As our understanding of hip function and disease improves, it is evident that the acetabular fossa has received little attention, despite it comprising over half of the acetabulum’s surface area and showing the first signs of degeneration. The fossa’s function is expected to be more than augmenting static stability with the ligamentum teres and being a templating landmark in arthroplasty. Indeed, the fossa, which is almost mature at 16 weeks of intrauterine development, plays a key role in hip development, enabling its nutrition through vascularization and synovial fluid, as well as the influx of chondrogenic stem/progenitor cells that build articular cartilage. The pulvinar, a fibrofatty tissue in the fossa, has the same developmental origin as the synovium and articular cartilage and is a biologically active area. Its unique anatomy allows for homogeneous distribution of the axial loads into the joint. It is composed of intra-articular adipose tissue (IAAT), which has adipocytes, fibroblasts, leucocytes, and abundant mast cells, which participate in the inflammatory cascade after an insult to the joint. Hence, the fossa and pulvinar should be considered in decision-making and surgical outcomes in hip preservation surgery, not only for their size, shape, and extent, but also for their biological capacity as a source of cytokines, immune cells, and chondrogenic stem cells. Cite this article:
This systematic review examines the current literature regarding surgical techniques for restoring articular cartilage in the hip, from the older microfracture techniques involving perforation to the subchondral bone, to adaptations of this technique using nanofractures and scaffolds. This review discusses the autologous and allograft transfer systems and the autologous matrix-induced chondrogenesis (AMIC) technique, as well as a summary of the previously discussed techniques, which could become common practice for restoring articular cartilage, thus reducing the need for total hip arthroplasty. Using the
In this study, we compared the pain behaviour and osteoarthritis (OA) progression between anterior cruciate ligament transection (ACLT) and osteochondral injury in surgically-induced OA rat models. OA was induced in the knee joints of male Wistar rats using transection of the ACL or induction of osteochondral injury. Changes in the percentage of high limb weight distribution (%HLWD) on the operated hind limb were used to determine the pain behaviour in these models. The development of OA was assessed and compared using a histological evaluation based on the Osteoarthritis Research Society International (OARSI) cartilage OA histopathology score.Objectives
Methods
Objectives. Sustained intra-articular delivery of pharmacological agents is an attractive modality but requires use of a safe carrier that would not induce cartilage damage or fibrosis. Collagen scaffolds are widely available and could be used intra-articularly, but no investigation has looked at the safety of collagen scaffolds within synovial joints. The aim of this study was to determine the safety of collagen scaffold implantation in a validated in vivo animal model of knee arthrofibrosis. Materials and Methods. A total of 96 rabbits were randomly and equally assigned to four different groups: arthrotomy alone; arthrotomy and collagen scaffold placement; contracture surgery; and contracture surgery and collagen scaffold placement. Animals were killed in equal numbers at 72 hours, two weeks, eight weeks, and 24 weeks. Joint contracture was measured, and cartilage and synovial samples underwent histological analysis. Results. Animals that underwent arthrotomy had equivalent joint contractures regardless of scaffold implantation (-13.9° versus -10.9°, equivalence limit 15°). Animals that underwent surgery to induce contracture did not demonstrate equivalent joint contractures with (41.8°) or without (53.9°) collagen scaffold implantation.
Medial unicompartmental knee arthroplasty (UKA) is associated
with successful outcomes in carefully selected patient cohorts.
We hypothesised that severity and location of patellofemoral cartilage
lesions significantly influences functional outcome after Oxford
medial compartmental knee arthroplasty. We reviewed 100 consecutive UKAs at minimum eight-year follow-up
(96 to 132). A single surgeon performed all procedures. Patients
were selected based on clinical and plain radiographic assessment.
All patients had end-stage medial compartment osteoarthritis (OA)
with sparing of the lateral compartment and intact anterior cruciate ligaments.
None of the patients had end-stage patellofemoral OA, but patients
with anterior knee pain or partial thickness chondral loss were
not excluded. There were 57 male and 43 female patients. The mean
age at surgery was 69 years (41 to 82). At surgery the joint was
carefully inspected for patellofemoral chondral loss and this was documented
based on severity of cartilage loss (0 to 4 Outerbridge grading)
and topographic location (medial, lateral, central, and superior
or inferior). Functional scores collected included Oxford Knee Score
(OKS), patient satisfaction scale and University College Hospital
(UCH) knee score. Intraclass correlation was used to compare chondral
damage to outcomes.Aims
Patients and Methods
Osteochondral injuries, if not treated adequately, often lead
to severe osteoarthritis. Possible treatment options include refixation
of the fragment or replacement therapies such as Pridie drilling,
microfracture or osteochondral grafts, all of which have certain
disadvantages. Only refixation of the fragment can produce a smooth
and resilient joint surface. The aim of this study was the evaluation
of an ultrasound-activated bioresorbable pin for the refixation of
osteochondral fragments under physiological conditions. In 16 Merino sheep, specific osteochondral fragments of the medial
femoral condyle were produced and refixed with one of conventional
bioresorbable pins, titanium screws or ultrasound-activated pins.
Macro- and microscopic scoring was undertaken after three months. Objectives
Methods
Femoroacetabular impingement (FAI) causes pain
and chondrolabral damage via mechanical overload during movement
of the hip. It is caused by many different types of pathoanatomy,
including the cam ‘bump’, decreased head–neck offset, acetabular
retroversion, global acetabular overcoverage, prominent anterior–inferior
iliac spine, slipped capital femoral epiphysis, and the sequelae
of childhood Perthes’ disease. Both evolutionary and developmental factors may cause FAI. Prevalence
studies show that anatomic variations that cause FAI are common
in the asymptomatic population. Young athletes may be predisposed
to FAI because of the stress on the physis during development. Other
factors, including the soft tissues, may also influence symptoms and
chondrolabral damage. FAI and the resultant chondrolabral pathology are often treated
arthroscopically. Although the results are favourable, morphologies
can be complex, patient expectations are high and the surgery is
challenging. The long-term outcomes of hip arthroscopy are still
forthcoming and it is unknown if treatment of FAI will prevent arthrosis.
