Septic arthritis of the cervical facet joint: Clinical report and review of the literature.

BACKGROUND: Facet joint septic arthritis (FJSA) is an uncommon cause of neck pain, most frequently occurring in the lumbosacral spine. Cervical facet joint septic arthritis is particularly rare. Symptoms typically include spinal or paraspinal pain and tenderness, with severe infections potentially causing neurological impairments. This condition can progress to discitis and osteomyelitis. High clinical suspicion is required for accurate diagnosis and timely treatment. OBJECTIVE: To present the first known case of cervical spine FJSA caused by Moraxella species and provide an updated narrative review of cervical spine FJSA. METHODS: A case study of a 66-year-old male with cervical spine FJSA caused by Moraxella osloensis is detailed. Additionally, a librarian-assisted literature search was conducted on MEDLINE Pubmed, filtering for adult human trials and including various study types, resulting in the inclusion of 9 relevant manuscripts. RESULTS: The patient's symptoms included neck, right upper thoracic, and periscapular pain, with episodes of numbness and tingling. MRI revealed septic arthritis at the C7-T1 facet joint and associated osteomyelitis. Cultures identified Moraxella osloensis as the causative agent. The patient was successfully treated with antibiotics and experienced significant symptom improvement. Literature review highlights that Staphylococcus aureus is the most common causative agent of cervical FJSA, with diagnosis typically involving MRI and culture tests. Treatment generally includes long-term antibiotics, with some cases requiring surgical intervention. CONCLUSIONS: This report underscores the need for high clinical suspicion in diagnosing FJSA and highlights the importance of early intervention. It documents the first known case of cervical spine FJSA caused by Moraxella osloensis, contributing valuable information to the limited literature on this rare condition.

Chemoresistance to additive PARP/PI3K dual inhibition in triple-negative breast cancer cell lines is associated with adaptive stem cell-like prevalence.

Cancer stem-like cells (CSCs) are posited to exhibit specialized oncogenic capacity to drive malignancies. CSCs are distinguished by enhanced hallmarks of cancer, including apoptosis avoidance, phenotypic plasticity and aberrant growth pathway signaling. Standard-of-care chemotherapies targeted to rapidly cycling cells routinely fail to eliminate this resistant subpopulation, leading to disease recurrence and metastasis. Triple-negative breast cancer (TNBC), a highly aggressive subtype of breast cancer, is enriched for tumor-propagating CD44+/CD24-/low CSCs, which are poorly ablated by chemotherapeutics and are associated with poor prognosis. CD44 governs sustained PI3K signaling in breast cancer, which is essential for CSC maintenance. PI3K inhibition can elicit DNA damage and down-regulate BRCA1 expression, which in turn enhance the synthetic lethality of PARP inhibitors. Here, we examined a dual chemotherapeutic approach targeting these pathways by combining a pan-PI3K inhibitor (Buparlisib) and a PARP1 inhibitor (Olaparib) on a panel of TNBC cell lines with distinct mutational profiles and proportions of CSCs. We observed differential sensitivity to this dual inhibition strategy and varying cellular stress and resistance responses across eight TNBC lines. The dual chemotherapeutic effect is associated with a reduction in S-phase cells, an increased in apoptotic cells and elevated expression of cleaved PARP, indicating a provoked replicative stress response. We observed that PARP/PI3K inhibition efficacy was potentiated by repeated administration in some TNBC lines and identified critical treatment schedules, which further potentiated the dual chemotherapeutic effect. Dual inhibition induced small but significant increases in CSC relative abundance as marked by CD44+/CD24-/low or ALDH1+ cells and increased stress and survival signaling in multiple TNBC cell lines, suggesting this sub-population contributes to TNBC chemoresistance. These results suggest the additive effects of PARP and PI3K inhibition against CSC phenotypes may be enhanced by temporally-staged administration in TNBC cells.

Lancinating lumbar facet syndrome: a congenitally absent facet joint.

Congenitally absent or hypoplastic L5-S1 facet (zygapophyseal) joints are an aberrated rarity, with less than 30 reported cases. This absence of facet joint and contralateral hypertrophic facet provides a continuum of presentations that can complicate low back pain diagnoses and management. A broad differential including lumbar facet syndrome, disc degeneration, spinal stenosis, herniated radiculopathy, spondyloarthropathies and sacroiliac joint pain should be considered initially, with the flexibility for other diagnoses. Understanding the effects of different anatomical, biomechanical and physiological changes on spinal health is essential for patient care. We report a progression of lumbar radiculopathy complicated by the presence of a congenitally absent left L5-S1 facet joint and hypertrophic right L5-S1 facet joint. Furthermore, our discussion concentrates on pathophysiology, differential diagnoses and management of congenitally absent facet joints and the impact they can have on low back pain and spinal health.