to the pathogenictheories of dry socket. We analyze and critize the different drugsand their results.
In conclusion from the revised data, we think it is possible todefend a pathogenic model in which the bacterial fibrinolyticmechanisms and the microorganism of the own patient may contribute toproduce the dry socket.

Key words: Dry socket, alveolar osteitis, postextractioncomplications.

CONCEPT

Dry socket is a postoperative complication that occurs after adental extraction. It has been defined in the classic books of OralSurgery as a local inflammation of the alveolus. In case thisinflammation should surpass the alveolar walls, it would result in alocated osteitis.

The first time that this term appeared in the literature was in1896, used by Crawford (1). Ever since many terms have been used assynonyms of dry socket, including painful dry socket, alveolalgia,osteomielitis, fibrinolytic osteitis, alveolar osteitis,osteomielytic postextraction syndrome, fibrinolytic alveolitis andlocated alveolar osteitis. In our opinion, the most appropriate termis the one given by Birn (2), fibrinolytic alveolitis, though it isthe least used one (3).

17 different definitions of dry socket have been reported. Themost recent we have found in the literature defines dry socket as apostoperative pain inside and around the dental alveolus, which isincreased in severity in some moment between the first and the thirdday after a dental extraction, accompanied by a partial or totaldisintegration of the intraalveolar clot sanguine, accompanied or notof halitosis. (3).

We can distinguish among dry sockets that occur in patients thatsuffer some type of hipovascularization condition in the maxillarybone (vascular or hematologic disorders, osteorradionecrosis,osteopetrosis, Paget´s illnes, etc.) and those where thesecondition are not detected, denominated true dry socket in theliterature revised (3,4).

EPIDEMIOLOGY

The frequency of appearance of dry socket has been reported in avery wide margin, from 1% to 70% (3,5). It is generally accepted thatmost dry sockets appear after extraction of third included molars, inwhich the occurrence of this complication is about 20-30% of dentalextractions, ten times more than in the rest of dental extractions(3). According to different authors, the average percentage of drysockets in the group of all tooth extraction is about 3-4% (6).

Such wide margins in figures of dry socket appearance are due tothe differences in diagnostic criteria, in evaluation methods, inmixture of data coming from simple extractions and of retained teeth,as well as to the variability in surgical treatment and postsugicalmanagement. We should distrust those studies showing dry socketspercentages smaller than 1% (for lack of clinical credibility), aswell as those studies showing dry socket percentages greater than 35%(suggesting variables or uncontrolled risk factors, a small number ofpatients, or extreme situations, or important lacks, as we find inthe article published by Simon and Matee (percentage of dry socket of48,7%) (3,7).

Since the aetiology of this affection is not known, the advisedtherapy is prevention. The epidemiologic studies have detecteddifferent risk factors in the development of dry socket: thedifficulty of the dental extraction, the surgeon’s inexperience,the use of oral contraceptives, an inadequate intraoperatoryirrigation, advanced age of patients, female sex, tobacco,inmunosupression, and surgical trauma.

Since we do not know the true causes of dry socket, the way thatthese factors of risk influence in the appearance of the affectionare, by now, theories more or less guessed right, more or lesscorroborated by this epidemiologic studies.

In his studies of 1991 and 1992, Larsen (8-10) did not demonstratethat the difficulty of the extraction and the surgical trauma, forexample, were risk factors. Perhaps the surgical interventionduration is not a good indicator of the difficulty of the extractionor still more important, of the trauma that is taking place. However,most authors agree that the surgeon’s inexperience could berelated to a bigger trauma occurred during the extraction (9). Abigger trauma would produce a delay in the alveolar healing, and itcould provoke a thrombosis of the underlying vessels as well as asmaller resistance to the infection in the alveolar bone.

Oral contraceptives and female sex has also been related to drysocket frequency. Estrogens and other drugs would activate thefibrinolytic system in an indirect way (increasing the factors II,VII, VIII, X and the plasminogen), contributing to the prematuredestruction of the clot and the development of dry socket (Figure1).The changing endogenous estrogens during the menstrual cycle wouldalso influence, diminishing the fibrinolytic system in the days 23 to28 of the menstrual cycle. To sum up, dry socket may affect women inrelationship of 5:1 in respect to the masculine sex, with a biggerfrequency among women that take oral contraceptives (3).

A review of the literature (1)

It is supposed that tobacco may increase the frequency of drysocket about 500% (12% in front of 2,6%). Blum quantifies that drysocket rate increases 20% in patients that smoke more than a packageper day, and 40% if the patient smokes on the day of the surgery orin the immediate postoperative period (3). The mechanism that tobaccointerferes in alveolar healing is through the incorporation ofpollutants to the wound or the suction effect on the clot information. It does not exist scientific data that relate tobacco tothe heat, the smoke or the systemic effects in dry socket development(3).

Some factors that diminish the irrigation of the alveolus havealso been related to dry socket appearance such as the use of ananaesthetic solution with vasoconstrictor, or an intraligamentoustechnique of anaesthetic in which the anaesthetic is deposited verynear to the alveolus, mainly if the anaesthetic is colder than thecorporal temperature (10). Some authors assert that this increase inthe incidence of dry socket is due to the bacterial disseminationinside the periodontal ligament produced by these anaesthetictechniques. Tsirlis and cols. discussed that intraligamentousanaesthetic technique increased the percentage of dry socketpostextraction (11).

Some authors associated a poorer mandibular vascularization,mainly in later sectors (cortical thick, small medullary spaces,etc.) to an increase of the presence of dry socket in this locations.Birn demonstrated that these macroscopic impressions were erroneousand that the area inferior molar was a very vascularized region, evenmore than the anteroinferior area (3).

The exaggerated or excessive irrigation of the alveolus after adental extraction has also been proposed by some authors as apossible cause of alveolar bone lesion, although the lack ofscientific data and the difficulty of evaluating this variable makeit impossible for us to pronounce ourselves in this aspect (3).

The advanced age has also been detected by some authors as afactor associated to bigger rates of dry socket, although it has notalways been statistically significant (8,9). In inmunosupresed ordiabetic patients healing can be altered, being these patients proneto develop dry socket (12).

CLINICAL FORMS AND DIAGNOSTIC

It is clinically recognizable by the existence of a naked alveoluswithout presence of sanguine clot, exposed bony walls and separationof gingival borders. After a dental extraction, the sanguine clotgets lost in a premature, first way adopting a grizzly coloration, itstops later and disappears completely. Although suppuration is notevidenced, a very important, sharp and stormy pain persists thatincreases with the suction or the mastication which lasts severaldays. It is not rare pain irradiation to the ear and the hom*olateralside of the head. Though rarely, it has also been reported theappearance of lymphatic nodes.

The affection has its typical appearance on the second or thirdday after the extraction, and it usually lasts, either with orwithout treatment, about ten or fifteen days. The patient notices aslight initial uneasiness, followed by a light improvement and asudden worsening, in form of important pain that is difficult tocontrol even with analgesic potent.

The appearance of a dry socket before the first day ofpostoperative is exceptional, because the clot needs a time to beaffected by the plasmina before its disintegration takes place.

Radiological studies do nor show important alterations, and inadvanced phases we can detect rarefaction areas that, from thecortical alveolar reach the adjacent bone. Histologically acircunscrict osteitis is observed in the alveolar sheet with tendencyto expand to the nearly bone.

PRONOSTIC AND TREATMENT

Although not the rule, some authors do not accept speaking of drysocket treatment as long as its aetiology it is not properly known.The treatment can only aim to control the pain during the period ofcure of the affection, and this is mainly achieved by means ofpalliative measures.

Even when the affection heals after ten or fifteen days ofevolution, with or without medication, the global tendency is tocarry out analgesic symptomatic treatment, accompanied byantinflamatory treatment and antibiotics (this last point is notadvised by all the authors).

After the anaesthesia of the area which allows a momentary relief,we should remove any suture that avoids a correct healing of thealveolus. The alveolus should be irrigated with a saline solution tocorporal temperature or with anaesthetic solution, followed by acareful aspiration of the material that overflows the alveolus. Someauthors do not advice a curettage of the alveolus to force thebleeding in it and the formation of a new clot (13). Potent analgesicshould be prescribed and the patient should be informed. The patientshould be irrigated daily with saline solution using a needlesssyringe.

Some authors advise the placement of antiseptic intraalveolarpastes (14). These pastes, according to their active principle, canbe classified into antimicrobial dressings, soothing dressings ordressings with local anaesthetics. In a study published by Garibaldiand cols. they compared the advantage of the treatment with eugenol,lidocaine and clorhexidine to 0,12% dressings, finding that the firstof them produced a bigger reduction of healing time (15).

The use of these pastes would diminish the patient’suneasiness during the recovery of the dry socket, although thesestatements are generally based on the experiences of the authors.Although the literature does not show clear evidences in favour ofthe placement of these pastes, they can help in the treatment of drysocket, because they increase locally the drug concentration,diminishing their secondary effects and avoiding the entrance ofremains of food to the alveolus. The number of secondarycomplications to the placement of dressings in the treatment of anestablished dry socket is ignored, although some local complicationshave been described after the placement of these dressings (neuritis,reactions of giant cells to strange body) (3, 16, 17).

Nevertheless, we should insist that we do not have more treatmentthan the symptomatic one while the organism is reestablished of drysocket, since the etiologic treatment does not exist at the presenttime. Because of this, the best option is prevention. That is whyimportant efforts have been done in getting effective methods andprotocols in this aspect (3).

ETIOPATHOGENIC

It is necessary to review the main etiopathogenic theories thathave intended to explain the dry socket to understand the differentpreventive strategies that have been elaborated. These areBirn´s fibrinolityc theory and the bacterial theory.

According to Birn´s fibrinolityc theory, after the extractionof a tooth an inflammatory process begins that could affect to theformation and retention of the clot. Laboratory and clinical studieshave shown an increase of the fibrinolytic activity in the pathogenicof dry socket (Figure 2) (2). The fibrin would disintegrate foreffect of the kinasas liberated in the inflammation process or due toa direct or indirect activation of the plasminogen, affecting to thestability of the clot and facilitating the development of a drysocket (3,8,9).

A review of the literature (2)

For Birn, this would be the main factor in the generation of thesocket. The reason to explain that in multiple extractions the socketrate is smaller, in spite of a bigger trauma, is the existence of abigger surgical bed that would contribute a great quantity of bloodand would allow the formation of an appropriate clot as first step ofa normal healing (2).

The plasminogen activator factors can be direct or indirect (notphysiologic). They can also be classified in extrinsic (not presentin the sanguine plasma) or intrinsic activators. Inside the intrinsicdirect activators we have the dependent activator of the XII factorand the urokinasa, mediated by leukocytes. The extrinsic directplasminogen activators include the plasminogen tisular activator andthe plasminogen endothelial activator. The indirect activators wouldbe formed in their biggest part by substances like the streptokinaseand the estafilokinase. This last point could unify bothetiopathogenic theories (the second of those which we will see next),whenever an important role of these indirect activators wasrecognized in the genesis of dry socket by means of a fibrinolitycprocess, according to the reductions in the socket frequency foundwhen rehearsing antimicrobial substances (3).

The existence of radicular tooth or bony in the alveolar bed aftera dental extraction can lead to the appearance of complications,among them the dry socket although some authors discard thispossibility in studies on animals (3).

The second theory, denominated bacterial theory, comes endorsed bythe existence of a high recount of pre and postoperative bacteriasaround the extraction place in patients that suffered alveolarosteitis with respect to those that did not suffer it (8). Theanaerobia microorganism would be mainly founded and the alveolar painwould be due to the effect of the bacterial toxins in the nervousterminations of the alveolus.

Dry socket would be also more frequent in patient with worse oralhygiene (18), or when it existed previous pericoronaritis orconcomitant periodontal illness (19). This theory would come endorsedby the descent in the appearance of the dry socket after the use ofantimicrobial agents.

Actinomyces viscous and the Streptococcus mutants have beenrelated to dry socket, because it has been demonstrated that theyretard the alveolar postextraction healing in an animal model. Also,a fibrinolytic activity has been observed increased with TreponemaDenticola, a periodontopatogenic microorganism. This affection neverappears in children, before colonization of the mouth by TreponemaDenticola (3).

It has not been universally accepted a etiopathogenic hypothesis,among other reasons, because there are not conclusive data to rejector to accept some of them. It is not even dishevelled to think thatthe socket is caused by a etiopathogenic mechanism of the sum of boththeories.

PREVENTION

According to the theories of the dry socket, for its preventionhave been considered antifibrinolytic agents, laundries, antisepticand antibiotics (Figures 3).

A review of the literature (3)

The antifibrinolytic agents are used in order to avoid the earlydisintegration of the clot. The use of tranexamic acid in a topicalform (0,5 mg) did not reduce the socket rate (23% in group control infront of 22% in experimental group), but this failure has not beendetected with other antifibrinolytic like the PEPH (propilic ester ofthe p-hidroxibenzoico acid: 24% of the group control in front of 0%in the experimental group); however, the use of this is accompaniedby important secondary effects (12).

Other authors have proposed the use of laundries with salinesolution. In studies where the alveolus was rinsed with differentquantities of saline solution after a tooth extraction (25 ml, 175 mland 350 ml), smaller rates of dry socket were found as the irrigationwas increased (10,9%, 5,7% and 3,2% of dry socket in each group,respectively) (3). Other protocols such as use of sterile glovesinstead of clean gloves but not sterile, have not demonstratedutility in the prevention of the dry socket (20).

The use of soothing dressings has also been applied with successin the reduction of the postextraction dry socket in a recent study(21). It has been broadly documented in the literature the positiveeffect of the eugenol usually contained in these dressings in spiteof the delay in the wound healing and the local irritatingeffect.

The polylactic acid has also been rehearsed for the control of drysocket, an biodegradable ester that would provide an additionalsupport to the clot and it would avoid or it would hinder itsdisintegration. In the initial studies they found percentages of drysocket near to 2% in the experimental group in front of 18,1% of thegroup control. In later studies they have found higher percentages ofdry socket (in a study that the group control used this type ofsupport treated with clorhexidine, the socket rate was of 23,6% inthe experimental group in front of 13,6% in the control group) in theexperimental group that in the control (3, 22).

The drugs that have probably been more successful in theprevention of the socket are the antiseptic and the antibiotics. In astudy carried out by Ragno and Szkutnik (23), the chlorhexidinegluconate oral rinse to 0,12% produced an important reduction of thepostextraction alveolar osteitis in impacted mandibular third molars(17,5% in the experimental group in front of 36% in the groupcontrol). These data were corroborated by Larsen in 1991 and theyconfirmed those found by Berwick and Lessin (8,24) that also informedof its effectiveness in concentrations of chlorhexidine gluconateoral rinse to 0,12% with smaller secondary effects that if aconcentration of 0,2% was used, as it was made in the initialrehearsals. Some authors think that in spite of the antiseptic powerof the clorhexidine, and reduce the bacterial salivary recount inmore than 95%, the saliva would contain enough number of bacterias toproduce dry socket (24).

Deepening in the bacterial theory, systemic antibiotics were usedas a measure of prevention of the dry socket, alone or pluscorticoids, but this association did not improved the results. On theother hand, the use of the corticoids alone did not reducesignificantly dry socket incidence.

Although the use of penicillin was not able to improve dry socketrate after the extraction of included third molars, the use oftopical antibiotics have rendered good results. Ritzau and cols. in1992 used 1 gram of metronidazole via oral preoperatory as apreventive strategy (25), although it did not reduce significantlythe percentages of dry socket. The antibiotic with a better resultshave shown in the prevention of dry socket is the tetracycline, in asystemic administration, proven in a study of Swanson and cols. in1966 (26), who found a reduction from 37,5% to 2,6%; as in a topicaladministration (in sponges or in intraalveolar placement), proven ina study of David and cols. (9,3% of the control group in front of2,7% of the experimental group) (27). Besides, there are otherreported works where the antibiotic treatment has not had influencein the reduction of dry socket (28).

To sum up, although the antifibrinolytic agents have shown apreventive activity in dry socket, its secondary effects shoulddissuade their use. The use of laundries of serum has provedeffective and should be incorporated to the protocol of extraction ofthe included third molars. The use of antiseptics provide reductionsof 50% in dry socket rates after the extraction of third mandibularmolars and it is considered an appropriate preventive measure. Theuse of antibiotics in a systemic administration, though it is aproper treatment in the prevention of this affection, has been verydiscussed, due to secondary effects, the creation of resistances, andtheir toxicity, the topical use being recommended.

If we apply the data that we have found in the studies revisedpreviously to the etiopathogenic theories presented above, we canthink, without leaving the territory of the hypothesis, of apathogenic model in which the bacterial fibrinolytic mechanisms andof the microorganism of the own patient may contribute to produce thedry socket.

REFERENCES

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2. Birn H. Bacterial and fibrinolytic activity in “dry socket”. Acta Odontol Scand 1970;28:773-83.[Links]

3. Blum IR. Contemporary views on dry socket (alveolar osteitis): a clinical appraisal of standardization, aetiopathogenesis and management: a critical review. Int J Oral Maxillofac Surg 2002;31:309-17.[Links]

4. Houston JP, McCollum J, Pietz D, Schneck D. Alveolar osteitis: a review of its etiology, prevention, and treatment modalities. Gen Dent 2002;50:457-63.[Links]

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6. Jaafar N, Nor GM. The prevalence of post-extraction complications in an outpatient dental clinic in Kuala Lumpur Malaysia--a retrospective survey. Singapore Dent J 2000;23:24-8.[Links]

7. Simon E, Matee M Post-extraction complications seen at a referral dental clinic Dar Es Salaam,Tanzania. Int Dent J 2001;51:273-6.[Links]

8. Larsen PE. The effect of a chlorhexidine rinse on the incidence of alveolar osteitis following the surgical removal of impacted mandibular third molar. J Oral Maxillofacial Surg 1991;49:932-7.[Links]

9. Larsen PE. Alveolar osteitis after surgical removal of impacted mandibular third molars. Oral Surg Oral Med Oral Pathol 1992;73:393-7.[Links]

10. Alexander RE. Dental Extraction wound management. A case against medicating postextraction sockets. J Oral Maxillofac Surg 2000;58:538-51.[Links]

11. Tsirlis AT, Lakovidis DP, Parissis NA. Dry socket: frecuency of occurrence after intraligamentary anestesia. Quint Int 1992;23:575-7.[Links]

12. García Murcia MJ, Peñarrocha Diago M. Alveolitos seca: Revisión de la literatura y metaanálisis. Rev Act Odontoestomatol Esp 1994;44:25-34.[Links]

13. Iamaroon A, Linpisarn S, Kuansuwan C. Iron and vitamin B12 deficiency anaemia in a vegetarian: a diagnostic approach by enzyme-linked immunosorbent assay and radioimmunoassay. Dent Update 2002;29:223-4.[Links]

14. Poor MR, Hall JE, Poor AS. Reduction in the incidence of alveolar osteitis in patients treated with the SaliCept patch, containing Acemannan hydrogel. J Oral Maxillofac Surg 2002;60:374-9.[Links]

15. Garibaldi JA, Greenlaw J, Choi J, Fotovatjah M. Treatment of post-operative pain. J Calif Dent Assoc 1995;23:71-4.[Links]

16. C Moore JW, Brekke JH. Foreign body giant cell reaction related to placement of tetracycline-treated polylactic acid. Reported of 18 cases. J Oral Maxillofacial Surg 1990;48:808-12.[Links]

17. Zúñiga JR, Leist JC. Topical tetracycline-induced neuritis: a case report. J Oral Maxillofac Surg 1995;53:196-9.[Links]

18. Peñarrocha M, Sanchos JM, Sáez U, Gay C, Bagán JV. Oral higiene and postoperative pain after mandibular third molar surgery. Oral surg Oral Med Oral Pathol Radiol Endod 2001;92:260-4.[Links]

19. Rud J. Removal of impacted lower third molars with acute pericoronaritis and necrotising gingivitis. Br J Oral Surg 1970;7:153-60.[Links]

20. Cheung LK, Chow LK, Tsang MH, Tung LK. An evaluation of complications following dental extractions using either sterile or clean gloves. Int J Oral Maxillofac Surg 2001;30:550-4.[Links]

21. Bloomer CR. Alveolar osteitis prevention by immediate placement of medicated packing Oral Surg Oral Med Oral Patholg Radiol Endod 2000;90:282-4.[Links]

22. Hooley JR, Golden DP. The effect of polylactic acid granules on the incidence of alveolar osteitis after mandibular third molar surgery. A prospective randomized study. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1995; 80:279-83.[Links]

23. Ragno JR Jr, Szkutnik AJ. Evaluation of 0.12% chlorhexidine rinse on the prevention of alveolar osteitit*. Oral Surg Oral Med Oral Pathol 1991;72: 524-6.[Links]

24. Berwick JE, Lessin ME. Effects of chlorhexidine gluconate oral rinse on the incidente of alveolar osteitis in mandibular third molar surgery. J Oral Maxillofacial Surg 1990;48:444- 8.[Links]

25. Ritzau M, Hillerup S, Branebjerg PE, Ersbol BK. Does metronidazole prevent alveolitis sicca dolorosa? A double- blind, placebo- controlled clinical study. J Oral Maxillofacial Surg 1992;21:299-302.[Links]

26. Swanson AE. A double-blind study on effectiveness of tetracycline in reducing the incidence of fibrinolytic alveolitis. J Oral Maxillofacial Surg 1989;47:165-7.[Links]

27. Davis WM Jr, Buchs AU, Davis WM. The use of granular gelatin-tetracycline compound after third molar removal” J Oral Surg 1981;39:36-7.[Links]

28. Monaco G, Staffolani C, Gatto MR, Checchi L. Antibiotic therapy in impacted third molar surgery. Eur J Oral Sci 1999;107:437-41.[Links]

A review of the literature (2024)
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