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Although orbital surgeons work extensively with the bony structures
of the orbit, the mechanism of bone healing has been a relatively neglected
topic in the ophthalmic literature. A detailed understanding of the basic
science of bone healing may pave the way for future innovations in surgical
and medical management of problems of the orbital bones. One factor long thought
to be important in bone healing is the hematoma overlying the fracture site.1,2 Some authors have proposed that
it acts as a mechanical and biochemical bridge for the migration of cells
that will eventually form a callus.3 Others,
however, have suggested that it does not play an important role in the healing
of bone fractures.4 In this report we describe
a case of a traumatic orbital subperiosteal hematoma with no obvious underlying
fracture and bone formation within the hematoma. This stage in bone healing
has rarely been captured histologically in a clinical setting, and appears
to support the importance of the role of the hematoma in osteoneogenesis.
Report of a Case
A 9-year-old boy was struck in the right periocular region by another
boy's head while participating in a sporting event. There was no immediate
change in vision or onset of symptoms other than a dull periorbital ache.
The following morning the vision was subjectively blurred with increased periocular
edema and ecchymosis. Five days following the injury the right eye became
proptotic and the patient complained of vertical diplopia. Medical attention
was sought. The patient's medical history was unremarkable; the only medication
he was taking was acetaminophen for the ache in the right eye. Ophthalmologic
examination revealed a best-corrected visual acuity of 20/40 OD and 20/20
OS. Pupils were symmetrically round and reactive without a relative afferent
pupillary defect. Ocular motility was full in the left eye but significantly
limited in supraduction and mildly limited in horizontal gaze in the right
eye with negative forced ductions. External examination results were unremarkable,
and fundus examination revealed a bulge in the supertemporal quadrant without
any chorioretinal folds. Hertel exophthalmometry measured 19 mm OD and 15
mm OS with a base of 83 mm. There was 3 mm of hypoglobus in the right eye,
and soft tissue could be palpated through the right upper eyelid. No resistance
to retropulsion was appreciated.
Orbital computed tomography revealed a large right superior orbital
mass contiguous with the orbital roof (Figure
1), suggesting a subperiosteal location with inferior displacement
of the extraocular muscles and globe. A diagnosis of right superior orbital
subperiosteal hematoma was made.
Coronal computed tomographic scan
demonstrating hematoma in a subperiosteal location in the right superior orbit.
An urgent anterior orbitotomy through an upper eyelid crease incision
was performed to improve vision and relieve the mass effect. Approximately
10 mm posterior to the superior orbital rim, a bluish-tinged mass was identified
beneath a thin, bulging periosteum. A 6 × 5-mm patch of this periosteum
was removed and submitted for histopathologic examination, with care being
taken to avoid the underlying bone and the medial portion of the orbit to
preserve the trochlea and neurovascular bundles. This resulted in expulsion
of a large volume of liquefied and coagulated blood, which was completely
irrigated. No fracture of the underlying bone was identified. On follow-up
examination 2 weeks postoperatively, the patient's vision had returned to
20/25 OD, and he was orthophoric in all positions of gaze. Hertel exophthalmometry
readings were 14 mm OD and 15 mm OS.
The gross specimen consisted of a triangular piece of black tissue measuring
6 × 5 × 4 mm. Light microscopic examination of routinely stained
sections (Figure 2) revealed red
blood cells and numerous polymorphonuclear and mononuclear inflammatory cells
within a highly vascular connective tissue matrix, consistent with granulation
tissue. In the granulation tissue was an island of osteoblasts within the
lacunae of an osseous matrix. A diagnosis of subperiosteal hematoma with granulation
tissue and foci of osteoneogenesis was made.
an island of osteoblasts within an osseous matrix developing within granulation
tissue (original magnification ×80).
While the etiology, epidemiology, and histopathology of orbital hematomas
have been described in the ophthalmic literature,5-9
the relationship of these hematomas to bone repair has not been described.
The sequence of events leading to osteoneogenesis after fractures has been
a subject of interest in the nonophthalmic literature.1,10,11
However, the exact biochemical and cellular mechanisms remain unclear and
are a subject of controversy among clinicians and basic scientists. The healing
process at the site of a fracture has conventionally been divided into 3 overlapping
morphologic stages: (1) an initial inflammatory stage, (2) a reparative stage,
and (3) a remodeling stage.1 The duration
of each stage is variable and depends on factors such as the size and severity
of the bony defect, as well as mechanical and biochemical influences at the
site of fracture. Our patient exhibited features of both stages 1 and 2. Stage
3 is a long-term process in which local forces and stress act to remodel and
establish the final shape and contour of the healed fracture and surrounding
bone, and was not considered in this case.
The first stage of bone fracture repair, the inflammatory stage, is
characterized by hematoma formation and inflammatory exudate from ruptured
blood vessels in bone, periosteum, and/or surrounding tissues.11
Within hours, platelets aggregate at the site of the injury, releasing cytokines,
which cause a marked inflammatory response and vasodilation. The ends of the
ruptured blood vessels soon clot off, and the loss of nutrition results in
necrosis of local tissues and osteocyte degeneration within 24 hours. Monocytes,
multinuclear phagocytes, and osteoclasts soon engulf and digest this necrotic
debris, including acellular bone.
The second stage, the reparative stage, is characterized by the formation
of a fracture callus and its subsequent transformation to mature bone. A proliferation
of blood vessels and loose connective tissue creates a bed of granulation
tissue within the periosteal tissues and marrow. The sources of the pluripotent
mesenchymal cells that transform into new bone are marrow, endosteum, periosteum,
endothelial cells, circulating cells, and surrounding muscle.12-18
These mesenchymal cells differentiate into osteoblasts, chondrocytes, and
fibroblasts, each laying down its own respective extracellular matrix. The
factors from fractured bone that attract and trigger the differentiation of
these osteoprogenitor cells remain elusive, but data obtained to date indicate
that these factors are numerous and have very complex interactions.19 The proteins most extensively studied have been
the bone morphogenetic proteins11,20,21
of the transforming growth factor β supergene family.
The process of differentiation of these primitive osteoprogenitor cells
begins within 2 to 3 days and is most marked by 1 week. By the fourth day,
nests of cartilage cells are apparent, and are soon replaced by bone tissue.15,16 By the end of the first week,
the tissue has matured to form a callus, which is of firmer consistency than
a hematoma and provides a natural internal fixation for the fracture. Subsequently,
mineralization and ossification of this new osteoid tissue progress, and new
bone tissue becomes visible radiographically as flecks of radiodense material
within approximately 1 to 3 weeks.
A hematoma occurring at the site of a bony fracture has long been suggested
to play a critical role in bone healing,2
and the absence of a fracture hematoma, whether due to surgical drainage or
anticoagulation by heparin, has been shown to result in a decrease in callus
production. In an interesting study using a rat animal model, Mizumo et al22 demonstrated that the hematoma surrounding a bony
fracture has inherent osteogenic potential, and that the osteogenic factor
arises from bone marrow.
Figure 2 shows an osseous
fleck developing within a subperiosteal hematoma. The specimen was collected
5 days after the development of the hematoma. The surrounding chronic inflammatory
exudate shows that this tissue is predominantly in the latter stages of the
stage I inflammatory process. In our patient, osteoneogenesis occurred without
any radiographic or clinical evidence of an underlying fracture. The absence
of an underlying fracture raises questions about the hypothesis developed
by Mizumo et al, that the osteogenic factor lies within the marrow. With further
understanding of these processes, it may be possible in the future to devise
less invasive and more satisfactory interventions in the management of orbital
We thank Daniel Aeschlimann, PhD, from the Department of Orthopedic
Surgery at the University of Wisconsin, Madison, for his critical review of
Corresponding author and reprints: Daniel M. Albert, MD, MS, Department
of Ophthalmology, F4/334 CSC, 600 Highland Ave, Madison, WI 53792-3220 (e-mail: firstname.lastname@example.org).
Sabet SJ, Tarbet KJ, Lemke BN, Smith ME, Albert DM. Subperiosteal Hematoma of the Orbit With Osteoneogenesis. Arch Ophthalmol. 2001;119(2):301–303. doi:
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