Ann OWl Rhiool LaryngollOl:1992
MAXILLARY SINUS ATELECTASIS PATRICK J. ANTONELLI, MD MlNNEAPOus, MINNEsOTA
ARNDT J. DUVALL III, MD
STEVEN L. TEITELBAUM, MD
MlNNEAPOus, MINNEsOTA
ST LoUIS, MISSOURI
Two patients are presented with maxillary bone loss and atelectasis of the sinus walls in association with chronic subclinical maxillarysinusitis.Maxillarysinusatelectasis resultsin a mildcosmeticdeformity, but mayalsocausediplopiaby involvingthe orbital floor. Ostialobstructionand inflammation-mediated osteopeniaare postulatedto be the responsiblemechanisms. Surgicaltreatmentof the sinusitismay prevent progressionof the bone loss. KEY WORDS- atelectasis, maxillarysinus, sinusitis.
INTRODUCTION
tuberculosis that was treated for 1 full year, ending approximately 1 year prior to presentation to the otolaryngology service. Following the treatment for tuberculosis, the patient was treated for asthma with bronchodilators. He had no history of nasal polyps or chronic sinusitis, but did suffer one episode of bilateral acute sinusitis 2 years prior to presentation that was radiographically confirmed and responded well to oral antibiotics and nasal decongestants.
The sequelae and complications of sinusitis that have been reported are primarily suppurative.' Asymptomatic maxillary bone loss with atelectasis of the maxillary sinus is not widely recognized as a sequela of chronic maxillary sinusitis, even when there is associated osteomyelitis with demineralization. 2 The purpose of this paper is to describe two patients who presented with atelectasis of the maxillary sinus in association with only subclinical chronic sinusitis, and to offer insight into the possible causative mechanisms.
. Sinus endoscopy revealed lateral bowing of the nght lateral nasal wall. Exploration of the right maxillary sinus through a Caldwell-Luc operation revealed no erosive lesions. The anterior maxillary wall bone was very thin and bowed posteriorly, but with-
CASEREPORTS
Case 1. A 32-year-old man developed excruciating pain in his right upper teeth during a pressurized commercial airplane flight. He was without further symptoms until a few days later. While he was watching television, the right side of his face felt unusual. On inspection, he felt that his right cheek was depressed. He did not have any facial pain, symptoms referable to the sinuses, or vision changes, such as diplopia. He did not seek medical evaluation until approximately 1 year later. Computed tomograms of the face revealed collapse of the anterior, posterior, and medial walls of the right maxillary sinus (Fig 1); hence, the patient was referred to the otolaryngology service. The dentition was healthy and the occlusion was subjectively unchanged. The facial and trigeminal nerves were symmetrically intact. No enophthalmos was apparent. The remainder of the head and neck examination yielded unremarkable findings. The medical history was significant for pulmonary
Fig 1.(Case1)Computedtomogramof paranasalsinuses.
From the Department of Otolaryngology, University of Minnesota School of Medicine, Minneapolis, Minnesota (Antonelli, Duvall), and the Department of Pathology, Jewish Hospital at Washington University School of Medicine, St Louis, Missouri (Teitelbaum). REPRINTS - Patrick J. Antonelli, MD, Box 396 UMHC, 420 Delaware SI SE, Minneapolis, MN 55455.
977
978
Antonelliet al, Maxillary Sinus Atelectasis
Fig 2. (Case 1) Photomicrographs. A) Right maxillary sinus bone appears normal. B) Overlying mucosa is inflamed.
out signs of necrosis. The antrum was collapsed and lined with pale, edematous mucosa. Histopathologic examination revealed normal-appearing bone in a fibrocellular stroma and chronic inflammation ofthe mucosa (Fig 2). Cultures of sinus bone and mucosa revealed normal oral flora and no bacterial or fungal pathogens. No additional treatment was prescribed. The patient has failed to keep follow-up appointments, but his family reports that he is doing well, without additional symptoms or facial changes, 6 months postoperatively.
Examination revealed an obvious depression of the left cheek, just below the infraorbital rim. Anterior rhinoscopy was limited by a bilateral septal deviation, more marked on the left. Flexible nasal endoscopy revealed fullness in the left middle meatus, but no erosive lesions or discrete tumors. A left anterior maxillary wall defect and atrophic lateral buttress were palpable transorally. The palate was intact and the left maxillary canine and premolar were secure. Facial and trigeminal nerve function was symmetrically intact.
Case 2. A 65-year-old man presented to the otolaryngology service with a 2-month history of gradual left cheek depression and bilateral nasal obstruction since childhood, but no other symptoms referable to the nose or sinuses. His medical history was significant for routine dental extractions, prostate cancer that was treated by radical prostatectomy 2 years prior to presentation, type II diabetes mellitus, remote alcohol abuse, and coronary artery disease.
Sinus films taken 3 months prior to presentation were interpreted by a radiologist as normal, but revealed bone loss of the left lateral buttress. Sinus films taken on the initial otolaryngologic evaluation confirmed this finding. Axial computed tomograms with coronal reconstruction showed collapse of the anterior, posterior, and superior maxillary sinus walls; however, no tumor was identified in or around the sinus (Fig 3). A bone scan, done just prior to presen-
Antonelliet al, Maxillary Sinus Atelectasis
979
can cause maxillary bone loss in Western populations. Acute sinusitis usually results in a lytic osteitis, whereas low-grade repeated infections are more commonly associated with a blastic osteitis," Chronic osteolytic sinusitis resulting from inhaling cocaine has been reported.f Maxillary mucoceles, which are thought to result from chronic or recurrent sinusitis, rarely result in bony erosion.? When the roof of the maxillary sinus is eroded by a mucocele, enophthalmos may develop.l?
Fig 3. (Case 2) Computed tomogram ofparanasal sinuses.
tation in follow-up for the prostate cancer, was interpreted as normal. A Caldwell-Luc operation was performed. The bone of the entire maxillary sinus was extremely thin and soft, but was without necrosis or erosions. The sinus mucosa was pale and no pus was seen. A polyp measuring lOx 8 x 5 mm was removed from the floor ofthe sinus. Polypoid mucosa was also removed from the area surrounding the natural ostium. Microscopic examination revealed unremarkable bone (Fig 4A). There was chronic mucosal inflammation and marked stromal edema with plasma cell infiltrate in the polyp (Fig 4B). No additional treatment was prescribed and the patient is doing well 6 months postoperatively.
DISCUSSION Occult maxillary bone loss is a potentially ominous radiographic finding, as the diagnosis is carcinoma until proven otherwise.r Maxillary bone loss may result from many disease processes. Unfortunately, the clinical history and objective findings do not always suggest the underlying cause for the bone loss. For instance, osteomyelitis, which results in focal bone loss, most often develops from an odontogenic infection,3,4 but may occur in the absence of oral disease or local trauma. 2,4Rare disorders, such as massive osteolysis, or phantom bone syndrome, also result in asymptomatic maxillary bone loss.s These asymptomatic and unusual causes of maxillary bone loss generally require histologic examination to establish a diagnosis.f Sinusitis is one of the most common diseases that
Chronic sinusitis as a cause of maxillary bone loss and collapse of the sinus walls has been reported previously. In 1981, Wilkins and Kulwin, 11 ophthalmologists, described five patients who developed spontaneous collapse of the orbital floor and enophthalmos in the presence ofchronic or recurrent sinusitis. All of these patients had a long history of maxillary sinusitis or allergic rhinitis. None were described as having sinus atelectasis. In 1986, Wesley et al 12 presented a similar case in the otolaryngologic literature. In 1991, Isaacs et aI13 described two patients who developed enophthalmos and atelectasis of the maxillary sinus in association with chronic subclinical sinusitis. Both of the patients whom we have presented developed maxillary sinus atelectasis, without clinical evidence of enophthalmos. In both of our patients, the historical and histologic data suggested that the sole cause for the maxillary sinus atelectasis was mild chronic maxillary sinusitis. Obstruction of the sinus ostium may be the critical factor in the development of maxillary sinus atelectasis. Ostial obstruction is thought to be the principal factor in the initiation of both acute and chronic sinusitis.l'' The first patient's history of maxillary pain during an airplane flight shortly before he noticed the depression in his cheek was presumably a result of change in environmental pressure. This indicates that some degree or period ofthe sinus ostial obstruction was present prior to the "collapse" of the sinus. Local stress is known to influence the remodeling of bone. 15 Since bone mass is ultimately a reflection of the remodeling process, changes in the rate ofremodeling can theoretically cause collapse of the sinus walls. In this regard, both patients with maxillary collapse had evidence for maxillary bone loss. Ostial obstruction with development of negative pressure may serve as an example of a bone resorptive agonist, as pressure changes have been shown to result in bone resorption in vitro. 16 It is well recognized that a pressure difference between the sinuses (or middle ear) and the environment causes pain. The absence of notable symptoms in both patients suggests that minimal or transient negative pressure was
980
Antonelliet al, Maxillary Sinus Atelectasis
Fig 4. (Case 2) Photomicrographs. A) Left maxillary sinus bone and mucosa are unremarkable. B) Antral polyp has marked stromal edema and plasma cell infiltrate.
necessary to develop sinus collapse. Hence, it is unlikely that a pressure differential was the only causative mechanism. Because inflammation is known to promote osteopenia.!? chronic maxillary sinusitis may have prompted the bone loss. Cytokines produced by inflammatory cells might mediate the bone loss in inflammation-mediated osteopenia by inhibiting osteoblast cell replication and collagen synthesis 18•19 and/or stimulating bone resorption.P Osteoblasts, as well as immunocompetent cells, produce cytokines, and their production is modulated by other cytokines. 21 Thus, the regulation of cytokine-mediated bone metabolism is a complex process, but one that is receiving increased attention. In both patients presented in this paper, the bone loss was limited to the maxilla, and the only local
abnormality was chronic sinusitis. The absence of increased osteoclastic activity suggests that the bone loss is most likely a result of decreased bone formation, as seen in inflammation-mediated osteopenia. Hence, inflammation-mediated osteopenia may have arole in the development ofmaxillary sinus atelectasis.
If maxillary sinus atelectasis is caused by chronic subclinical sinusitis, traditional treatment modalities for chronic sinusitis could be expected to arrest or reverse the disease process. For diagnostic purposes, we performed a Caldwell-Luc operation on both patients, and each has done well for at least 6 months. It is not clear why maxillary sinus atelectasis developed in these two patients, and not in many other patients with chronic maxillary sinusitis. These patients may represent extreme cases along a spec-
Antonelliet al, Maxillary SinusAtelectasis
trum, with less dramatic maxillary sinus collapse not being recognized clinically or radiographically. Alternatively, sinus atelectasis may reflect an unusual biologic response to inflammation. In order to deter-
981
mine the pathogenesis and optimal treatment for maxillary sinus atelectasis, further investigation into the metabolism of maxillary bone in the presence of sinus inflammation is necessary.
REFERENCES 12. WesleyRE, Johnson11II, Cate RC. Spontaneous enoph1. Rood SR, SchrammVL, Maseiotra NJ, DuBoisP. Comthalmos from chronic maxillary sinusitis. Laryngoscope 1986; plicationsofacuteandchronicsinusitis. Washington, DC:Ameri96:353-5. canAcademyof Otolaryngology-Head andNeckSurgeryFoundation, 1982:11-47. 13. IsaacsRS, EdelsteinDR, AnandVK, LismanR. Spontaneous enophthalmos associated with the atelectatic maxillary 2. Johnson EE, Duvall AI ill, Donaldson JA. Infectious sinus [Abstract]. Otolaryngol Head Neck Surg 1991;105:274. osteonecrosis of the maxilla. ArchOtolaryngoll962;76:558-61. 14. Reilly JS. The sinusitis cycle. Otolaryngol Head Neck 3. Adekeye EO, Comah J. Osteomyelitis of the jaws: a Surg 1990;103:856-62. reviewof 141 cases. Br J Oral Maxillofac Surg 1985;23:24-35. 15. SledgeCB, RubinCT. Formation andresorption of bone. 4. KrotchdoffOJ, Runstad L. Unusually aggressive osteoIn: KellyWN,HarrisEDJr, RuddyS, SledgeCB,eds.Textbook myelitis ofthejaws.OralSurgOral MedOralPatho11989;67:499ofrheumatology.Philadelphia, Pa: WB Saunders, 1989:54-75. 507. 16. Imamura K, Ozawa H, Hiraide T, et al. Continuously 5. OhayaT, ShibataS, TakedaY. Massiveosteolysis of the maxillofacial bones.Oral SurgOralMedOralPathoI199O;70:698applied pressureinducesboneresorption by a mechanism involving prostaglandin E2 synthesis. J Cell PhysioI1990;I44:222-8. 703. 6. Shafer WG, Hine MK, Levy BM. A textbook of oral 17. MinneHW,PfeilschifterJ, ScharlaS,etal.Inflammationpathology. 4th ed. Philadelphia, Pa: WB Saunders, 1983:674mediated osteopeniaintherat:anewanimalmodelforpathologi718. cal loss of bone mass.Endocrinology 1984;115:50-4. 7. Dolan KD. Radiology. In: Cummings CW, Fredrickson 18. StashenkoP, DewhirstFE, Rooney ML, Desjardins LA, 1M, HarkerLA, KrauseCJ, SchullerDE, eds. OtolaryngologyHeeleyro. Interleukin-lPis a potentinhibitorof boneformation head and neck surgery.St Louis,Mo: CV Mosby, 1986:853-86. in vitro.J Bone Mineral Res 1987;6:559-65. 8. SchweitzerVG. Osteolyticsinusitis and pneumomedia19. SmithDO, GowenM, MundyGR. Effectsof interferonstinum: deceptiveotolaryngologiccomplications ofcocaineabuse. y and other cytokines on collagen synthesis in fetal rat bone Laryngoscope 1986;96:206-10. cultures. Endocrinology 1987;120:2494-9. 9. JohnsonIT. Infections. In: Cummings CW, Fredrickson 20. Amano S, Hanazawa S, Hirose K, Ohmori Y, KitanoS. 1M, HarkerLA, KrauseCJ, SchullerDE, eds. OtolaryngologyStimulatoryeffecton boneresorptionof'imerleukin-l-likecytoheadandnecksurgery.St Louis,Mo:CVMosby,1986:887-900. kineproducedbyanosteoblast-rich population ofmousecalvarial cells.CalcifTissue Int 1988;43:88-91. 10. Montgomery WW.Mucocele ofthe maxillary sinuscausing enophthalmos. Eye Ear NoseThroat Mon 1964;43:41-4. 21. GowenM, ChapmanK, Littlewood A, Hughes 0, Evans 0, Russell G. Production of tumor necrosis factor by human 11. Wilkins RB, Kulwin DR. Spontaneous enophthalmos osteoblasts ismodulatedbyothercytokines, butnotbyosteotropic associatedwithchronicmaxillary sinusitis. Ophthalmology 1981; hormones. Endocrinology 1990;126:1250-5. 88:981-5.
THE PROSPER MENIERE SOCIETY The annualmeetingof the ProsperMeniereSocietywillbe heldin Aspen,Colorado,February21-28, 1993.For moreinformation, please contact Apryl Salz or Jane Wells, Meeting Coordinatos, c/o I. Kaufman Arenberg, MD, FACS, Program Chairman. 300 E HampdenAve, Suite 401, Englewood, CO 80110;phone303-850-9545; fax 303-788-4234.
MAXILLARY SINUS ATELECTASIS PATRICK J. ANTONELLI, MD MlNNEAPOus, MINNEsOTA
ARNDT J. DUVALL III, MD
STEVEN L. TEITELBAUM, MD
MlNNEAPOus, MINNEsOTA
ST LoUIS, MISSOURI
Two patients are presented with maxillary bone loss and atelectasis of the sinus walls in association with chronic subclinical maxillarysinusitis.Maxillarysinusatelectasis resultsin a mildcosmeticdeformity, but mayalsocausediplopiaby involvingthe orbital floor. Ostialobstructionand inflammation-mediated osteopeniaare postulatedto be the responsiblemechanisms. Surgicaltreatmentof the sinusitismay prevent progressionof the bone loss. KEY WORDS- atelectasis, maxillarysinus, sinusitis.
INTRODUCTION
tuberculosis that was treated for 1 full year, ending approximately 1 year prior to presentation to the otolaryngology service. Following the treatment for tuberculosis, the patient was treated for asthma with bronchodilators. He had no history of nasal polyps or chronic sinusitis, but did suffer one episode of bilateral acute sinusitis 2 years prior to presentation that was radiographically confirmed and responded well to oral antibiotics and nasal decongestants.
The sequelae and complications of sinusitis that have been reported are primarily suppurative.' Asymptomatic maxillary bone loss with atelectasis of the maxillary sinus is not widely recognized as a sequela of chronic maxillary sinusitis, even when there is associated osteomyelitis with demineralization. 2 The purpose of this paper is to describe two patients who presented with atelectasis of the maxillary sinus in association with only subclinical chronic sinusitis, and to offer insight into the possible causative mechanisms.
. Sinus endoscopy revealed lateral bowing of the nght lateral nasal wall. Exploration of the right maxillary sinus through a Caldwell-Luc operation revealed no erosive lesions. The anterior maxillary wall bone was very thin and bowed posteriorly, but with-
CASEREPORTS
Case 1. A 32-year-old man developed excruciating pain in his right upper teeth during a pressurized commercial airplane flight. He was without further symptoms until a few days later. While he was watching television, the right side of his face felt unusual. On inspection, he felt that his right cheek was depressed. He did not have any facial pain, symptoms referable to the sinuses, or vision changes, such as diplopia. He did not seek medical evaluation until approximately 1 year later. Computed tomograms of the face revealed collapse of the anterior, posterior, and medial walls of the right maxillary sinus (Fig 1); hence, the patient was referred to the otolaryngology service. The dentition was healthy and the occlusion was subjectively unchanged. The facial and trigeminal nerves were symmetrically intact. No enophthalmos was apparent. The remainder of the head and neck examination yielded unremarkable findings. The medical history was significant for pulmonary
Fig 1.(Case1)Computedtomogramof paranasalsinuses.
From the Department of Otolaryngology, University of Minnesota School of Medicine, Minneapolis, Minnesota (Antonelli, Duvall), and the Department of Pathology, Jewish Hospital at Washington University School of Medicine, St Louis, Missouri (Teitelbaum). REPRINTS - Patrick J. Antonelli, MD, Box 396 UMHC, 420 Delaware SI SE, Minneapolis, MN 55455.
977
978
Antonelliet al, Maxillary Sinus Atelectasis
Fig 2. (Case 1) Photomicrographs. A) Right maxillary sinus bone appears normal. B) Overlying mucosa is inflamed.
out signs of necrosis. The antrum was collapsed and lined with pale, edematous mucosa. Histopathologic examination revealed normal-appearing bone in a fibrocellular stroma and chronic inflammation ofthe mucosa (Fig 2). Cultures of sinus bone and mucosa revealed normal oral flora and no bacterial or fungal pathogens. No additional treatment was prescribed. The patient has failed to keep follow-up appointments, but his family reports that he is doing well, without additional symptoms or facial changes, 6 months postoperatively.
Examination revealed an obvious depression of the left cheek, just below the infraorbital rim. Anterior rhinoscopy was limited by a bilateral septal deviation, more marked on the left. Flexible nasal endoscopy revealed fullness in the left middle meatus, but no erosive lesions or discrete tumors. A left anterior maxillary wall defect and atrophic lateral buttress were palpable transorally. The palate was intact and the left maxillary canine and premolar were secure. Facial and trigeminal nerve function was symmetrically intact.
Case 2. A 65-year-old man presented to the otolaryngology service with a 2-month history of gradual left cheek depression and bilateral nasal obstruction since childhood, but no other symptoms referable to the nose or sinuses. His medical history was significant for routine dental extractions, prostate cancer that was treated by radical prostatectomy 2 years prior to presentation, type II diabetes mellitus, remote alcohol abuse, and coronary artery disease.
Sinus films taken 3 months prior to presentation were interpreted by a radiologist as normal, but revealed bone loss of the left lateral buttress. Sinus films taken on the initial otolaryngologic evaluation confirmed this finding. Axial computed tomograms with coronal reconstruction showed collapse of the anterior, posterior, and superior maxillary sinus walls; however, no tumor was identified in or around the sinus (Fig 3). A bone scan, done just prior to presen-
Antonelliet al, Maxillary Sinus Atelectasis
979
can cause maxillary bone loss in Western populations. Acute sinusitis usually results in a lytic osteitis, whereas low-grade repeated infections are more commonly associated with a blastic osteitis," Chronic osteolytic sinusitis resulting from inhaling cocaine has been reported.f Maxillary mucoceles, which are thought to result from chronic or recurrent sinusitis, rarely result in bony erosion.? When the roof of the maxillary sinus is eroded by a mucocele, enophthalmos may develop.l?
Fig 3. (Case 2) Computed tomogram ofparanasal sinuses.
tation in follow-up for the prostate cancer, was interpreted as normal. A Caldwell-Luc operation was performed. The bone of the entire maxillary sinus was extremely thin and soft, but was without necrosis or erosions. The sinus mucosa was pale and no pus was seen. A polyp measuring lOx 8 x 5 mm was removed from the floor ofthe sinus. Polypoid mucosa was also removed from the area surrounding the natural ostium. Microscopic examination revealed unremarkable bone (Fig 4A). There was chronic mucosal inflammation and marked stromal edema with plasma cell infiltrate in the polyp (Fig 4B). No additional treatment was prescribed and the patient is doing well 6 months postoperatively.
DISCUSSION Occult maxillary bone loss is a potentially ominous radiographic finding, as the diagnosis is carcinoma until proven otherwise.r Maxillary bone loss may result from many disease processes. Unfortunately, the clinical history and objective findings do not always suggest the underlying cause for the bone loss. For instance, osteomyelitis, which results in focal bone loss, most often develops from an odontogenic infection,3,4 but may occur in the absence of oral disease or local trauma. 2,4Rare disorders, such as massive osteolysis, or phantom bone syndrome, also result in asymptomatic maxillary bone loss.s These asymptomatic and unusual causes of maxillary bone loss generally require histologic examination to establish a diagnosis.f Sinusitis is one of the most common diseases that
Chronic sinusitis as a cause of maxillary bone loss and collapse of the sinus walls has been reported previously. In 1981, Wilkins and Kulwin, 11 ophthalmologists, described five patients who developed spontaneous collapse of the orbital floor and enophthalmos in the presence ofchronic or recurrent sinusitis. All of these patients had a long history of maxillary sinusitis or allergic rhinitis. None were described as having sinus atelectasis. In 1986, Wesley et al 12 presented a similar case in the otolaryngologic literature. In 1991, Isaacs et aI13 described two patients who developed enophthalmos and atelectasis of the maxillary sinus in association with chronic subclinical sinusitis. Both of the patients whom we have presented developed maxillary sinus atelectasis, without clinical evidence of enophthalmos. In both of our patients, the historical and histologic data suggested that the sole cause for the maxillary sinus atelectasis was mild chronic maxillary sinusitis. Obstruction of the sinus ostium may be the critical factor in the development of maxillary sinus atelectasis. Ostial obstruction is thought to be the principal factor in the initiation of both acute and chronic sinusitis.l'' The first patient's history of maxillary pain during an airplane flight shortly before he noticed the depression in his cheek was presumably a result of change in environmental pressure. This indicates that some degree or period ofthe sinus ostial obstruction was present prior to the "collapse" of the sinus. Local stress is known to influence the remodeling of bone. 15 Since bone mass is ultimately a reflection of the remodeling process, changes in the rate ofremodeling can theoretically cause collapse of the sinus walls. In this regard, both patients with maxillary collapse had evidence for maxillary bone loss. Ostial obstruction with development of negative pressure may serve as an example of a bone resorptive agonist, as pressure changes have been shown to result in bone resorption in vitro. 16 It is well recognized that a pressure difference between the sinuses (or middle ear) and the environment causes pain. The absence of notable symptoms in both patients suggests that minimal or transient negative pressure was
980
Antonelliet al, Maxillary Sinus Atelectasis
Fig 4. (Case 2) Photomicrographs. A) Left maxillary sinus bone and mucosa are unremarkable. B) Antral polyp has marked stromal edema and plasma cell infiltrate.
necessary to develop sinus collapse. Hence, it is unlikely that a pressure differential was the only causative mechanism. Because inflammation is known to promote osteopenia.!? chronic maxillary sinusitis may have prompted the bone loss. Cytokines produced by inflammatory cells might mediate the bone loss in inflammation-mediated osteopenia by inhibiting osteoblast cell replication and collagen synthesis 18•19 and/or stimulating bone resorption.P Osteoblasts, as well as immunocompetent cells, produce cytokines, and their production is modulated by other cytokines. 21 Thus, the regulation of cytokine-mediated bone metabolism is a complex process, but one that is receiving increased attention. In both patients presented in this paper, the bone loss was limited to the maxilla, and the only local
abnormality was chronic sinusitis. The absence of increased osteoclastic activity suggests that the bone loss is most likely a result of decreased bone formation, as seen in inflammation-mediated osteopenia. Hence, inflammation-mediated osteopenia may have arole in the development ofmaxillary sinus atelectasis.
If maxillary sinus atelectasis is caused by chronic subclinical sinusitis, traditional treatment modalities for chronic sinusitis could be expected to arrest or reverse the disease process. For diagnostic purposes, we performed a Caldwell-Luc operation on both patients, and each has done well for at least 6 months. It is not clear why maxillary sinus atelectasis developed in these two patients, and not in many other patients with chronic maxillary sinusitis. These patients may represent extreme cases along a spec-
Antonelliet al, Maxillary SinusAtelectasis
trum, with less dramatic maxillary sinus collapse not being recognized clinically or radiographically. Alternatively, sinus atelectasis may reflect an unusual biologic response to inflammation. In order to deter-
981
mine the pathogenesis and optimal treatment for maxillary sinus atelectasis, further investigation into the metabolism of maxillary bone in the presence of sinus inflammation is necessary.
REFERENCES 12. WesleyRE, Johnson11II, Cate RC. Spontaneous enoph1. Rood SR, SchrammVL, Maseiotra NJ, DuBoisP. Comthalmos from chronic maxillary sinusitis. Laryngoscope 1986; plicationsofacuteandchronicsinusitis. Washington, DC:Ameri96:353-5. canAcademyof Otolaryngology-Head andNeckSurgeryFoundation, 1982:11-47. 13. IsaacsRS, EdelsteinDR, AnandVK, LismanR. Spontaneous enophthalmos associated with the atelectatic maxillary 2. Johnson EE, Duvall AI ill, Donaldson JA. Infectious sinus [Abstract]. Otolaryngol Head Neck Surg 1991;105:274. osteonecrosis of the maxilla. ArchOtolaryngoll962;76:558-61. 14. Reilly JS. The sinusitis cycle. Otolaryngol Head Neck 3. Adekeye EO, Comah J. Osteomyelitis of the jaws: a Surg 1990;103:856-62. reviewof 141 cases. Br J Oral Maxillofac Surg 1985;23:24-35. 15. SledgeCB, RubinCT. Formation andresorption of bone. 4. KrotchdoffOJ, Runstad L. Unusually aggressive osteoIn: KellyWN,HarrisEDJr, RuddyS, SledgeCB,eds.Textbook myelitis ofthejaws.OralSurgOral MedOralPatho11989;67:499ofrheumatology.Philadelphia, Pa: WB Saunders, 1989:54-75. 507. 16. Imamura K, Ozawa H, Hiraide T, et al. Continuously 5. OhayaT, ShibataS, TakedaY. Massiveosteolysis of the maxillofacial bones.Oral SurgOralMedOralPathoI199O;70:698applied pressureinducesboneresorption by a mechanism involving prostaglandin E2 synthesis. J Cell PhysioI1990;I44:222-8. 703. 6. Shafer WG, Hine MK, Levy BM. A textbook of oral 17. MinneHW,PfeilschifterJ, ScharlaS,etal.Inflammationpathology. 4th ed. Philadelphia, Pa: WB Saunders, 1983:674mediated osteopeniaintherat:anewanimalmodelforpathologi718. cal loss of bone mass.Endocrinology 1984;115:50-4. 7. Dolan KD. Radiology. In: Cummings CW, Fredrickson 18. StashenkoP, DewhirstFE, Rooney ML, Desjardins LA, 1M, HarkerLA, KrauseCJ, SchullerDE, eds. OtolaryngologyHeeleyro. Interleukin-lPis a potentinhibitorof boneformation head and neck surgery.St Louis,Mo: CV Mosby, 1986:853-86. in vitro.J Bone Mineral Res 1987;6:559-65. 8. SchweitzerVG. Osteolyticsinusitis and pneumomedia19. SmithDO, GowenM, MundyGR. Effectsof interferonstinum: deceptiveotolaryngologiccomplications ofcocaineabuse. y and other cytokines on collagen synthesis in fetal rat bone Laryngoscope 1986;96:206-10. cultures. Endocrinology 1987;120:2494-9. 9. JohnsonIT. Infections. In: Cummings CW, Fredrickson 20. Amano S, Hanazawa S, Hirose K, Ohmori Y, KitanoS. 1M, HarkerLA, KrauseCJ, SchullerDE, eds. OtolaryngologyStimulatoryeffecton boneresorptionof'imerleukin-l-likecytoheadandnecksurgery.St Louis,Mo:CVMosby,1986:887-900. kineproducedbyanosteoblast-rich population ofmousecalvarial cells.CalcifTissue Int 1988;43:88-91. 10. Montgomery WW.Mucocele ofthe maxillary sinuscausing enophthalmos. Eye Ear NoseThroat Mon 1964;43:41-4. 21. GowenM, ChapmanK, Littlewood A, Hughes 0, Evans 0, Russell G. Production of tumor necrosis factor by human 11. Wilkins RB, Kulwin DR. Spontaneous enophthalmos osteoblasts ismodulatedbyothercytokines, butnotbyosteotropic associatedwithchronicmaxillary sinusitis. Ophthalmology 1981; hormones. Endocrinology 1990;126:1250-5. 88:981-5.
THE PROSPER MENIERE SOCIETY The annualmeetingof the ProsperMeniereSocietywillbe heldin Aspen,Colorado,February21-28, 1993.For moreinformation, please contact Apryl Salz or Jane Wells, Meeting Coordinatos, c/o I. Kaufman Arenberg, MD, FACS, Program Chairman. 300 E HampdenAve, Suite 401, Englewood, CO 80110;phone303-850-9545; fax 303-788-4234.
