Patellofemoral articular cartilage damage is associated with poorer patient-reported outcomes following isolated medial patellofemoral ligament reconstruction.

PURPOSE: The purpose of this study was to investigate the impact of articular cartilage damage on outcomes following medial patellofemoral ligament (MPFL) reconstruction. METHODS: Record review identified 160 patients who underwent isolated MPFL reconstruction at a single institution between 2008 and 2016. Patient demographics, patellofemoral articular cartilage status at surgery, and patient anatomical measures from imaging were obtained via chart review. Patients were contacted and outcomes assessed through collection of Norwich Patellar Instability (NPI) score, Knee injury and Osteoarthritis Outcome Score (KOOS), and Marx activity score as well as an assessment for recurrent patellar dislocation. Outcomes of patients with grade 0-II patellofemoral cartilage damage were compared to those of patients with grade III-IV cartilage damage. RESULTS: One hundred twenty-two patients (76%) with a minimum of one year follow-up were contacted at a mean of 4.8 years post-operatively. A total of 63 patients (52%) had grade III or IV patellofemoral chondral damage at the time of surgery. The majority of the defects was on the medial patella (46 patients-72%) and the mean patellar defect size was 2.8 cm2. Among 93 patients who completed patient-reported outcome scores, the 52 with grade III or IV chondral damage reported a significantly poorer KOOS Quality of Life than the 44 patients with grade 0 to II chondral damage (p = 0.041), controlling for patient age, sex, BMI, and anatomical factors. CONCLUSION: Patients with grade III or IV articular cartilage damage of the patellofemoral joint at the time of MPFL reconstruction demonstrated poorer KOOS knee-related quality of life than patients without grade III or IV articular cartilage damage at a mean of 4.8 years following isolated MPFL reconstruction. LEVEL OF EVIDENCE: Level II.

The role of neuroinflammation in the transition of acute to chronic pain and the opioid-induced hyperalgesia and tolerance.

Current evidence suggests that activation of glial and immune cells leads to increased production of proinflammatory mediators, creating a neuroinflammatory state. Neuroinflammation has been proven to be a fundamental mechanism in the genesis of acute pain and its transition to neuropathic and chronic pain. A noxious event that stimulates peripheral afferent nerve fibers may also activate pronociceptive receptors situated at the dorsal root ganglion and dorsal horn of the spinal cord, as well as peripheral glial cells, setting off the so-called peripheral sensitization and spreading neuroinflammation to the brain. Once activated, microglia produce cytokines, chemokines, and neuropeptides that can increase the sensitivity and firing properties of second-order neurons, upregulating the signaling of nociceptive information to the cerebral cortex. This process, known as central sensitization, is crucial for chronification of acute pain. Immune-neuronal interactions are also implicated in the lesser-known complex regulatory relationship between pain and opioids. Current evidence suggests that activated immune and glial cells can alter neuronal function, induce, and maintain pathological pain, and disrupt the analgesic effects of opioid drugs by contributing to the development of tolerance and dependence, even causing paradoxical hyperalgesia. Such alterations may occur when the neuronal environment is impacted by trauma, inflammation, and immune-derived molecules, or when opioids induce proinflammatory glial activation. Hence, understanding these intricate interactions may help in managing pain signaling and opioid efficacy beyond the classical pharmacological approach.