The importance of OsteoChondral unit. A review of over 20 years of personal clinical, surgical and imaging journey through numerous osteochondral and subchondral issues. Still more questions than answers!

1. The Importance of Subchondral Bone
and Osteochondral Unit
Vladimir Bobić, MD FRCS Ed
Chester Knee Clinic www.kneeclinic.info office@kneeclinic.info @ChesterKnee
SEEFORT 2019
www.slideshare.net/vbobic

2. Do not bother writing and taking pictures - just watch and listen!
entire presentation will be available later today on: www.slideshare.net/vbo

4. MR Imaging Protocol 1997: Dr David Ritchie, Consultant Musculoskeletal Radiologist, Liverpool (now Glasgow), UK

5. “Chronic” BME and Cartilage Delamination
CKC UK

8. Osteochondral Functional Unit
Source: Dr Carl Winalski, Boston, USA, 2003

10. ” … recent studies have shown that cartilage and subchondral bone act as a
single functional unit. This review highlights this novel concept.” ...
Osteoporosis Int. 2012
Cartilage + Subchondral Bone = a single functional unit

11. ... well, not exactly a brand new concept:
Source: Francis Berenbaum, 3 November 2016

12. Nothing New!
Source: Francis Berenbaum, 3 November 2016

13. OsteoArthritis or OsteoArthrosis?
Or just wear and tear? Or PTOA?

15. The Subchondral Unit: A New Frontier
re-drawn from Imhof et al. 1999
Henning Madry, Saarland University, Homburg/Saar, Germany
Imhof H, Breitenseher M, Kainberger F, Rand T, Trattnig S. (1999): Importance of
subchondral bone to articular cartilage in health and disease. Top Magn Reson Imaging
10:180–192

16. The Structure of Subchondral Bone
Redrawn from: Imhof H, Breitenseher M, Kainberger F, Rand T, Trattnig S. (1999): Importance of subchondral bone to
articular cartilage in health and disease. Top Magn Reson Imaging 10:180–192
A surprisingly high number of arterial and venous vessels, as well
as nerves, can be seen in the subchondral region sending tiny
branches into the calcified cartilage …

17. The Structure of Subchondral Bone
•This is extremely important for cartilage repair: the
tidemark is crossed by collagen fibrils extending
from the articular cartilage into the calcified
cartilage, while no collagen fibrils connect the
calcified cartilage to the subchondral bone plate.
• Blood vessels from the subchondral region can extend into
the overlying calcified cartilage through canals in the
subchondral bone plate.
• Therefore, nutrients can reach chondrocytes in the
calcified zone via these perforations.
CKC UK

18. The Structure of Subchondral Bone
Unsurprisinly, the changes in the thickness of the subchondral bone plate
depend on the location and mechanical loads
Henning Madry, Saarland University, Homburg/Saar, Germany

19. … the structural integrity of articular cartilage
is dependent on normal subchondral bone
turnover, intact chondrocyte function and
ordinary biomechanics stresses …

20. • VB to DR email, 2006:
• Subject: SONK and all that jazz (re confusing MRI
appearance of different subchondral events):
• VB: “ There is something there and it seems it’s all
connected. We are probably looking at different stages of the
same thing:
• … it seems that subchondral repair and remodelling are a
common denominator, some of which is successful (traumatic
bone bruising, transient osteoporosis, SONK), partially
successful (persisting bone marrow oedema) or not at all
(progressive chronic bone marrow oedema, subchondral
cysts, AVN, osteonecrosis, and in the end secondary
osteoarthrosis). I don’t know, for some people most of this is
probably at various places on the same timeline, but I am not
sure if that makes sense.”
• DR: “The terminology is a bit confusing … “
• I would like to thank Dr David Ritchie and Dr Carl Winalski for
their unreserved help and patience over many years
(“Vladimir, stop staring at MR images and stick to your day
job.”)
Subchondral Events in a Nutshell:

21. The Terminology is a Bit Confusing …
• Disclosure: Arthrex (OATS inventor), principal investigator for UK BioPoly clinical trial, former clinical advisor for TiGenix CCI.
• This is a non-EBM (orthopaedic surgeon’s) clinical overview of “subchondral events”, based on our clinical and MR imaging
experience since 1996.
• We have a problem at the outset: what are we actually talking about? How do
we treat a wide range of osteochondral problems which are still poorly defined and
understood?
• Bone Bruise (BB): a transient traumatic event = a series of trabecular
microfractures. No surgical treatment required.
• Bone Marrow Oedema (BME): MRI evidence of increased subchondral metabolic
activity. Remodelling or reparative process, or a failure of subchondral remodelling
or repair = a degenerative process? Initially a reparative process, but if persistent it
is probably a degenerative process (often associated with initial formation of
subchondral cysts, which are a consequence of failed local repair). No surgical
treatment required, but … . Possibly associated with CRPS (Sudeck’s Algodystrophy)
• Transient Osteoporosis (TOP): no history of trauma, the knee pain is
spontaneous and disabling, exacerbated on weight-bearing. Usually gets better over
many months, back to normal MRI and clinically. When multiple joints are involved
(in approx. 40% of patients) the condition is referred to as Transient Regional
Migratory Osteoporosis (TRMO). No surgical treatment required.
CKC UK

22. No Edema in Bone Marrow Edema!
• The correlation of bone marrow lesions with pain in knee OA has been
convincingly established. Here, another compelling association is established
between bone marrow (edema) lesions and risk for progression of knee OA.
What remains to be established is the cause-and-effect relationship between
the various variables.
• It is interesting that, histologically, the lesions that appear as bone
marrow edema on MRI contain very little edema at all. Rather, they
demonstrate fibrosis, osteonecrosis, and extensive bony REMODELLING
and are likely the result of contusions and focal microfractures.
• Also, it is not clear, whether an initial injury to articular cartilage
leads to mechanical malalignment and subsequent subchondral bone
destruction or rather subchondral bone damage leads to mechanical
malalignment and subsequent articular cartilage destruction.
Does bone marrow edema predict progression of knee arthritis?
A summary of Felson’s 2001 and 2003 AIM articles written by Jon Gilles, M.D., The John Hopkins Arthritis Center, 2003.
http://www.hopkins-arthritis.org/arthritis-news/2003/bone_edema_oa.html

23. Conclusion:
A majority of acutely
ACL injured knees
(92%) had a cortical
depression fracture,
which was associated
with larger BME
volumes.
This indicates strong
compressive forces
to the articular
cartilage at the time
of injury, which may
constitute an additional
risk factor for later
knee OA development.
CKC UK

24. ACL injury + extensive BB
CKC MRI 110206
7 months later

25. MFC ACI, 6/12: “In the medial
compartment, the ACI graft has
been placed over the central
weight-bearing portion of the
medial femoral condyle. Small
cartilage flap at the interface
peripherally in keeping with
minor delamination but
otherwise the graft appears good
with no cartilage overgrowth or
major defects. The
inhomogeneity of the implant
cartilage and mild marrow
oedema-like signal beneath
the graft are expected normal
findings 6 months after the
procedure.”
Unedited MRI report.
Dr David Ritchie, Glasgow, UK
CKC MRI 260906
“Normal” Bone Marrow Oedema 6/12 after MFC ACI

26. Transient Regional Migratory Osteoporosis:
MRI report: “The diffuse bone marrow oedema pattern with development of subchondral linear fractures
would therefore suggest regional migratory osteoporosis rather than typical SONK lesions.”

27. Transient Osteoporosis – Extreme Bone Remodeling?
CKC UK
• The aetiology of TO and TRMO remains unclear:
• One of the likely explanations for the pathogenesis of TO is perhaps
that proposed by Frost and others.
• He stated that under noxious tissue stimuli, the ordinary biological
processes, including blood flow, cell metabolism and turnover
and also tissue modelling and remodelling, might be greatly
accelerated, called the Regional Acceleratory Phenomenon
(RAP). In his opinion a prolonged or exaggerated RAP in which a
large number of bone turnover foci are activated, is the cause of
TO.
• It has been hypothesized that symptoms may be related to bone
marrow edema demonstrated at MRI and to a transitory regional
arterial hyperflow observed at the early scintigraphic analysis.
Bone tissue micro damage is the most frequent noxious
stimulus that provokes RAP and bone tissue micro fracture is
the main consequence.
• Several elements support this hypothesis. The repeatedly observed
histological findings in patients with TO showing mild inflammatory
changes and osteoporosis, associated with an elevated bone
turnover with increased bone resorption and reactive bone
formation are a good description of ongoing TRMO.

28. The Terminology is Even More Confusing …
• Spontaneous Osteonecrosis (SONK, Ahlback): is the term used to
describe a subchondral insufficiency fracture that causes osteonecrosis.
MRI appearance: a thin linear hypointense subchondral focus on T1W and
T2W that blends in with overlying cortex and is typically surrounded by
diffuse BME. With or without subchondral fractures/deformity.
• Avascular Necrosis (AVN): an osteonecrotic lesion, low signal rim on
T1W and double line sign on T2W, with or without BME. The necrotic focus
often extends some distance away from the articular margin and may contain
fat, blood, fluid, fibrous tissue. With or without subchondral
fractures/deformity.
• Osteochondritis Dissecans (OCD): semidetached osteochondral fragment
(essentially a non-union) with fluid layer at osseous interface and seemingly
intact articulating surface. A traumatic or metabolic event, or both?
• Secondary Osteoarthrosis (not –itis): if localized, this is perhaps the end
result of more extensive progressive failure of subchondral remodelling.
Increased but unsuccessful subchondral activity (progressive BME + multiple
cysts?) seems to be a primary event, with secondary loss of articulating
surface, which fails gradually as it is not supported by normal elastic
trabecular bone. May go as far back as injury-induced bone bruise, with or
without visible initial chondral damage.
CKC UK

29. BME and Insufficiency Fracture
Recent localised incomplete subarticular fracture of the outer aspect of the MFC (15 x 5 x 3
mm) with slight depression of the overlying articular cortex and prominent surrounding
marrow and soft tissue oedema but no obvious disruption of the overlying articular
cartilage or unstable osteochondral fragment.
CKC UK

30. Insufficiency Fracture and BME

31. Insufficiency Fracture and BME

32. Insufficiency Fracture and BME

33. AJSM 2011

34. SONK (Spontaneous Osteonecrosis)
CKC UK

35. Spontaneous Osteonecrosis (SONK)
• Ahlback et al first described
spontaneous osteonecrosis of the
knee as a distinct clinical entity in
1968.
• Osteonecrosis of the knee has also
been described as a postsurgical
complication following
arthroscopic meniscectomy
(Muscolo et al., Prues-Latour et al.)
and following radiofrequency-
assisted arthroscopic treatments,
mainly in 50+ age groups.
• The pathophysiology of osteonecrosis
following these arthroscopic
procedures is not fully understood
(vascular isufficiency, trabecular
microfractures?), or, more likely, a
consequence of pre-arthrosopy
osteopoenia and altered focal
biomechanics (bone density
should be looked into).

36. Spontaneous Osteonecrosis of Both Femoral Condyles
Shifting Bone Marrow Oedema is a self-contained disorder involving both femoral condyles. On MRI it
exhibits vast marrow oedema and is most likely an event on the SONK timeline.

37. Spontaneous Osteonecrosis (SONK) and Beyond
CKC UK

38. MFC BME + Subchondral Cyst Following ACL Surgery
No problems with ACL reconstruction, good functional
result, no meniscal deficiency.

39. ACI MRI FU: 3/12: Bone marrow edema, 12/12: Subcortical cyst
Subchondral Cysts Following ACI Surgery

40. Subchondral Cysts Following ACI Surgery
CKC UK

41. Subchondral Cyst Formation Following ACI Surgery
Subchondral cysts are bad news as they represent a
terminal failure (trabecular necrosis and structural
collapse) of local subchondral remodelling.

43. •Conclusions: Delivery of bone
marrow concentrate can result in
healing of acute full-thickness
cartilage defects that is superior
to that after microfracture alone
in an equine model.
•If this is the case, looking at
osteochondral defects, is this
combination working better because
microfracture (multiple perforations
and tunnelling) of subchondral bone
is making it less stiff but also allows
“biologic fuel” (bone marrow, blood
and who knows what else) to reach
deeper areas, re-establish nutrition
and facilitate local osteochondral
repair?
ABMA: An Essential Ingredient for Osteochondral Repair?
JBJS A August 2010

45. JBJS B June 2006

46. “Pre-TKR” option: OATS combined with autologous bone marrow aspirate

47. Autologous Bone Marrow Aspirate

48. Lateral Femoral Trochlea:
a reliable source of good cancellous bone and bone marrow, even in advanced OA
CKC UK
MFC AVN

49. An alternative approach to the treatment of
femoral and tibial Osteonecrosis, Chronic SONK
and Secondary OA:
• The knee is often not too bad (all 3 compartments) or it is too early
for a partial or a full knee replacement.
• Classic Microfracture and Core Decompression are probably not deep
enough.
• Looking at most MRIs it seems that we need to reach at least 15 to 20
mm deep into subchondral bone, which is where any cylindrical
osteochondral harvesters are very handy.
• Effectively, this is a combination of OAT and deep core (subchondral)
decompression, with a hand driven K-wire, through the bottom of the
recipient socket, with
• a mixture of autologous blood + bone marrow injected into the
recipient socket,
• and capped with 10 mm OATS plug, which was soaked in the same
mixture of bone marrow and blood.
• This “integrated” subchondral repair concept makes sense, it gives
most people quick and durable pain relief and better knee function,
but it is based on huge assumptions.
• The main question is weather unprocessed (and not concentrated)
autologous bone marrow, is powerful enough biologically?
CKC UK

50. SONK Before and After Subchondral Decompression
(“the road to hell is paved with good intentions”)
• 15/12/08: subarticular insufficiency
fracture and slight flattening of the
MFC and prominent subarticular marrow
oedema more marked on the femoral
side. Since 04/04/08, significant
deterioration in the medial compartment
with SONK-like process, progressive
degenerative changes …
• 11/09/09: Comparison is made with the
previous scan 15/12/2008. In the
medial compartment, following the
subchondral decompression, there
is now evidence of articular
irregularity, deficiency and thinning
of articular cartilage, slight increase
in the subarticular marrow oedema
and early subarticular cyst
formation in the outer aspect of the
MFC …

51. SONK: sudden onset,
severe knee pain
MRI: “In the outer weight-
bearing portion of the medial
femoral condyle, there is an
osteochondral lesion (22mm ant-
post x 10mm med-lat x 2mm
deep), with fluid at the interface
with parent bone, mild reactive
marrow oedema and a cortical
break peripherally in keeping
with instability. Degenerative
changes in the medial
compartment with spontaneous
osteonecrosis of the medial
femoral condyle (SONK) and
unstable fragment.”
David Ritchie, Glasgow
CKC MRI 060506

52. FU MRI: “In the medial
compartment, the graft over the
central weight-bearing portion of
the medial femoral condyle has
incorporated with adjacent
bone and the overlying
articular cartilage is flush
with adjacent native
cartilage. A small focus of
marrow oedema is noted directly
beneath the graft but overall
there has been a reduction in
marrow oedema around the
graft. A small trace of
subcortical fluid in the peripheral
portion of the medial femoral
condyle is similar to the pre-
operative scan - presumably not
included in the repair.”
Dr David Ritchie, Glasgow
CKC MRI 030307

53. The Subchondroplasty
Procedure

54. The Subchondroplasty Procedure
Great idea, but it seems that this entirely new concept (as it is) is based on huge
assumptions.
Arguably, subchondroplasty is indicated mainly for the treatment of subchondral
cysts and cavities, rather than various bone marrow oedema conditions.
Bone marrow oedema, as metabolic (vascular) “event” does not lack bone
(therefore injecting bone substitute is not the right ingredient). To the contrary,
injecting bone paste will clog many interconnected cellular spaces, may block
vascular pathways and slow down or prevent subchondral repair and remodelling.
Not surprised to hear that patients "should expect 3 days of severe pain" (!) as
injected and cured bone paste will increase intra-osseous pressure (which is already
higher than normal and which is why some conditions like SONK are very painful to
start with).
However, the real (biologically) desirable ingredient is autologous bone marrow
aspirate (or autologous stem cells or even autologous PRP) delivered to the area
affected with bone marrow oedema.
This is when subchondroplasty becomes a bit more intelligent and gets entirely new
biological meaning.
Vladimir Bobic CKC: Articular Cartilage, Subchondral Bone and Osteochondral Unit. 4th BKS Meeting, Cardiff, UK 1-2 February 2018.

55. The Subchondroplasty Procedure
Tweeted on 23rd April 2019

57. • Well, mainly because we still do not seem to understand
(well enough) complex biological and mechanical interaction
of articulating surface and subchondral bone.
• This is probably the reason why all mainstream cartilage
repair technologies suffer from two major problems:
• insufficient peripheral chondral integration
(biomechanical problem?)
• insufficient longitudinal subchondral integration
(nutritional and biomechanical problem?).
• However, we may have to accept that this is as good as it
gets, at this point in time.
So, Why is Cartilage Repair Still a Problem?

58. Thank You for Your Attention
Everything We Know About
Articular Cartilage
A Lot More We do Not Know
About Subchondral Bone and
Osteochondral Unit
(Unknown Unknowns)
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