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Surgical Treatment of
Symptomatic Subchondral Activity
(or Bone Marrow Oedema or Bone Marrow Lesion)
What are we treating? Why? How?
Mr Vladimir Bobić, MD FRCS Ed, Consultant Orthopaedic Knee Surgeon
Chester Knee Clinic, Chester UK
www.kneeclinic.info office@kneeclinic.info @ChesterKnee
The entire presentation is available on: www.slideshare.net/vbobic
ICRS Approved Knee & Ankle Course
Wrocław, Poznań, Poland, 8th & 9th October 2020
MARIARC MRI, UK (1997)
The orange pixels correspond to normal T2 values for bone. The blue and
purple pixels are anomalous: the T2 relaxation times are elevated because the
tissue is "wetter" than normal (the fluid interface between recipient and
donor bone).
OAT MRI analysis
MR Imaging Protocol 1997: Dr David Ritchie, Consultant Musculoskeletal Radiologist, Liverpool (now Glasgow), UK
Osteochondral Functional Unit
Source: Dr Carl Winalski, Boston, USA, 2003
CKC UK
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 …
The Terminology is a Bit Confusing …
• 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 …
• 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
The BME is not necessarily a problem!
CKC UK
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
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
ACL injury + extensive BB
CKC MRI 110206
Gone after 7 months
Traumatic bone bruise = many local microtrabecular fractures
CKC UK
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
CKC UK
BME After ACI: Quite Common After 3 Years
Long term ACI FU & MRI and BME
CKC UK
VB: I know, but for how long?
CKC UK
Spontaneous BME + Insufficiency Fracture
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.
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.”
Shifting Bone Marrow Oedema = Remodelling Overdrive?
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. Gets better (asymptomatic), eventually!
CKC UK
The Terminology is Even More Confusing …
• Spontaneous Osteonecrosis (SONK): 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 BB,
with or without visible initial chondral damage.
CKC UK
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
Insufficiency Fracture and BME
CKC UK
SONK (Spontaneous Osteonecrosis)
CKC UK
Post-arthroscopy 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).
CKC UK
Post-arthroscopy BME (SONK?)
CKC UK 2018
SONK Before and After Subchondral Decompression
• 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 …
CKC UK
Insufficiency Fracture and BME - Things get better, given time!
CKC UK
CKC UK
Spontaneous SONK + Insufficiency Fracture:
relatively asymptomatic, getting better slowly …
SONK (Spontaneous Osteonecrosis)
with Residual Insufficiency Fracture
CKC UK
Symptomatic Treatable Subchondral Cyst (with CP and BMC)
CKC UK
CKC UK
Subchondral Cysts Are Not Good But Do not Need Treatment
CKC UK
Symptomatic Treatable MTC BME (with intraosseous BMA)
Subchondroplasty
Procedure with CP
Subchondroplasty: 1st Take Home Message:
CKC UK
CKC UK
The 1st report on complications after
a calcium phosphate subchondroplasty
CKC UK
CKC UK
The CP Subchondroplasty Procedure:
Arguably, subchondroplasty with bone substitute 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 and will slow
down or prevent subchondral repair and remodelling.
Injected and cured bone paste will increase intra-osseous pressure (which is
already higher than normal and which is why SONK-like conditions are very painful
to start with) and block metabolic (vascular) pathways!
However, the real (biologically) desirable ingredient is autologous bone marrow
aspirate (or autologous stem cells or even PRP), delivered to the area affected
with bone marrow oedema.
Vladimir Bobic CKC: Articular Cartilage, Subchondral Bone and Osteochondral Unit. 4th BKS Meeting, Cardiff, UK 1-2 February 2018.
The Importance of Autologous Bone Marrow
CKC UK
Dr Philippe Hernigou, Paris
James Cook, UMSM “Pre-TKR” option: OATS combined with ABMC
Targeted Intraosseous Delivery of Autologous Bone Marrow
CKC UK
Symptomatic Medial OA + BME: PT Declined UKR or HTO
CKC UK
Asymptomatic Medial OA + BME 1 Year After OATS + SCD + ABMI
CKC UK
Other Take Home Messages …
Do you really have to treat painful bone marrow
oedema? Think twice!
Do not treat MR images - treat the patient, holistically!
Take time: wait, review, repeat the scan …
If you decide to treat “symptomatic bone marrow
oedema”, discuss everything with the patient and
document everything.
Do not use bone substitutes, use autologous bone
marrow.
Do not restrict WB and ROM!
And finally, remember:
CKC UK
… and the Last Take Home Message:
Thank You for Your Attention
Everything We Know About
Articular Cartilage
A Lot More We do Not Know About
Subchondral Bone and
Osteochondral Unit
(Known and Unknown Unknowns)
www.slideshare.net/vbobic
CKC UK

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Bobic Subchondral Events - ICRS Wroclaw 091020

  • 1. Surgical Treatment of Symptomatic Subchondral Activity (or Bone Marrow Oedema or Bone Marrow Lesion) What are we treating? Why? How? Mr Vladimir Bobić, MD FRCS Ed, Consultant Orthopaedic Knee Surgeon Chester Knee Clinic, Chester UK www.kneeclinic.info office@kneeclinic.info @ChesterKnee
  • 2. The entire presentation is available on: www.slideshare.net/vbobic ICRS Approved Knee & Ankle Course Wrocław, Poznań, Poland, 8th & 9th October 2020
  • 3. MARIARC MRI, UK (1997) The orange pixels correspond to normal T2 values for bone. The blue and purple pixels are anomalous: the T2 relaxation times are elevated because the tissue is "wetter" than normal (the fluid interface between recipient and donor bone). OAT MRI analysis MR Imaging Protocol 1997: Dr David Ritchie, Consultant Musculoskeletal Radiologist, Liverpool (now Glasgow), UK
  • 4. Osteochondral Functional Unit Source: Dr Carl Winalski, Boston, USA, 2003 CKC UK
  • 5. 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 …
  • 6. The Terminology is a Bit Confusing … • 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 … • 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
  • 7. The BME is not necessarily a problem! CKC UK
  • 8. 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
  • 9. 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
  • 10. ACL injury + extensive BB CKC MRI 110206 Gone after 7 months Traumatic bone bruise = many local microtrabecular fractures CKC UK
  • 11. 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
  • 12. CKC UK BME After ACI: Quite Common After 3 Years
  • 13. Long term ACI FU & MRI and BME CKC UK VB: I know, but for how long?
  • 14. CKC UK Spontaneous BME + Insufficiency Fracture
  • 15. 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.
  • 16. 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.”
  • 17. Shifting Bone Marrow Oedema = Remodelling Overdrive? 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. Gets better (asymptomatic), eventually! CKC UK
  • 18. The Terminology is Even More Confusing … • Spontaneous Osteonecrosis (SONK): 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 BB, with or without visible initial chondral damage. CKC UK
  • 19. 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
  • 22. Post-arthroscopy 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). CKC UK
  • 24. SONK Before and After Subchondral Decompression • 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 … CKC UK
  • 25. Insufficiency Fracture and BME - Things get better, given time! CKC UK
  • 26. CKC UK Spontaneous SONK + Insufficiency Fracture: relatively asymptomatic, getting better slowly …
  • 27. SONK (Spontaneous Osteonecrosis) with Residual Insufficiency Fracture CKC UK
  • 28. Symptomatic Treatable Subchondral Cyst (with CP and BMC) CKC UK
  • 29. CKC UK Subchondral Cysts Are Not Good But Do not Need Treatment
  • 30. CKC UK Symptomatic Treatable MTC BME (with intraosseous BMA)
  • 32. Subchondroplasty: 1st Take Home Message: CKC UK
  • 34. The 1st report on complications after a calcium phosphate subchondroplasty CKC UK
  • 36. The CP Subchondroplasty Procedure: Arguably, subchondroplasty with bone substitute 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 and will slow down or prevent subchondral repair and remodelling. Injected and cured bone paste will increase intra-osseous pressure (which is already higher than normal and which is why SONK-like conditions are very painful to start with) and block metabolic (vascular) pathways! However, the real (biologically) desirable ingredient is autologous bone marrow aspirate (or autologous stem cells or even PRP), delivered to the area affected with bone marrow oedema. Vladimir Bobic CKC: Articular Cartilage, Subchondral Bone and Osteochondral Unit. 4th BKS Meeting, Cardiff, UK 1-2 February 2018.
  • 37. The Importance of Autologous Bone Marrow CKC UK Dr Philippe Hernigou, Paris
  • 38. James Cook, UMSM “Pre-TKR” option: OATS combined with ABMC
  • 39.
  • 40. Targeted Intraosseous Delivery of Autologous Bone Marrow CKC UK
  • 41. Symptomatic Medial OA + BME: PT Declined UKR or HTO CKC UK
  • 42. Asymptomatic Medial OA + BME 1 Year After OATS + SCD + ABMI CKC UK
  • 43. Other Take Home Messages … Do you really have to treat painful bone marrow oedema? Think twice! Do not treat MR images - treat the patient, holistically! Take time: wait, review, repeat the scan … If you decide to treat “symptomatic bone marrow oedema”, discuss everything with the patient and document everything. Do not use bone substitutes, use autologous bone marrow. Do not restrict WB and ROM! And finally, remember: CKC UK
  • 44. … and the Last Take Home Message:
  • 45. Thank You for Your Attention Everything We Know About Articular Cartilage A Lot More We do Not Know About Subchondral Bone and Osteochondral Unit (Known and Unknown Unknowns) www.slideshare.net/vbobic CKC UK