Exploring the Efficacy of Biologics in Knee Osteoarthritis: Ultrasound Evaluation of Cartilage Regeneration Effects.

Introduction: Biologics like growth factors, stem cells, and platelet-rich plasma show potential in stimulating cartilage regrowth and reducing inflammation. By synthesizing preclinical and clinical studies, this study offers insights into how these biologics work and their effectiveness in treating knee osteoarthritis. Methods and Materials: Twenty-four participants with knee osteoarthritis (Kellgren - Lawrence grade II or III) were enrolled after obtaining consent. They received three doses of 2 ml intraarticular platelet-rich plasma at 1 month intervals. The clinical assessment involved the oxford knee score (OKS) and visual analogue scale (VAS) for pain on Days 0, 90, and 180. Ultrasound measured femoral and trochlear cartilage thickness pre- (Day 0) and post-PRP (Day 90-180). Results: Before treatment, the average pain score was 7.2 (p = 1.03). On Day 90 post-PRP, it decreased to 5 (p = 0.81), and by Day 180, it further reduced to 4.5 (p = 0.97). The initial total OKS was 33.5 (p = 1.76), which increased to 36 (p = 1.71) on Day 90 and 38.5 (p = 1.89) on Day 180. The femoral and trochlear cartilage thickness also showed improvement from baseline (0.92) to Day 90 (0.96) and Day 180 (1.01), indicating significant cartilage healing post-PRP administration. Conclusion: Our study highlights the probability of PRP in treating knee OA, highlighting their ability to alleviate symptoms, enhance joint function, and promote articular cartilage regeneration.

Clinical Outcomes of Arthroscopic Adhesiolysis: A Case Series of 40 Patients With Postoperative Knee Stiffness.

Introduction Restricted range of motion over the knee joint is a known complication following the surgical procedure. Aggressive rehabilitation protocols can initially manage knee stiffness due to arthrofibrosis. If conservative management fails, surgical (open or arthroscopic) release is the preferred modality of management. We present a series of 40 patients with postoperative knee stiffness who were treated with arthroscopic adhesiolysis. Material and methods This is a retrospective study conducted at Phoenix Orthopedic Superspeciality Hospital, Nagpur, India, from 2017 to 2021. Our study included 40 patients with postoperative knee joint stiffness, of whom 27 were males and 13 were females. The study considered the duration of stiffness, which ranged from six months to five years. All patients underwent arthroscopic knee release. A rigorously supervised physical therapy program followed this procedure. Patients were examined at three months, six months, and one year to assess improvement in knee range of movement. Results Out of 40 patients, six were classified as Shelbourne type 4, and the remaining were Shelbourne type 3. Twenty-three of 40 patients developed arthrofibrosis following intra-articular or peri-articular fracture fixation surgery; 11 patients were operated on arthroscopically for anterior cruciate ligament (ACL) or posterior cruciate ligament (PCL) reconstruction. Three patients developed stiffness following total knee replacement, one following patellectomy, and three following infection after fracture fixation. The mean pre-op knee range of motion (ROM) was 48.875 degrees. Following arthroscopic release, the mean improvement in ROM was 60 degrees intra-operatively. The average postoperative range was 108.25 degrees. Conclusion Arthroscopic adhesiolysis and quadriceps release are reliable methods for dealing with postoperative knee stiffness. It prevents wound complications and increases the chances of surgical site infection due to smaller incisions. Postoperatively, we achieved an average increase of 60 degrees in ROM over the knee joint.

Unveiling Enigma: Navigating the Diagnostic Labyrinth of an Atypical Medial Clavicular Enchondroma.

Benign cartilaginous lesions called enchondromas usually appear in the long bones of the limbs. This case report, however, draws attention to an uncommon and unusual appearance of enchondroma near the medial end of clavicle. Because of the unusual location, the diagnostic process was very complex, which presented a challengefor the physicians. We provide the clinical, radiological and histological results that finally allowed for an accurate diagnosis. This example highlights the need of taking into account atypical location for benign lesions and highlights the necessity of a thorough diagnostic approach in unexpected clinical settings. Since the occurrence of clavicular enchondromas is a rare entity and can at times mislead the clinician, healthcare providers must be vigilant enough to guarantee a prompt and accurate diagnosis for timely intervention.

Reconstructive Surgical Intervention for Malunited Distal End Radius and Ulna Fracture: A Case Report Demonstrating Improved Patient Outcomes.

This case report explores the efficacy of reconstructive surgical intervention in addressing malunited fractures of the distal end of the radius and ulna. The study presents a detailed analysis of a specific case, highlighting the surgical techniques employed and their impact on patient outcomes. The report emphasizes the importance of precision in addressing malunited fractures and showcases how the intervention led to improved patient outcomes. By documenting this case, the study contributes valuable insights into the field of orthopedic surgery, providing a basis for further research and enhancing the understanding of optimal approaches to managing such complex fractures.

Tenosynovial giant cell tumour of the finger: a case report.

Giant cell tumour most commonly occuring in epiphysis of the long bone, present and with pain, tenderness and swelling. It is a solitary lesion with restricted movement and tenderness over the lesion. The tendon sheath is where tenosynovial giant cell tumours typically develop. Because of its remarkably peculiar position, we present a case of giant cell tumour (GCT) tenosynovial of bone in the middle phalaynx in a 33-year-old female with complaints of swelling, pain in ring finger of left hand since 2 months which is rarely seen. After clinical, radiological, pathological investigations tenosynovial giant cell tumour was diagnosed. Following fine needle aspiration cytology, histopathology was utilized to confirm the tumour's diagnosis which was later treated as resection of excision of the tumour with allo/autograft reconstruction. Our case report showed no evidence of recurrence in 2 years of follow-up. Hence our case report proves that early and complete resection of the tumour shows evidence of regain of complete range of motion and decrease recurrence rate.

Heterologous expression of hAID in E. coli leads to the production of a splice isoform of AID: hAIDδC, a mystery to be explored.

Activation-induced cytidine deaminase (AID) is a key player that initiates antibody diversification in activated B-cell. AID mediates somatic hypermutation (SHM) and class switch recombination (CSR) via the deamination of cytosine to uracil at the Ig locus, resulting in the production of high-affinity antibodies. AID is predominantly restricted to Ig genes, whereas off-targeting of AID leads to lymphocyte-related malignancies. Interestingly, apart from FL-AID other splice isoforms of AID are highly expressed in the lymphocyte malignancies. In our study, we found that the heterologous expression of hAID-FL in E. coli cells produced two induced bands of hAID as demonstrated by SDS-PAGE and western blotting. Remarkably, peptide mapping data predicted that one band is hAID-FL and the other is its splice isoform, hAIDδE4a. To get an insight into why E. coli cells expressed hAID-FL and hAID variant, we mutated the 5' and 3' splice site of a putative intron of hAID, but it failed to produce only hAID-FL. Incidentally, hAID expressed with fusion partners also displayed two bands, and peptide mapping data strongly suggest that besides hAID-FL, the lower band showed a significant number of amino acids missing towards the C-terminal domain (named as hAIDδC). Our results are the first report to show that expression of recombinant hAID alone or irrespective of solubilization tags in E. coli cells produced hAID-FL and hAIDδC. It will be fascinating to explore the potential mechanism underlying the expression of hAIDδC from recombinant hAID plasmid in E. coli cells.

Unfolding the Role of Splicing Factors and RNA Debranching in AID Mediated Antibody Diversification.

Activated B-cells diversify their antibody repertoire via somatic hypermutation (SHM) and class switch recombination (CSR). SHM is restricted to the variable region, whereas, CSR is confined to the constant region of immunoglobulin (Ig) genes. Activation-induced cytidine deaminase (AID) is a crucial player in the diversification of antibodies in the activated B-cell. AID catalyzes the deamination of cytidine (C) into uracil (U) at Ig genes. Subsequently, low fidelity repair of U:G mismatches may lead to mutations. Transcription is essential for the AID action, as it provides a transient single-strand DNA substrate. Since splicing is a co-transcriptional event, various splicing factors or regulators influence the transcription. Numerous splicing factors are known to regulate the AID targeting, function, Ig transcription, and AID splicing, which eventually influence antibody diversification processes. Splicing regulator SRSF1-3, a splicing isoform of serine arginine-rich splicing factor (SRSF1), and CTNNBL1, a spliceosome interacting factor, interact with AID and play a critical role in SHM. Likewise, a splicing regulator polypyrimidine tract binding protein-2 (PTBP2) and the debranching enzyme (DBR1) debranches primary switch transcripts which later forms G-quadruplex structures, and the S region guide RNAs direct AID to S region DNA. Moreover, AID shows several alternate splicing isoforms, like AID devoid of exon-4 (AIDΔE4) that is expressed in various pathological conditions. Interestingly, RBM5, a splicing regulator, is responsible for the skipping of AID exon 4. In this review, we discuss the role and significance of splicing factors in the AID mediated antibody diversification.

AID Biology: A pathological and clinical perspective.

Activation-induced cytidine deaminase (AID), primarily expressed in activated mature B lymphocytes in germinal centers, is the key factor in adaptive immune response against foreign antigens. AID is responsible for producing high-affinity and high-specificity antibodies against an infectious agent, through the physiological DNA alteration processes of antibody genes by somatic hypermutation (SHM) and class-switch recombination (CSR) and functions by deaminating deoxycytidines (dC) to deoxyuridines (dU), thereby introducing point mutations and double-stranded chromosomal breaks (DSBs). The beneficial physiological role of AID in antibody diversification is outweighed by its detrimental role in the genesis of several chronic immune diseases, under non-physiological conditions. This review offers a comprehensive and better understanding of AID biology and its pathological aspects, as well as addresses the challenges involved in AID-related cancer therapeutics, based on various recent advances and evidence available in the literature till date. In this article, we discuss ways through which our interpretation of AID biology may reflect upon novel clinical insights, which could be successfully translated into designing clinical trials and improving patient prognosis and disease management.