Meniscal tear as potential steering factor for inflammation may aggravate arthritis: two case reports

Abstract

IntroductionMeniscal tear is thought to play a crucial role in onset as well as progression of arthritis. However, role of cytokine response to meniscal injury and resulting inflammation is not clearly understood. Because synovial fluid is juxtaposed to cartilage and serves as a biological connection between chondrocytes and synoviocytes, we chose synovial fluid analysis to ascertain biochemical response associated with a meniscal tear.Case presentationWe report the cases of two patients with clinically different inflammatory arthritis, both of whom are Indian men. Patient 1 was 30 years of age, and patient 2 was 50 years of age. They both had a history of meniscal tear, which we confirmed by magnetic resonance imaging scans. Synovial fluid samples obtained from these two patients were analyzed for proinflammatory markers, such as interleukin 1β (IL-1β) and nitric oxide, and also for glycosaminoglycan as a cartilage degradation indicator. Relatively high levels of IL-1β (2000.0±15.7pg/ml) and nitric oxide (4.73±0.05μM/ml) and relatively low glycosaminoglycan (93.75±6.3μg/ml) were observed in patient 1, corroborating the diagnosis of traumatic meniscal tear. Compared to patient 1, Patient 2 had relatively low levels of IL-1β (54.55±14.5pg/ml) and nitric oxide (20.00±0.6μM/ml) and remarkably high glycosaminoglycan levels (553.33±1.7μg/ml), coupled with significant osteophytes and profound cartilage loss, which indicated severe arthritis and a diagnosis of degenerative meniscal tear.ConclusionThe elevated levels of inflammatory IL-1β aggravated the severity of arthritis attributable to meniscal tear in both patients, as found in follow-up visits. This was quite evident in patient 2, whereas patient 1, being younger, had less serious symptoms. Meniscal tear has emerged as a potential confounding factor in arthritis with different clinical backgrounds, which leads to increased levels of inflammation and results in accelerated disease progression.

The use of eponyms in medical case reports: etymological, quantitative, and structural analysis

“…We found ten cases of an “erroneous” Biblical eponym with the name “Lazarus” (five articles) [ 39 – 43 ], for example, “CDH was first described in 1679 by Lazarus Riverius” [ 39 ], “They were first described by Lazarus and Trombetta in 1978” [ 42 ], and “ Lazarus and Chiang examined patients that had a bone marrow transplant later followed by a solid organ” [ 43 ]. There were four cases of “pseudo” Roman eponyms with the name “Hercules” (four articles) [ 44 – 47 ], for example, “After incubation at room temperature for ten minutes, the absorbance was measured at 540 nm in a spectrophotometer (Bio-Rad Laboratories, Hercules , CA, USA)” [ 45 ], and one case for “Venus”: “We report the unusual case of a girl diagnosed with Neisseria gonorrhoeae after bathing in a heavily frequented hot pool at the edge of the crater lake Specchio di Venere (“Mirror of Venus ”) on Pantelleria Island, Italy” [ 48 ]. As a result, we did not include the eponym “the Hercules complex” from Roman mythology [ 36 ] in our study.…”

The Effects of an Osteoarthritic Joint Environment on ACL Damage and Degeneration: A Yucatan Miniature Pig Model

“…Patients who sustain an intra-articular joint injury are at greater risk of suffering from future cartilage degeneration due to a complex interaction between mechanical and biological factors [ 2 ]. Beyond ACL tears, lesions to the meniscus and posterior cruciate ligament, as well as intra-articular osseous fractures, are common injuries requiring surgical treatment [ 2 , 16 , 17 , 18 , 19 ]. Uncontrolled inflammation, through the upregulation of TNF-α, IL-1β, and IL-6, remains even after surgical stabilization and places the injured joint in a catabolic environment [ 20 , 21 ].…”

Systems Based Study of the Therapeutic Potential of Small Charged Molecules for the Inhibition of IL-1 Mediated Cartilage Degradation

“…We also note that for constant therapeutic effect, drug concentration may be ‘traded-off’ with the dissociation constant. It has been reported that IL-1α levels in synovial fluid increases significantly following traumatic injury to cartilage tissue [14, 92, 93]. The results presented here show that even small molecules with a very strong negative charge (MW = 3 kDa and Z d = -16) can completely inhibit IL-1α mediated aggrecan catabolism provided it binds strongly to IL-1α with a dissociation constant of 10 nM or smaller (see Fig 6 and Table 5).…”