Keywords
discoid lateral meniscus - histology - children - knee - development
Introduction
Discoid lateral meniscus is the most frequent variant of the meniscus and it is bilateral
in up to 20% of cases.[1] Discoid menisci can be classified according to Watanabe et al[2] in complete, incomplete, and Wrisberg's variants. A ring-shaped variant was subsequently
described.[3]
There is still debate about the etiology of discoid meniscus. Smillie[4] first proposed that it is normally present at some stages during fetal development.
However, most of the authors believe that it is anomalous also during prenatal development
and arises through variant morphogenesis.[5]
[6] In fact, it is frequently associated to other abnormalities, often an incidental
finding, and commonly asymptomatic.[1]
Although the histology of normal menisci in children and in adults has been well described,[2] few studies focused on the histology of discoid menisci, unfortunately including
a great number of adults and meniscal tears.[7]
[8]
[9]
[10]
The aim of the present study was to report the histological findings of discoid lateral
meniscus in children and adolescents, after arthroscopic partial resection, to give
a possible explanation of its developmental etiology.
Methods
This study is conformed to the Declaration of Helsinki as revised in 2000. Approval
from the Institutional Review Board was waived for this study at the author's Institution.
Parents of the young patients signed a written informed consent prior to surgery,
authorizing histological examination of the specimens.
From 2012 to 2016, all the children and adolescents presenting for a symptomatic (locking,
caching, popping, and/or pain) discoid lateral meniscus at the authors' Institution
were prospectively scrutinized and enrolled in the study. There were no exclusion
criteria for this study.
Five patients were arthroscopically operated on for a symptomatic discoid lateral
meniscus at our Department. During each intervention, partial meniscectomy (saucerization)
with preservation of a stable peripheral rim was performed to obtain the shape of
a normal meniscus. The resected tissue was decalcified in ethylenediaminetretracetic
acid (EDTA) buffered for 2 hours, fixed in 4% buffered formaldehyde for 24 hours,
and placed in a series of graded ethanol solution for paraffin embedding. From the
paraffin blocks, 3-µm thick sections were cut both parallel and perpendicular to the
articular horizontal plane and stained with hematoxylin and eosin, Masson trichromic,
and Alcian-Periodic acid-Schiff reaction (PAS). The sections were examined with an
Axioskop microscope (Carl Zeiss Light Microscopy, Göttingen, Germany) and photographed
with a digital camera (Rt Slider, Diagnostic Instrument Inc., Germany).
Results
There were one female and four male patients aged 9, 10, 13, 15, and 17 years. The
right knee was involved in two cases. At preoperative magnetic resonance imaging (MRI)
and at arthroscopic examination, a complete variant was diagnosed.[2]
At full-thickness sections cut perpendicular to the surface, the tibial surface appeared
mainly smooth, while the femoral surface appeared undulated, frayed or in some cases
with clefts; the extracellular matrix, showed a lower intensity of staining, on the
periphery of both the tibial and femoral surfaces. The decreasing cell gradient of
the normal meniscus was completely absent ([Fig. 1]).
Fig. 1 Section perpendicular to the articular surfaces of a discoid lateral meniscus in
a 13-year-old patient (×5 magnification, Masson's trichrome). The femoral surface
(F) shows an irregular and notched profile unlike the tibial surface (T) which appears
smooth and more regular. Within the fibrocartilaginous tissue, areas of wide tissue
degeneration are evident, represented both by a lower intensity of staining and by
the presence of completely disorganized collagen fibers. There are also areas of tissue
lacerations associated with a lower cell density (asterisks). It is possible to observe
the different aspect of the cell component. On the articular sides, cells have a more
flattened aspect while in the innermost portion the cells appear more rounded.
The collagen fibers in the inner part showed a woven arrangement, while peripheral
parts were larger and formed a tighter network ([Fig. 2]). Several tears were observed (asterisks in [Fig. 1]). Degenerated extracellular matrix with disorganized and less-dense collagen fibers
was observed in some areas of the different sections. ([Figs. 1]
[2]
[3]
[4]). On both meniscal surfaces, cells had a more flattened, fusiform morphology (similar
to fibroblasts). In contrast, the central portion cell was more rounded (similar to
chondrocytes; [Figs. 1] and [2]). The vascular supply was completely absent in all specimens.
Fig. 2 Section perpendicular to the articular surfaces of a discoid lateral meniscus in
a 13-year-old patient (×10 magnification, hematoxylin and eosin). This picture shows
how the thickness and orientation of the collagen fibers vary from the surface to
the innermost portion of the tissue. On the surface, we observe thick fibers with
parallel orientation to the surface. Moving toward the center, we observe collagen
fibers with random orientation and considerably reduced thickness. Edematous areas
were also evident in the tissue.
Fig. 3 Section perpendicular to the articular surfaces of a discoid lateral meniscus in
a 17-year-old patient (×20 magnification, hematoxylin and eosin). This section shows
a markedly degenerated fibrocartilaginous tissue with large areas of tissue breakdown.
Note the complete absence of the cellular component in the most degenerated areas.
Fig. 4 Section parallel to the articular surfaces of a discoid lateral meniscus in a 17-year-old
patient (×10 magnification Masson's trichrome). Tissue degeneration is even more marked
here, especially in the innermost portion of the meniscus. Edema associated with a
poor presence of the cellular component and an important alteration of the extracellular
matrix are evident in this section.
Both on the tibial and femoral side, cells were randomly scattered, the collagen fibers
were irregularly represented, with a loose texture. Some areas of hypocellularity
as a sign of degeneration were present ([Fig. 4]).
On sections cut parallel to the articular surface, thick bundles of almost homogeneous
size, with variable directions, were observed, cells had a round morphology, and a
random distribution ([Fig. 4]). A lower intensity of staining, with disorganized and inhomogeneous aspect, was
observed in some areas, with collagen fibers distributed without a definite arrangement.
Cells were decreased and irregularly distributed ([Figs. 4] and [5]).
Fig. 5 Section parallel to the articular surfaces in a 17-year-old patient (×10 magnification,
Masson's trichrome). In this image it is possible to observe the presence of collagen
fibers with a different orientation and a cell component randomly scattered inside
the different areas of the tissue.
Discussion
The histologic findings of our study seem to confirm that discoid lateral meniscus
is different from a normal meniscus in terms of distribution and shape of the cells,
vascularity, and organization of collagen fibers, irrespectively of the age of the
patients.
Discoid meniscus represents the most common congenital abnormality of the knee meniscus.
Cadaveric studies reported the prevalence of discoid lateral meniscus to be between
0 and 7%, while arthroscopic studies reported a prevalence from 0.4 to 16.6%,[11] with the highest values in the Asian population (20%).[1] The exact pathologic alterations and cause of this discoid shape is still debated.
Smillie,[4] who proposed the first theory about the discoid meniscus, considered that it resulted
from the persistence of a normal fetal stage of normal development, consequence of
a failure of resorption of the central area of a cartilaginous disc. Kaplan[6] refuted this theory and proposed a developmental theory, considering the discoid
shape to be the consequence of the abnormal meniscal motion due to the lack of attachment
to the tibia, and definitely revealed that the menisci are never discoid during the
development. This last conclusion was confirmed also by Clark and Ogden[5] in their prenatal and postnatal cadaver knee studies of the developmental changes
that occur in the menisci prior to skeletal maturity. Le Minor[12] reported also that no embriological study in humans had ever shown a discoid shape
in lateral menisci, and concluded that discoid lateral meniscus does not originate
from a persistence of normal embryonic structure. Murlimanju et al,[13] studying the lateral meniscus of the knee in South Indian human fetuses, reported
an incidence of a discoid-shaped lateral meniscus in only 17.9% of the cases, while
the majority of the knees had a nondiscoid shape. They concluded that the lateral
meniscus is anomalous and arises from variant morphogenesis.
Despite the large number of anatomic, clinical, and arthroscopic studies on discoid
lateral meniscus, there are limited data in the literature regarding its histology
that can help to understand its possible developmental etiology.
Only few papers described the histology of discoid meniscus. Atay et al[7] reported a decrease in the number of collagen fibers with a heterogeneous course
in discoid menisci. Cui and Min[9] reported the femoral surface of discoid meniscus to be covered by dense and well-arranged
thick fibrils, while the tibial surface to have an irregular orientation of fibers.
This significant disorganization of the circular collagen network in the discoid meniscus
with a heterogeneous course of the circumferentially arranged collagen fibers with
areas of degeneration was confirmed by Papadopoulos et al.[8] He concluded that the discoid meniscus represents a structural lesion rather than
a morphologic variant.
The limitations of those studies are the inclusion of a great percentage of adults
and meniscal tears.
The main finding of the current study is the description of the histologic features
of discoid lateral meniscus in a group composed only by children and adolescents without
a meniscal tear. In our study, the significant disorganization of the circular collagen
network in the discoid meniscus with a heterogeneous course of the circumferentially
arranged collagen fibers was observed, together with areas of degeneration with lower
density of extracellular matrix, evidenced by a lower intensity of staining.
Most authors also believe that the discoid meniscus must be of congenital origin,
and support that the congenital theory comes from evidence of familial transmission
and reports of occurrence in twins. Discoid meniscus has also been described associated
with agenesis of anterior cruciate ligament,[14] with cord-like anterior intermeniscal ligament,[15] and with hypoplasia of the medial femoral condyle.[16] These last reports seem to confirm that the discoid lateral meniscus is a complete
different entity from the normal meniscus with a possible genetic transmission, and
not a consequence of an altered meniscal development. Furthermore, regrowth of a discoid
lateral meniscus after arthroscopic reshaping has been described in an adolescent,
as to indicate the genetic information to obtain the discoid shape at the end of skeletal
growth.[17]
We observed also a scattered distribution of the cells in the discoid meniscus. They
appeared also very different depending on where they were observed in the tissue:
from a very flat shape close to the outer part of the meniscus to an oval/round shape
(like chondrocytes) in the inner part. These histological observations have never
been described in a normal meniscus.
All our samples were obtained at surgery from children or adolescent patients. We
did not find differences in the different samples examined at different ages.
These findings suggest that discoid lateral meniscus is different from a normal meniscus
in terms of cellularity and organization of collagen fibers. We speculate that the
disorganization of collagen is a native feature of discoid lateral meniscus, and not
a consequence of the degeneration induced by the altered mechanics. Thus, we agree
with Murlimanju et al[13] that the discoid lateral meniscus must be anomalous and due to a variant morphogenesis.
Limitations
The main limitation of the current study is the lack of comparison with a normal meniscus,
but there were no meniscal tears in children and adolescents during the study period
that required resection (we usually perform meniscal repair in these young patients).
Conclusion
In conclusion, the histologic findings of our study seem to confirm that discoid lateral
meniscus is different from a normal meniscus in terms of distribution and shape of
the cells, vascularity, and organization of collagen fibers, irrespective of the patients'
age. This features may predispose discoid lateral meniscus to degeneration, damage,
and tear in young patients also.
