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Actinomycosis of the jaws
Int. J. Oral Surg. 1985: 14: 195-199 (Key words: injection, specific; actinomycosis; maxilla; mandible; surgery, oral)
Actinomycosis of the jaws 2 case reports R. BENOLIEL AND J. ASQUITH Department of Oral & Maxillofacial Surgery, Queen Mary's Hospital, Roehampton, London, England ABSTRACT - The diagnosis of actinomycosis is not always straightforward. It has been described as a masquerader, and 2 cases are presented which exemplify this. Their mode of presentation and natural history are contrasted.
(Received for publication 24 January, accepted 12 April 1984)
The failure to include actinomycosis in the differential diagnosis of relevant cases has previously been reported 1 0, and this often results in delayed diagnosis. Actinomycosis merits consideration in any persistent, chronic orofacial infection, although it may not always present as such; hence the delay in diagnosis. The first case described had extensive and rapid local destruction and this questions the view that actinomycosis is of low virulence. The second case, with a long latent period suggests an organism of low virulence. This possible variation in pathogenicity has previously been discussed'. In the absence of positive culture, histology demonstrating organisms and sulphur granules is the only definitive diagnostic test.
Review Actinomycosis was first described as a clin-
ical entity nearly 200 years ago!", The infection is caused by organisms of the order actinomycetales. Members of this group are considered to be transitional forms between bacteria and fungi. Their characteristic appearance under the light microscope has given rise to the descriptive term 'Ray Fungus". However, certain biochemical and structural characteristics suggest that they should be classified as bacteria 14. Originally, Actinomycosis israelii was considered to be the sole pathogen, although subsequently several other populations have been recovered from lesions". Some different species (e.g., Arachnia propionica) are morphologically identical and can only be distinguished by their difference in end products of glucose metabolism, antigenic components or cell wall composition'". Actinomyces boots and Actinomyces naeslundii have occasionally been isolated from clinical infections. These organisms are anaerobic
196
BENOLIEL AND ASQUITH
or microaerophillic and appear as wavy non-septate branching hyphae or filaments. On solid media such as blood agar, they grow as tangled masses, although they are notoriously difficult to culture. Actinomycosis appears to be a 'cooperative disease' with synergism being particularly strong with streptococci and staphylococci. This predilection for mixed infection along with its anaerobic qualities explains the difficulty in culturing the organisms. Actinomyces are members of the normal oral flora. In a study of the predominant flora from approximal plaque in 12-year-old children, Actinomyces israelii accounted for 16.5% and Actinomyces oiscosuslnaelundii for 19.1 % of the total'". Of recorded cases, cervicofacial actinomycosis accounts for 55%, ileocaecal 25% and pulmonary 15%. Subcutaneous and other sites account for the remaining 5% 7. Cervicofacial actinomycosis usually occurs in young adults, males being affected twice as frequently as females 11. Some authorities state that the mandible is more commonly affected than the maxillav'", whilst WEIR & BUCK 1 4 found the maxillary central incisor to be the most commonly involved. Infection is usually endogenous. Trauma, either accidental (e.g., fracture) or from dental treatment such as root canal therapy or extraction is believed to be the most likely portal of entry of the organism 1 5 . 'Punch Actinomycosis', a hand infection caused by implantation of a tooth fragment following a punch, has also been reported". Classically, Actinomycotic infection presents as a slowly enlarging dusky blue or reddish swelling, slightly tender which may become indurated due to scar formation. Sinuses mayor may not be present and are often multiple. Characteristically, lesions have granules (often termed 'sulphur granules') within the purulent exudate, although
purulent discharge is not necessarilly a presenting sign. The sulphur granules are coated with an Arginine-rich polypeptide and contain the causative organisms together with calcium phosphate. Granule formation may play an important role in the pathogenicity of the species. Such organisms are protected from the host defences and are more resistant to antibiotics'". The presence of sulphur granules is almost pathognomonic of actinomycosis. Bone involvement occurs in the later stages when expansion, destruction and cyst formation may be seen. Actinomycosis does not spread to the lymph nodes 6 •1 3 . 2 cases presenting at the department of Oral and Maxillofacial Surgery, Queen Mary's Hospital, Roehampton, are now described. They illustrate the widely variable modes of presentation and diagnostic difficulties associated with this disease.
Fig. 1. Epulis viewed from buccal aspect (a) and
Palatal aspect (b).
ACTINOMYCOSIS
Case reports Case 1 A 31-year-old white male was seen in the department on August 27, 1982. He had been referred by his dental practitioner with a complaint of pain associated with gingival swellings in the /1-4 region, which bled easily on toothbrushing. During the course of February 1982, his dental practitioner had initially treated this lesion by gingivectomy and curettage, followed by root canal therapy to L.!L This afforded temporary relief from his symptoms, but the swellings recurred within a period of 2 months. The previous medical history revealed nothing of significance. On examination, there were no extra-oral physical signs, no lymphadenopathy and no pyrexia. Intra-orally, the /123 were mobile, tender and non-vital. The surrounding gingival tissues were grossly hyperplastic. There was no ulceration but the lesion bled easily on gentle probing (Fig. 1). The standard of oral hygiene was poor, but there was no other active disease process noted. Radiographs revealed well-demarwithout root resorpcated bone loss around tion (Fig. 2). A differential diagnosis was made as follows:
m
1. pyogenic granuloma 2. peripheral giant cell reparative granuloma 3. malignant neoplasm The rapid destruction in a short period of time suggested that malignancy may be involved and an incisional biopsy was performed on the day of presentation. Appearances consistent with those of actinomycosis were reported.
Fig. 2. Upper occlussal radiograph of L!.b.
197
Routine haematological tests were within normal limits and a chest X-ray was reported as normal. Due to the appearance and presentation of the lesions, it was suspected that the actinomycosis was a secondary phenomenon masking an underlying aggressive neoplasm. The patient was therefore admitted to hospital for exploration of the area under general anaesthesia. At surgery, on September 10, 1982, the affected soft tissue was excised and the underlying bone explored. There was extensive bone loss around ~ These teeth were removed and the area thoroughly curetted. No pus was found at operation. The patient made an uneventful recovery and was discharged home the next day. Antibiotic therapy was instigated consisting of Phenoxymethyl penicillin 500 rng, 4 x daily. A pathology report of the excised tissue reported appearances consistent with actinomycosis with no sign of malignancy. In view of the diagnosis, penicillin therapy was continued for 3 months. During follow-up review, a small area of granulation was noted. Culture was attempted but was negative for actinomycosis. This, however, healed spontaneously and at review on January 26, 1983 there was no sign of residual disease (Fig. 3). Case 2 A 25-year-old black female was seen in the department on July 13, 1979. She complained of pain on the right side of her face of 2 days
Fig. 3. View, from buccal aspect, of affected area 4 months post-operatively; there is no sign of residual disease.
198
BENOLIEL AND ASQUITH
duration. The pain radiated to the right cheek and there was pain on, and restriction of mandibular movement. The patient was apyrexial, Previous medical history revealed nothing of significance. The 8/ had been removed 10 years previously and this had been uneventful. On examination , there was no lymphadenopathy and lip sensation was normal. Intra-orally, there was expansion of the buccal plate adjacent to 765(. Lingually there was a fluctuant mass which was tender on gentle pressure. 765/ were vital and otherwise the patient had a healthy dentition and soft tissue environment. Radiographs revealed a radiolucent area associated with 76/ (Fig. 4). Routine haematological tests were within normal limits. A differential diagnosis was made as follows:
extensively, up to the distal root of 7/. The mass had infiltrated the floor of the mouth which made complete removal difficult. 76/ were removed and the mass enucleated . A pathology report of the enucleated mass showed that the mass consisted of chronic inflammatory tissue with actinomycotic colonies . Immediate antibiotic therapy consisting of phenoxymethyl penicillin 500 mg 4 x daily was instigated . The patient made an uneventful recovery and was discharged the next day. She was kept under regular review, but returned to the West Indies in the latter part of October 1979 and was then lost to follow-up.
I. 2. 3. 4. 5.
It is interesting to speculate on the aetiology
radicular cyst keratocyst odontogenic tumour cementoblastoma metastatic tumour
The patient was admit ted to hospital for exploration of the area under general anaesthesia. At surgery on July 20, 1979, a solid grey mass was found. This had perforated the lingual plate
Fig. 4. Radiograph showing radiolucent area associated with 76/ (enlarged from orthopantomograph).
Discussion of the disease in the first case. Soft tissues are more commonly involved in actinomycotic infections 15, and this would suggest that the epulis was the original source of the infection. This probably originated from a periodontal pocket with suitable anaerobic conditions favourable to the growth of actinomycosis organisms. Actinomyces organisms are predominant populations in gingivitis and early periodontitis''". The subsequent gingivectomy would then have spread the organism more deeply within the tissues, an attempt then being made by the dental practitioner to treat this by conventional root canal therapy. In this case, bone involvement occurred early with rapid destruction. As previously mentioned, this may be due to a variation in pathogenicity or, may be a reflection of the host's resistance . Interestingly, when actinomyces organisms are specifically looked for in cultures of infected root canals, they have been found in 10.6% of positive cultures.'. Neither case presented with chronic sinuses and purulent discharge, factors often claimed to be reliable guides to diagnosis. The second case presented with no history of recent trauma. One may only speculate whether actinomycosis, which may be of
ACTINOMYCOSIS
low virulence, can remain in the tissues for 10 years and therefore be related to the extraction of 8/. One cannot assume the presence of an actinomycotic lesion without classical clinical features or a positive culture or histology. OWEN & MACANSH 9 reported a case of actinomycosis of the mandible that lasted for more than 3 years without displaying typical signs such as board-like swelling and multiple abscesses and sinuses. CRAN & HANNAM 3 suggested that actinomycotic infection might be more common than previously thought, but often remaining undiagnosed. Thus we cannot ignore the possibility that the infection entered the tissues through the extraction socket and remained there for a long time before a clinically obvious lesion presented. Actinomyces israelii is highly sensitive to many antibiotics and there are no recorded cases of resistance to penicillin 7 • Treatment should be prolonged and thus for the first case, where total surgical excision had been accomplished, the antibiotic was continued for 3 months. In the second case, due to the high probability of residual infected tissue, the antibiotic was continued for 6 months.
Conclusion The points discussed stress the importance of routinely submitting all excision specimens and biopsies for histological examination. Actinomycosis must be considered in persistent orofacial infections whilst remembering that this disease may masquerade and present atypically.
References I. BHASKAR, S. N.: Synopsis oforal pathology. C. V. Mosby Company, St. Louis 1981, p. 679. 2. BORSSEN, E. & SUNDQUIST, G.: Actinomyces of infected dental root canals. Oral Surg, 1981: 51: 643-648. 3. CRAN, J. A. & HANNAM, A. G.: Cervicofacial actinomycosis. Aust. Dent. J. 1963: 8: 106108. 4. DOVE, 1.: Actinomycosis in surgical biopsies. J. Roy. Soc. Med. 1979: 72: 106-108. 5. FERGUS, H. S. & SAVORD, E. G.: Actinomycosis involving a periapical cyst in the anterior maxilla. Oral Surg, 1980: 49: 390-393. 6. GOLDSTEfN, B. H., SCIRBA, 1. J. & LASKIN, D. M.: Actinomycosis of the maxilla. J. Oral Surg, 1972: 30: 362-366. 7. HENSHER, R. & BOWERMAN, J. Eo: Actinomycosis of the parotid gland. Br. J. Oral Surg., in press. 8. MARSH, P.: Oral microbiology. Thomas Nelson & Sons Ltd., Surrey 1980. (a) p. 78, (b) p. 78, (c) p. 48, (d) p. 78, (e) ppo 64-65. 9. OWEN, M. D. & MACANSH, Jo: Actinomycosis of the mandible. Med. J. Aust. 1965: 52: 962963. 10. RANKOW, R. M. & ABRAHAM, D. M.: Actinomycosis: masquerader in the head and neck. Ann. Otol. Rhinol. Laryngol. 1978: 87: 230-237. II. STENHOUSE, D. & MACDONALD, D. G.: Low grade osteomyelitis of the jaws with actinomycosis. Int. J. Oral Surg, 1974: 3: 60-64. 12. SHAFER, W. G., HfNE, M. K. & LEVY, B. M.: A textbook of oral pathology. W. B. Saunders Company, Philadelphia 1974, p. 349. 13. WALTER, J. B., HAMILTON, M. C. & ISRAEL, M. S.: Principles of pathology for dental students. Churchill Livingstone, Edinburgh 1981, p. 234. 14. WEIR, J. C. & BUCK, W. H.: Periapical actinomycosis; report of a case and review of the literature. Oral Surg. 1982: 54: 336-340. 15. YAKATA, H., NAKAJIMA, T., YAMADA, H. & TOKIWA, N.: Actinomycotic osteomyelitis of the mandible; report of case. J. Oral Surg, 1978: 36: 720-724. Address:
Acknowledgements - We would like to thank Mr. J. D. Langdon for allowing us to document these 2 cases and for his kind advice in the preparation of this paper. Additionally we would like to thank the photographic department of Queen Mary's Hospital, Roehampton, for preparing the figures.
199
R. Benoliel cio J. D. Langdon Department of Oral & Maxillofacial Surgery King's College Hospital Dental School Denmark Hill London, SE5 8RX England
Actinomycosis of the jaws 2 case reports R. BENOLIEL AND J. ASQUITH Department of Oral & Maxillofacial Surgery, Queen Mary's Hospital, Roehampton, London, England ABSTRACT - The diagnosis of actinomycosis is not always straightforward. It has been described as a masquerader, and 2 cases are presented which exemplify this. Their mode of presentation and natural history are contrasted.
(Received for publication 24 January, accepted 12 April 1984)
The failure to include actinomycosis in the differential diagnosis of relevant cases has previously been reported 1 0, and this often results in delayed diagnosis. Actinomycosis merits consideration in any persistent, chronic orofacial infection, although it may not always present as such; hence the delay in diagnosis. The first case described had extensive and rapid local destruction and this questions the view that actinomycosis is of low virulence. The second case, with a long latent period suggests an organism of low virulence. This possible variation in pathogenicity has previously been discussed'. In the absence of positive culture, histology demonstrating organisms and sulphur granules is the only definitive diagnostic test.
Review Actinomycosis was first described as a clin-
ical entity nearly 200 years ago!", The infection is caused by organisms of the order actinomycetales. Members of this group are considered to be transitional forms between bacteria and fungi. Their characteristic appearance under the light microscope has given rise to the descriptive term 'Ray Fungus". However, certain biochemical and structural characteristics suggest that they should be classified as bacteria 14. Originally, Actinomycosis israelii was considered to be the sole pathogen, although subsequently several other populations have been recovered from lesions". Some different species (e.g., Arachnia propionica) are morphologically identical and can only be distinguished by their difference in end products of glucose metabolism, antigenic components or cell wall composition'". Actinomyces boots and Actinomyces naeslundii have occasionally been isolated from clinical infections. These organisms are anaerobic
196
BENOLIEL AND ASQUITH
or microaerophillic and appear as wavy non-septate branching hyphae or filaments. On solid media such as blood agar, they grow as tangled masses, although they are notoriously difficult to culture. Actinomycosis appears to be a 'cooperative disease' with synergism being particularly strong with streptococci and staphylococci. This predilection for mixed infection along with its anaerobic qualities explains the difficulty in culturing the organisms. Actinomyces are members of the normal oral flora. In a study of the predominant flora from approximal plaque in 12-year-old children, Actinomyces israelii accounted for 16.5% and Actinomyces oiscosuslnaelundii for 19.1 % of the total'". Of recorded cases, cervicofacial actinomycosis accounts for 55%, ileocaecal 25% and pulmonary 15%. Subcutaneous and other sites account for the remaining 5% 7. Cervicofacial actinomycosis usually occurs in young adults, males being affected twice as frequently as females 11. Some authorities state that the mandible is more commonly affected than the maxillav'", whilst WEIR & BUCK 1 4 found the maxillary central incisor to be the most commonly involved. Infection is usually endogenous. Trauma, either accidental (e.g., fracture) or from dental treatment such as root canal therapy or extraction is believed to be the most likely portal of entry of the organism 1 5 . 'Punch Actinomycosis', a hand infection caused by implantation of a tooth fragment following a punch, has also been reported". Classically, Actinomycotic infection presents as a slowly enlarging dusky blue or reddish swelling, slightly tender which may become indurated due to scar formation. Sinuses mayor may not be present and are often multiple. Characteristically, lesions have granules (often termed 'sulphur granules') within the purulent exudate, although
purulent discharge is not necessarilly a presenting sign. The sulphur granules are coated with an Arginine-rich polypeptide and contain the causative organisms together with calcium phosphate. Granule formation may play an important role in the pathogenicity of the species. Such organisms are protected from the host defences and are more resistant to antibiotics'". The presence of sulphur granules is almost pathognomonic of actinomycosis. Bone involvement occurs in the later stages when expansion, destruction and cyst formation may be seen. Actinomycosis does not spread to the lymph nodes 6 •1 3 . 2 cases presenting at the department of Oral and Maxillofacial Surgery, Queen Mary's Hospital, Roehampton, are now described. They illustrate the widely variable modes of presentation and diagnostic difficulties associated with this disease.
Fig. 1. Epulis viewed from buccal aspect (a) and
Palatal aspect (b).
ACTINOMYCOSIS
Case reports Case 1 A 31-year-old white male was seen in the department on August 27, 1982. He had been referred by his dental practitioner with a complaint of pain associated with gingival swellings in the /1-4 region, which bled easily on toothbrushing. During the course of February 1982, his dental practitioner had initially treated this lesion by gingivectomy and curettage, followed by root canal therapy to L.!L This afforded temporary relief from his symptoms, but the swellings recurred within a period of 2 months. The previous medical history revealed nothing of significance. On examination, there were no extra-oral physical signs, no lymphadenopathy and no pyrexia. Intra-orally, the /123 were mobile, tender and non-vital. The surrounding gingival tissues were grossly hyperplastic. There was no ulceration but the lesion bled easily on gentle probing (Fig. 1). The standard of oral hygiene was poor, but there was no other active disease process noted. Radiographs revealed well-demarwithout root resorpcated bone loss around tion (Fig. 2). A differential diagnosis was made as follows:
m
1. pyogenic granuloma 2. peripheral giant cell reparative granuloma 3. malignant neoplasm The rapid destruction in a short period of time suggested that malignancy may be involved and an incisional biopsy was performed on the day of presentation. Appearances consistent with those of actinomycosis were reported.
Fig. 2. Upper occlussal radiograph of L!.b.
197
Routine haematological tests were within normal limits and a chest X-ray was reported as normal. Due to the appearance and presentation of the lesions, it was suspected that the actinomycosis was a secondary phenomenon masking an underlying aggressive neoplasm. The patient was therefore admitted to hospital for exploration of the area under general anaesthesia. At surgery, on September 10, 1982, the affected soft tissue was excised and the underlying bone explored. There was extensive bone loss around ~ These teeth were removed and the area thoroughly curetted. No pus was found at operation. The patient made an uneventful recovery and was discharged home the next day. Antibiotic therapy was instigated consisting of Phenoxymethyl penicillin 500 rng, 4 x daily. A pathology report of the excised tissue reported appearances consistent with actinomycosis with no sign of malignancy. In view of the diagnosis, penicillin therapy was continued for 3 months. During follow-up review, a small area of granulation was noted. Culture was attempted but was negative for actinomycosis. This, however, healed spontaneously and at review on January 26, 1983 there was no sign of residual disease (Fig. 3). Case 2 A 25-year-old black female was seen in the department on July 13, 1979. She complained of pain on the right side of her face of 2 days
Fig. 3. View, from buccal aspect, of affected area 4 months post-operatively; there is no sign of residual disease.
198
BENOLIEL AND ASQUITH
duration. The pain radiated to the right cheek and there was pain on, and restriction of mandibular movement. The patient was apyrexial, Previous medical history revealed nothing of significance. The 8/ had been removed 10 years previously and this had been uneventful. On examination , there was no lymphadenopathy and lip sensation was normal. Intra-orally, there was expansion of the buccal plate adjacent to 765(. Lingually there was a fluctuant mass which was tender on gentle pressure. 765/ were vital and otherwise the patient had a healthy dentition and soft tissue environment. Radiographs revealed a radiolucent area associated with 76/ (Fig. 4). Routine haematological tests were within normal limits. A differential diagnosis was made as follows:
extensively, up to the distal root of 7/. The mass had infiltrated the floor of the mouth which made complete removal difficult. 76/ were removed and the mass enucleated . A pathology report of the enucleated mass showed that the mass consisted of chronic inflammatory tissue with actinomycotic colonies . Immediate antibiotic therapy consisting of phenoxymethyl penicillin 500 mg 4 x daily was instigated . The patient made an uneventful recovery and was discharged the next day. She was kept under regular review, but returned to the West Indies in the latter part of October 1979 and was then lost to follow-up.
I. 2. 3. 4. 5.
It is interesting to speculate on the aetiology
radicular cyst keratocyst odontogenic tumour cementoblastoma metastatic tumour
The patient was admit ted to hospital for exploration of the area under general anaesthesia. At surgery on July 20, 1979, a solid grey mass was found. This had perforated the lingual plate
Fig. 4. Radiograph showing radiolucent area associated with 76/ (enlarged from orthopantomograph).
Discussion of the disease in the first case. Soft tissues are more commonly involved in actinomycotic infections 15, and this would suggest that the epulis was the original source of the infection. This probably originated from a periodontal pocket with suitable anaerobic conditions favourable to the growth of actinomycosis organisms. Actinomyces organisms are predominant populations in gingivitis and early periodontitis''". The subsequent gingivectomy would then have spread the organism more deeply within the tissues, an attempt then being made by the dental practitioner to treat this by conventional root canal therapy. In this case, bone involvement occurred early with rapid destruction. As previously mentioned, this may be due to a variation in pathogenicity or, may be a reflection of the host's resistance . Interestingly, when actinomyces organisms are specifically looked for in cultures of infected root canals, they have been found in 10.6% of positive cultures.'. Neither case presented with chronic sinuses and purulent discharge, factors often claimed to be reliable guides to diagnosis. The second case presented with no history of recent trauma. One may only speculate whether actinomycosis, which may be of
ACTINOMYCOSIS
low virulence, can remain in the tissues for 10 years and therefore be related to the extraction of 8/. One cannot assume the presence of an actinomycotic lesion without classical clinical features or a positive culture or histology. OWEN & MACANSH 9 reported a case of actinomycosis of the mandible that lasted for more than 3 years without displaying typical signs such as board-like swelling and multiple abscesses and sinuses. CRAN & HANNAM 3 suggested that actinomycotic infection might be more common than previously thought, but often remaining undiagnosed. Thus we cannot ignore the possibility that the infection entered the tissues through the extraction socket and remained there for a long time before a clinically obvious lesion presented. Actinomyces israelii is highly sensitive to many antibiotics and there are no recorded cases of resistance to penicillin 7 • Treatment should be prolonged and thus for the first case, where total surgical excision had been accomplished, the antibiotic was continued for 3 months. In the second case, due to the high probability of residual infected tissue, the antibiotic was continued for 6 months.
Conclusion The points discussed stress the importance of routinely submitting all excision specimens and biopsies for histological examination. Actinomycosis must be considered in persistent orofacial infections whilst remembering that this disease may masquerade and present atypically.
References I. BHASKAR, S. N.: Synopsis oforal pathology. C. V. Mosby Company, St. Louis 1981, p. 679. 2. BORSSEN, E. & SUNDQUIST, G.: Actinomyces of infected dental root canals. Oral Surg, 1981: 51: 643-648. 3. CRAN, J. A. & HANNAM, A. G.: Cervicofacial actinomycosis. Aust. Dent. J. 1963: 8: 106108. 4. DOVE, 1.: Actinomycosis in surgical biopsies. J. Roy. Soc. Med. 1979: 72: 106-108. 5. FERGUS, H. S. & SAVORD, E. G.: Actinomycosis involving a periapical cyst in the anterior maxilla. Oral Surg, 1980: 49: 390-393. 6. GOLDSTEfN, B. H., SCIRBA, 1. J. & LASKIN, D. M.: Actinomycosis of the maxilla. J. Oral Surg, 1972: 30: 362-366. 7. HENSHER, R. & BOWERMAN, J. Eo: Actinomycosis of the parotid gland. Br. J. Oral Surg., in press. 8. MARSH, P.: Oral microbiology. Thomas Nelson & Sons Ltd., Surrey 1980. (a) p. 78, (b) p. 78, (c) p. 48, (d) p. 78, (e) ppo 64-65. 9. OWEN, M. D. & MACANSH, Jo: Actinomycosis of the mandible. Med. J. Aust. 1965: 52: 962963. 10. RANKOW, R. M. & ABRAHAM, D. M.: Actinomycosis: masquerader in the head and neck. Ann. Otol. Rhinol. Laryngol. 1978: 87: 230-237. II. STENHOUSE, D. & MACDONALD, D. G.: Low grade osteomyelitis of the jaws with actinomycosis. Int. J. Oral Surg, 1974: 3: 60-64. 12. SHAFER, W. G., HfNE, M. K. & LEVY, B. M.: A textbook of oral pathology. W. B. Saunders Company, Philadelphia 1974, p. 349. 13. WALTER, J. B., HAMILTON, M. C. & ISRAEL, M. S.: Principles of pathology for dental students. Churchill Livingstone, Edinburgh 1981, p. 234. 14. WEIR, J. C. & BUCK, W. H.: Periapical actinomycosis; report of a case and review of the literature. Oral Surg. 1982: 54: 336-340. 15. YAKATA, H., NAKAJIMA, T., YAMADA, H. & TOKIWA, N.: Actinomycotic osteomyelitis of the mandible; report of case. J. Oral Surg, 1978: 36: 720-724. Address:
Acknowledgements - We would like to thank Mr. J. D. Langdon for allowing us to document these 2 cases and for his kind advice in the preparation of this paper. Additionally we would like to thank the photographic department of Queen Mary's Hospital, Roehampton, for preparing the figures.
199
R. Benoliel cio J. D. Langdon Department of Oral & Maxillofacial Surgery King's College Hospital Dental School Denmark Hill London, SE5 8RX England