BritishJournal ofOphthalmology, 1991,75, 61-63

Decalcification of a choroidal osteoma

Susan N Trimble, Howard Schatz

AbstractA 56-year-old man presented with a clearlydefined orange tumour in the posterior pole ofhis left eye. A choroidal osteoma was sus-pected, and ultrasonography confirmed thediagnosis. Fluorescein angiography demon-

strated subretinal neovascularisation on the

nasal edge of the tumour, which was treatedwith krypton laser photocoagulation twice.Recurrent subretinal neovascularisationoccurred one year later and was not amenableto treatment. Three years after the patient firstpresented, thinning of the tumour was notedon follow-up examination. During the next 15months the tumour completely disappeared,leaving an area ofretinal pigment epithelial andchoroidal atrophy. Total decalcification of the Figure lB Red-free photchoroidal osteoma was demonstrated by ultra- choroidal osteoma in the uppatch ofsubretinal neovascsonography. bundle adjacent to thefove

haemorrhage.

tograph left macula. Note thepper part ofthe macula. There is acularisation in the papillomacularea. Note afew spots ofsubretinal

Choroidal osteomas are juxtapapillary choroidallesions which contain bone, and have beenrecognised since 1978.1 2 We report a second caseof choroidal osteoma which gradually dis-appeared after laser treatment for subretinalneovascularisation.3 In both cases decalcificationoccurred, leaving an area of atrophic retinalpigment epithelium and choriocapillaris.

Case reportIn June 1982, a 56-year-old white male was seenin consultation with a three- or four-week historyof distorted vision in his left eye. The history wasnegative except for past thyroid cancer in 1955.A thyroid resection was done initially, andmetastic rib cage tumours were removed in 1963.When he presented to us, his visual acuity was20/20 in the right eye and 20/50 in the left eye. Awell defined, slightly elevated mass was seen inthe posterior pole of the left eye. The mass wasorange centrally and was yellow-white where theretinal pigment epithelium was thinned along

the margin (Fig lA). Fluorescein angiographydemonstrated the tumour and subretinal neo-vascularisation located nasal to the left fovea(Figs 1 B-D). On the ultrasonogram there wasvery high reflectivity and extreme acousticshadowing of orbital fat behind the globe consis-tent with the diagnosis of choroidal osteoma.The subretinal neovascularisation was treated

with krypton laser photocoagulation. Twomonths later the patient's vision dropped from20/40 to 8/200, and recurrent subretinal neo-vascularisation was again treated with laser. Hisvision did not improve, though the macularemained dry for the next year. In August 1983there was a new haemorrhage with serousdetachment in the macula, and recurrent sub-retinal neovascularisation was defined on thefluorescein angiogram (Figs 2, A-C). Since thenhis vision has remained 3/200.

Department ofOphthalmology, LoyolaUniversity MedicalCenter, Maywood,Illinois, USAS N Trimble

Retina Research Fund,St Mary's Hospital andMedical Center, andDepartment ofOphthalmology,University of California,San Francisco, USAH SchatzCorrespondence to:Howard Schatz, MD, 1 DanielBurnham Court, SanFrancisco, CA 94109, USA.Accepted for publication18 July 1990

Figure IA june 1982. Well defined choroidal osteoma withreddish centre andyellow-white edge. Note subretinalneovascularisation at inferior nasal edge oftumour.

Figure IC Midphase angiogram showing moderatefluorescence from the choroidal osteoma as well ashyperfluorescencefrom the ring ofsubretinalneovascularisation nasal to thefovea. The haemorrhagehypofluoresces.

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Trimble, Schatz

Figure ID Late phase fluorescein angiogram shows that thechoroidal osteoma stains and there is leakage into thesubretinal spacefrom the patch ofsubretinalneovascularisation.

Figure 2C Late phase angiogram shows leakagefrom thepatch ofsubretinal neovascularisation below and staining ofthe choroidal osteoma and previous laser treatment.

Figure 2A Fourteen months later. The patch ofsubretinal Figure 3 July 1986 Complete decalcification oftheneovascularisation has been treated, and there is an atrophic choroidal osteoma has occurred leaving an area ofpigmentscar in the papillomacular bundle. The subretinal epithelial and choroidal atrophy. Clumps ofpigment are seen.

neovascularisation has recurred just below the fovea. Thechoroidal osteoma appears thinner with visualisation ofchoroidal vessels. _

Figure 4A September 1988. Additional chorioretinalatrophy has occurred sinceJuly 1986.

Figure 2B Midphase angiograms showing hyperfluorescencefrom the patch ofsubretinal neovascularisation below themacula with a surrounding ring ofsubretinal haemorrhage(hypofluorescent ring), atrophyfrom the previous laser nasal tothefovea, and thinning ofthe choroidal osteoma above.

In April 1985 the tumour appeared to bethinning, and retinal pigment epithelial atrophywas noted. Ultrasonography still showedcalcification. Fifteen months later the pigmentepithelium was more atrophic (Fig 3), and totaldecalcification was confirmed by ultrasono-graphy. Examination in 1988 revealed additional

chorioretinal atrophy at the tumour site (Figs4A-D).

DiscussionChoroidal osteomas are yellow-white or orange,

peripapillary lesions with discrete, well definedborders. They are seen most often in young

white, healthy females. The aetiology is notknown, but one factor may be intraocularinflammation. They have been found in eyes

with associated inflammatory diseases.' Wehave reported a case ofan osteoma that developed

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Decalcification ofa choroidal osteoma

Figure 4B Red-free photograph. Atrophic areas are seen at Figure 4C Mid-phase angiography shows hypofluorescencethe previous tumour site. There is thinning and loss ofretinal in the areas ofchorioretinal atrophy. In the surrounding retinapigment epithelium and choroid with scattered pigment is hyperfluorescence due to visualisation ofchoriocapillarisclumping. where overlying retinal pigment epithelium is defective.

fl1E' '; :s.s 4-k' X ..w~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~........

..~~~~~~~~~~~ ~ ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~'.;;..Figure~~~~~~~.4D Late .tg .....lshow .yefloes.c

fromscleralstaining. Pigment clumps are hypofluorescent.~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~.......

at a site where focal choroiditis had occurred fiveyears previously.7Unexpected decalcification and disappearance ofa choroidal osteoma was observed and firstreported by us in 1988.3 In that case a 23-year-oldwoman had a choroidal osteoma confirmed byultrasonography and orbital tomography. Overfive years it grew slowly. Subretinal neo-

vascularisation developed and was treated withargon laser photocoagulation. Gradual thinningand tumour decalcification followed. Eighteenmonths later complete decalcification andatrophy had occurred. At that time a bed ofpigment epithelial and choriocapillaris atrophyremained. Disappearance of the choroidalosteoma and loss of calcium was confirmed byfluorescein angiography and ultrasonography.A second case is reported here in a 56-year-old

man. The development of parafoveal subretinalneovascularisation occurred in both patients and

was treated with laser photocoagulation.Whether this factor is of any significance in thesubsequent disappearance of the tumour isunknown.

Resorption of bone is initiated when there isosteoclast formation adjacent to bone. Osteo-clasts are multinucleated cells formed by thefusion of mononuclear precursors. In additionmononuclear phagocytic inflammatory cells(monocytes and macrophages) may participate inresorption of normal or pathological bone.

Reporting this second case is importantbecause the phenomenon of decalcification anddisappearance of choroidal osteomas could bepart of the natural course of the disease. Sincechoroidal osteomas were first identified in 1978,most cases have been followed up for a decade orless. Another factor in both our cases is that eachhad laser treatment for subretinal neovas-cularisation. Perhaps a cascade of osteoclastactivity was initiated after it which led to thedisappearance of the osteoma. In a patient whopresents with a well defined area of chorioretinalatrophy in the posterior pole a decalcifiedchoroidal osteoma should be considered in thedifferential diagnosis.

1 Williams AT, Font RL, VanDyk HJL, Riekhof FT. Osseouschoristoma of the choroid simulating a choroidal melanoma.Arch Ophthalmol 1978; 96: 1874-7.

2 Gass JDM, Guerry RK, Jack RL, Haris G. Choroidal osteoma.Arch Ophthalmol 1978; 96: 428-35.

3 Trimble SN, Schatz H, Schneider GB. Spontaneous decalcifi-cation of a choroidal osteoma. Ophthalmology 1988; 95:631-4.

4 Kline LB, Skalka HW, Davidson JD, Wilmes FJ. Bilateralchoroidal osteomas associated wth fatal systemic illness. AmJ7Ophthalmol 1982; 93: 192-97.

5 Gass JDM. Stereoscopic atlas of macular diseases. 3rd ed. St.Louis: 1987: 1:152, 153, 180.

6 Katz RS, Gass JDM. Multiple choroidal osteomas developing inassociation with recurrent orbital inflammatory pseudo-tumour. Arch Ophthalmol 1983; 101: 1724-7.

7 Trimble SN, Schatz H. Choroidal osteoma after intraocularinflammation. AmJ Ophthalmol 1982; 96: 759-64.

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