- Citado por SciELO
versión impresa ISSN 1698-4447
Med. oral patol. oral cir. bucal (Ed.impr.) vol.10 no.1 ene./feb. 2005
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.
Dry socket is a postoperative complication that occurs after a
dental extraction and has been defined as an inflammation of the
alveolus. If this inflammation should surpass the alveolar walls, it
would result in a located osteitis. The frequency of appearance of
dry socket has been reported in a very wide margin, from 1% until
70%. It is generally accepted that most dry sockets appear after
extraction of third retained molars, in which the occurrence of this
complication is about 20-30% of dental extractions, ten times more
than in the rest of dental extractions.
In this work we review the forms of clinical appearance, the risk factors related to this affection and the etiopathogenic theories that try to explain its appearance. The treatment management is also examined. Fibrinolitic agents, laundries, antiseptic, and antibiotics have been studied for its prevention, according to the pathogenic theories of dry socket. We analyze and critize the different drugs and their results.
In conclusion from the revised data, we think it is possible to defend a pathogenic model in which the bacterial fibrinolytic mechanisms and the microorganism of the own patient may contribute to produce the dry socket.
Key words: Dry socket, alveolar osteitis, postextraction complications.
Dry socket is a postoperative complication that occurs after a dental extraction. It has been defined in the classic books of Oral Surgery as a local inflammation of the alveolus. In case this inflammation should surpass the alveolar walls, it would result in a located osteitis.
The first time that this term appeared in the literature was in 1896, used by Crawford (1). Ever since many terms have been used as synonyms of dry socket, including painful dry socket, alveolalgia, osteomielitis, fibrinolytic osteitis, alveolar osteitis, osteomielytic postextraction syndrome, fibrinolytic alveolitis and located alveolar osteitis. In our opinion, the most appropriate term is the one given by Birn (2), fibrinolytic alveolitis, though it is the least used one (3).
17 different definitions of dry socket have been reported. The most recent we have found in the literature defines dry socket as a postoperative pain inside and around the dental alveolus, which is increased in severity in some moment between the first and the third day after a dental extraction, accompanied by a partial or total disintegration of the intraalveolar clot sanguine, accompanied or not of halitosis. (3).
We can distinguish among dry sockets that occur in patients that suffer some type of hipovascularization condition in the maxillary bone (vascular or hematologic disorders, osteorradionecrosis, osteopetrosis, Paget´s illnes, etc.) and those where these condition are not detected, denominated true dry socket in the literature revised (3,4).
The frequency of appearance of dry socket has been reported in a very wide margin, from 1% to 70% (3,5). It is generally accepted that most dry sockets appear after extraction of third included molars, in which the occurrence of this complication is about 20-30% of dental extractions, ten times more than in the rest of dental extractions (3). According to different authors, the average percentage of dry sockets in the group of all tooth extraction is about 3-4% (6).
Such wide margins in figures of dry socket appearance are due to the differences in diagnostic criteria, in evaluation methods, in mixture of data coming from simple extractions and of retained teeth, as well as to the variability in surgical treatment and postsugical management. We should distrust those studies showing dry sockets percentages smaller than 1% (for lack of clinical credibility), as well as those studies showing dry socket percentages greater than 35% (suggesting variables or uncontrolled risk factors, a small number of patients, or extreme situations, or important lacks, as we find in the article published by Simon and Matee (percentage of dry socket of 48,7%) (3,7).
Since the aetiology of this affection is not known, the advised therapy is prevention. The epidemiologic studies have detected different risk factors in the development of dry socket: the difficulty of the dental extraction, the surgeons inexperience, the use of oral contraceptives, an inadequate intraoperatory irrigation, advanced age of patients, female sex, tobacco, inmunosupression, and surgical trauma.
Since we do not know the true causes of dry socket, the way that these factors of risk influence in the appearance of the affection are, by now, theories more or less guessed right, more or less corroborated by this epidemiologic studies.
In his studies of 1991 and 1992, Larsen (8-10) did not demonstrate that the difficulty of the extraction and the surgical trauma, for example, were risk factors. Perhaps the surgical intervention duration is not a good indicator of the difficulty of the extraction or still more important, of the trauma that is taking place. However, most authors agree that the surgeons inexperience could be related to a bigger trauma occurred during the extraction (9). A bigger trauma would produce a delay in the alveolar healing, and it could provoke a thrombosis of the underlying vessels as well as a smaller resistance to the infection in the alveolar bone.
Oral contraceptives and female sex has also been related to dry socket frequency. Estrogens and other drugs would activate the fibrinolytic system in an indirect way (increasing the factors II, VII, VIII, X and the plasminogen), contributing to the premature destruction of the clot and the development of dry socket (Figure 1). The changing endogenous estrogens during the menstrual cycle would also influence, diminishing the fibrinolytic system in the days 23 to 28 of the menstrual cycle. To sum up, dry socket may affect women in relationship of 5:1 in respect to the masculine sex, with a bigger frequency among women that take oral contraceptives (3).
It is supposed that tobacco may increase the frequency of dry socket about 500% (12% in front of 2,6%). Blum quantifies that dry socket rate increases 20% in patients that smoke more than a package per day, and 40% if the patient smokes on the day of the surgery or in the immediate postoperative period (3). The mechanism that tobacco interferes in alveolar healing is through the incorporation of pollutants to the wound or the suction effect on the clot in formation. It does not exist scientific data that relate tobacco to the heat, the smoke or the systemic effects in dry socket development (3).
Some factors that diminish the irrigation of the alveolus have also been related to dry socket appearance such as the use of an anaesthetic solution with vasoconstrictor, or an intraligamentous technique of anaesthetic in which the anaesthetic is deposited very near to the alveolus, mainly if the anaesthetic is colder than the corporal temperature (10). Some authors assert that this increase in the incidence of dry socket is due to the bacterial dissemination inside the periodontal ligament produced by these anaesthetic techniques. Tsirlis and cols. discussed that intraligamentous anaesthetic technique increased the percentage of dry socket postextraction (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 erroneous and that the area inferior molar was a very vascularized region, even more than the anteroinferior area (3).
The exaggerated or excessive irrigation of the alveolus after a dental extraction has also been proposed by some authors as a possible cause of alveolar bone lesion, although the lack of scientific data and the difficulty of evaluating this variable make it impossible for us to pronounce ourselves in this aspect (3).
The advanced age has also been detected by some authors as a factor associated to bigger rates of dry socket, although it has not always been statistically significant (8,9). In inmunosupresed or diabetic patients healing can be altered, being these patients prone to develop dry socket (12).
CLINICAL FORMS AND DIAGNOSTIC
It is clinically recognizable by the existence of a naked alveolus without presence of sanguine clot, exposed bony walls and separation of gingival borders. After a dental extraction, the sanguine clot gets lost in a premature, first way adopting a grizzly coloration, it stops later and disappears completely. Although suppuration is not evidenced, a very important, sharp and stormy pain persists that increases with the suction or the mastication which lasts several days. It is not rare pain irradiation to the ear and the homolateral side of the head. Though rarely, it has also been reported the appearance of lymphatic nodes.
The affection has its typical appearance on the second or third day after the extraction, and it usually lasts, either with or without treatment, about ten or fifteen days. The patient notices a slight initial uneasiness, followed by a light improvement and a sudden worsening, in form of important pain that is difficult to control even with analgesic potent.
The appearance of a dry socket before the first day of postoperative is exceptional, because the clot needs a time to be affected by the plasmina before its disintegration takes place.
Radiological studies do nor show important alterations, and in advanced phases we can detect rarefaction areas that, from the cortical alveolar reach the adjacent bone. Histologically a circunscrict osteitis is observed in the alveolar sheet with tendency to expand to the nearly bone.
PRONOSTIC AND TREATMENT
Although not the rule, some authors do not accept speaking of dry socket treatment as long as its aetiology it is not properly known. The treatment can only aim to control the pain during the period of cure of the affection, and this is mainly achieved by means of palliative measures.
Even when the affection heals after ten or fifteen days of evolution, with or without medication, the global tendency is to carry out analgesic symptomatic treatment, accompanied by antinflamatory treatment and antibiotics (this last point is not advised 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 the alveolus. The alveolus should be irrigated with a saline solution to corporal temperature or with anaesthetic solution, followed by a careful aspiration of the material that overflows the alveolus. Some authors do not advice a curettage of the alveolus to force the bleeding in it and the formation of a new clot (13). Potent analgesic should be prescribed and the patient should be informed. The patient should be irrigated daily with saline solution using a needless syringe.
Some authors advise the placement of antiseptic intraalveolar pastes (14). These pastes, according to their active principle, can be classified into antimicrobial dressings, soothing dressings or dressings with local anaesthetics. In a study published by Garibaldi and cols. they compared the advantage of the treatment with eugenol, lidocaine and clorhexidine to 0,12% dressings, finding that the first of them produced a bigger reduction of healing time (15).
The use of these pastes would diminish the patients uneasiness during the recovery of the dry socket, although these statements are generally based on the experiences of the authors. Although the literature does not show clear evidences in favour of the placement of these pastes, they can help in the treatment of dry socket, because they increase locally the drug concentration, diminishing their secondary effects and avoiding the entrance of remains of food to the alveolus. The number of secondary complications to the placement of dressings in the treatment of an established dry socket is ignored, although some local complications have 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 treatment than the symptomatic one while the organism is reestablished of dry socket, since the etiologic treatment does not exist at the present time. Because of this, the best option is prevention. That is why important efforts have been done in getting effective methods and protocols in this aspect (3).
It is necessary to review the main etiopathogenic theories that have intended to explain the dry socket to understand the different preventive strategies that have been elaborated. These are Birn´s fibrinolityc theory and the bacterial theory.
According to Birn´s fibrinolityc theory, after the extraction of a tooth an inflammatory process begins that could affect to the formation and retention of the clot. Laboratory and clinical studies have shown an increase of the fibrinolytic activity in the pathogenic of dry socket (Figure 2) (2). The fibrin would disintegrate for effect of the kinasas liberated in the inflammation process or due to a direct or indirect activation of the plasminogen, affecting to the stability of the clot and facilitating the development of a dry socket (3,8,9).
For Birn, this would be the main factor in the generation of the socket. The reason to explain that in multiple extractions the socket rate is smaller, in spite of a bigger trauma, is the existence of a bigger surgical bed that would contribute a great quantity of blood and would allow the formation of an appropriate clot as first step of a normal healing (2).
The plasminogen activator factors can be direct or indirect (not physiologic). They can also be classified in extrinsic (not present in the sanguine plasma) or intrinsic activators. Inside the intrinsic direct activators we have the dependent activator of the XII factor and the urokinasa, mediated by leukocytes. The extrinsic direct plasminogen activators include the plasminogen tisular activator and the plasminogen endothelial activator. The indirect activators would be formed in their biggest part by substances like the streptokinase and the estafilokinase. This last point could unify both etiopathogenic theories (the second of those which we will see next), whenever an important role of these indirect activators was recognized in the genesis of dry socket by means of a fibrinolityc process, according to the reductions in the socket frequency found when rehearsing antimicrobial substances (3).
The existence of radicular tooth or bony in the alveolar bed after a dental extraction can lead to the appearance of complications, among them the dry socket although some authors discard this possibility in studies on animals (3).
The second theory, denominated bacterial theory, comes endorsed by the existence of a high recount of pre and postoperative bacterias around the extraction place in patients that suffered alveolar osteitis with respect to those that did not suffer it (8). The anaerobia microorganism would be mainly founded and the alveolar pain would be due to the effect of the bacterial toxins in the nervous terminations of the alveolus.
Dry socket would be also more frequent in patient with worse oral hygiene (18), or when it existed previous pericoronaritis or concomitant periodontal illness (19). This theory would come endorsed by the descent in the appearance of the dry socket after the use of antimicrobial agents.
Actinomyces viscous and the Streptococcus mutants have been related to dry socket, because it has been demonstrated that they retard the alveolar postextraction healing in an animal model. Also, a fibrinolytic activity has been observed increased with Treponema Denticola, a periodontopatogenic microorganism. This affection never appears in children, before colonization of the mouth by Treponema Denticola (3).
It has not been universally accepted a etiopathogenic hypothesis, among other reasons, because there are not conclusive data to reject or to accept some of them. It is not even dishevelled to think that the socket is caused by a etiopathogenic mechanism of the sum of both theories.
According to the theories of the dry socket, for its prevention have been considered antifibrinolytic agents, laundries, antiseptic and antibiotics (Figures 3).
The antifibrinolytic agents are used in order to avoid the early disintegration of the clot. The use of tranexamic acid in a topical form (0,5 mg) did not reduce the socket rate (23% in group control in front of 22% in experimental group), but this failure has not been detected with other antifibrinolytic like the PEPH (propilic ester of the p-hidroxibenzoico acid: 24% of the group control in front of 0% in the experimental group); however, the use of this is accompanied by important secondary effects (12).
Other authors have proposed the use of laundries with saline solution. In studies where the alveolus was rinsed with different quantities of saline solution after a tooth extraction (25 ml, 175 ml and 350 ml), smaller rates of dry socket were found as the irrigation was increased (10,9%, 5,7% and 3,2% of dry socket in each group, respectively) (3). Other protocols such as use of sterile gloves instead of clean gloves but not sterile, have not demonstrated utility in the prevention of the dry socket (20).
The use of soothing dressings has also been applied with success in the reduction of the postextraction dry socket in a recent study (21). It has been broadly documented in the literature the positive effect of the eugenol usually contained in these dressings in spite of the delay in the wound healing and the local irritating effect.
The polylactic acid has also been rehearsed for the control of dry socket, an biodegradable ester that would provide an additional support to the clot and it would avoid or it would hinder its disintegration. In the initial studies they found percentages of dry socket near to 2% in the experimental group in front of 18,1% of the group control. In later studies they have found higher percentages of dry socket (in a study that the group control used this type of support treated with clorhexidine, the socket rate was of 23,6% in the experimental group in front of 13,6% in the control group) in the experimental group that in the control (3, 22).
The drugs that have probably been more successful in the prevention of the socket are the antiseptic and the antibiotics. In a study carried out by Ragno and Szkutnik (23), the chlorhexidine gluconate oral rinse to 0,12% produced an important reduction of the postextraction alveolar osteitis in impacted mandibular third molars (17,5% in the experimental group in front of 36% in the group control). These data were corroborated by Larsen in 1991 and they confirmed those found by Berwick and Lessin (8,24) that also informed of its effectiveness in concentrations of chlorhexidine gluconate oral rinse to 0,12% with smaller secondary effects that if a concentration of 0,2% was used, as it was made in the initial rehearsals. Some authors think that in spite of the antiseptic power of the clorhexidine, and reduce the bacterial salivary recount in more than 95%, the saliva would contain enough number of bacterias to produce dry socket (24).
Deepening in the bacterial theory, systemic antibiotics were used as a measure of prevention of the dry socket, alone or plus corticoids, but this association did not improved the results. On the other hand, the use of the corticoids alone did not reduce significantly dry socket incidence.
Although the use of penicillin was not able to improve dry socket rate after the extraction of included third molars, the use of topical antibiotics have rendered good results. Ritzau and cols. in 1992 used 1 gram of metronidazole via oral preoperatory as a preventive strategy (25), although it did not reduce significantly the percentages of dry socket. The antibiotic with a better results have shown in the prevention of dry socket is the tetracycline, in a systemic administration, proven in a study of Swanson and cols. in 1966 (26), who found a reduction from 37,5% to 2,6%; as in a topical administration (in sponges or in intraalveolar placement), proven in a study of David and cols. (9,3% of the control group in front of 2,7% of the experimental group) (27). Besides, there are other reported works where the antibiotic treatment has not had influence in the reduction of dry socket (28).
To sum up, although the antifibrinolytic agents have shown a preventive activity in dry socket, its secondary effects should dissuade their use. The use of laundries of serum has proved effective and should be incorporated to the protocol of extraction of the included third molars. The use of antiseptics provide reductions of 50% in dry socket rates after the extraction of third mandibular molars and it is considered an appropriate preventive measure. The use of antibiotics in a systemic administration, though it is a proper treatment in the prevention of this affection, has been very discussed, due to secondary effects, the creation of resistances, and their toxicity, the topical use being recommended.
If we apply the data that we have found in the studies revised previously to the etiopathogenic theories presented above, we can think, without leaving the territory of the hypothesis, of a pathogenic model in which the bacterial fibrinolytic mechanisms and of the microorganism of the own patient may contribute to produce the dry socket.
1. Crawford JY. Dry socket. Dent Cosmos 1896;38:929. [ Links ]
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 ]
5. Ariza E, González J, Boneu F, Hueto JA, Raspall G. Incidencia de la alveolitis seca, tras la exodoncia quirúrgica de terceros molares mandibulares en nuestra Unidad de Cirugía Oral. Rev Esp Cir oral Maxilofac 1999;21:214-9. [ Links ]
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 osteitits. 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 ]