Aims. CRP is an acute-phase protein that is used as a biomarker to follow severity and progression in infectious and inflammatory diseases. Its pathophysiological mechanisms of action are still poorly defined. CRP in its pentameric form exhibits weak anti-inflammatory activity. The monomeric isoform (mCRP) exerts potent proinflammatory properties in chondrocytes, endothelial cells, and leucocytes. No data exist regarding mCRP effects in human intervertebral disc (IVD) cells. This work aimed to verify the pathophysiological relevance of mCRP in the aetiology and/or progression of IVD degeneration. Methods. We investigated the effects of mCRP and the signalling pathways that are involved in cultured human primary annulus fibrosus (AF) cells and in the human nucleus pulposus (NP) immortalized cell line HNPSV-1. We determined messenger RNA (mRNA) and protein levels of relevant factors involved in inflammatory responses, by quantitative real-time polymerase chain reaction (RT-qPCR) and western blot. We also studied the presence of mCRP in human AF and NP tissues by
This study was performed to explore the effect of melatonin on pyroptosis in nucleus pulposus cells (NPCs) and the underlying mechanism of that effect. This experiment included three patients diagnosed with lumbar disc herniation who failed conservative treatment. Nucleus pulposus tissue was isolated from these patients when they underwent surgical intervention, and primary NPCs were isolated and cultured. Western blotting, reverse transcription polymerase chain reaction, fluorescence staining, and other methods were used to detect changes in related signalling pathways and the ability of cells to resist pyroptosis.Aims
Methods
The belief that an intervertebral disc must degenerate
before it can herniate has clinical and medicolegal significance,
but lacks scientific validity. We hypothesised that tissue changes
in herniated discs differ from those in discs that degenerate without
herniation. Tissues were obtained at surgery from 21 herniated discs
and 11 non-herniated discs of similar degeneration as assessed by
the Pfirrmann grade. Thin sections were graded histologically, and
certain features were quantified using immunofluorescence combined
with confocal microscopy and image analysis. Herniated and degenerated
tissues were compared separately for each tissue type: nucleus, inner
annulus and outer annulus. Herniated tissues showed significantly greater proteoglycan loss
(outer annulus), neovascularisation (annulus), innervation (annulus),
cellularity/inflammation (annulus) and expression of matrix-degrading
enzymes (inner annulus) than degenerated discs. No significant differences
were seen in the nucleus tissue from herniated and degenerated discs.
Degenerative changes start in the nucleus, so it seems unlikely
that advanced degeneration caused herniation in 21 of these 32 discs.
On the contrary, specific changes in the annulus can be interpreted
as the consequences of herniation, when disruption allows local
swelling, proteoglycan loss, and the ingrowth of blood vessels,
nerves and inflammatory cells. In conclusion, it should not be assumed that degenerative changes
always precede disc herniation. Cite this article:
We have treated 175 patients with a chordoma over a ten-year period. Only two had a family history of the condition and we describe these in this paper. In one patient the tumour was at the craniocervical junction and in the other the lesion affected the sacrum. We have undertaken a literature review of familial chordoma and have identified chromosomal abnormalities associated with the condition.
