Therapeutic Effects of Intra-articular Botulinum Toxin Type A in Knee Osteoarthritis

Knee osteoarthritis (KOA) is an intractable and devastating consequence of degeneration that results in tremendous impact on daily activities. Painful disabling KOA occurs in more than 10% of people who are over 55 years old.

Those who are severely disabled account for up to 25% of aging people and KOA is a major cause of total knee replacement. Current osteoarthritis therapies largely rely on rest, weight loss, bracing and assistive devices, physical modalities, therapeutic exercises, and pharmacological interventions which are unsatisfactory for the majority of severe disabled patients, who are left with ambulation deficit despite vigorous treatment intervention.

Although numerous patients can be treated with surgery, some of them are not good candidates due to multiple co-morbidities. For these reasons, intra-articular (IA) treatments that reduce chronic joint pain and improve function is the long-term effective and safe alternative options. In a number of recent studies, pain intensity and functional performance resulted from osteoarthritis has been improved after IA injection of botulinum toxin type A

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Systemic Amyloidosis with Predominant Spine Involvement: A Case Report

In November 2011 a 57-year old man, with a 3 months history of back pain, was admitted at the Emergency Department because of difficulty maintaining upright position. He was admitted in our Department for an incomplete paraplegia with hypertonus, exhaustible bilateral clonus and acute urinary retention.

The CT scan and MRI showed a pathological fracture of T7 with the presence of a large soft tissue mass narrowing the spinal canal for more than 50% of its diameter (Figure 1 A-B). Anamnesis was negative for cancer and only revealed a history of HBV-related steatosis.

Laboratory tests showed elevation of Ca 19-9 (263.4), Ca 125 (96.1), alkaline phosphatase (199) and γ GT (325); at that time there was no serum monoclonal component. After arteriography and selective embolization (with pathological finding of a modest circle), he underwent urgently to tumor debulking, decompression and stabilization from T5 to T9 (Figure 2 A-B).

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Therapeutic Effects of Intra-articular Botulinum Toxin Type A in Knee Osteoarthritis

Knee osteoarthritis (KOA) is an intractable and devastating consequence of degeneration that results in tremendous impact on daily activities. Painful disabling KOA occurs in more than 10% of people who are over 55 years old.

Those who are severely disabled account for up to 25% of aging people and KOA is a major cause of total knee replacement. Current osteoarthritis therapies largely rely on rest, weight loss, bracing and assistive devices, physical modalities, therapeutic exercises, and pharmacological interventions which are unsatisfactory for the majority of severe disabled patients, who are left with ambulation deficit despite vigorous treatment intervention.

Although numerous patients can be treated with surgery, some of them are not good candidates due to multiple co-morbidities. For these reasons, intra-articular (IA) treatments that reduce chronic joint pain and improve function is the long-term effective and safe alternative options.

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Collagen Mutant Mouse Models Provide an Important Tool to Study Osteoarthritis

Mutations in the human type II (COL2A1) collagen gene appear to be the basis for many skeletal disorders such as spondyloepiphyseal dysplasia, achondrogenesis, Kniest, and Stickler syndrome. Several of these conditions include early-onset osteoarthritis in addition to the chondrodysplasia phenotype.

Other collagen genes are also involved etiologically in the chondrodysplasias, e.g., an autosomal dominant form of Stickler syndrome, characterized by mild spondyloepiphyseal dysplasia (SED) and early-onset osteoarthritis, results from a mutation involving the COL11A2 gene that encodes the α2 (XI) chain of the quantitatively minor fibrillar type XI collagen.

Multiple epiphyseal dysplasia in humans involving flattening of the epiphyses, shortening of endochondral bones, and early-onset osteoarthritis has been linked to a mutation in type IX collagen, and mice made transgenic for α1 (IX) mutation have been shown to develop osteoarthritis and intervertebral disc degeneration prematurely.

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Risk Factors Affecting Postoperative Walking Ability Following Hip Fracture Surgery in the Elderly

Hip fractures are frequent in elderly people, and subsequent Activities of Daily Living (ADL) depend on whether practical walking ability is achieved postoperatively. The aim of this study was to examine the factors affecting postoperative walking ability following a hip fracture.

A retrospective study of 95 patients (85 females, 10 males, mean age 77.4 ± 10.8 years) was conducted. All patients were operated in our hospital between 2007 and 2014. Information about age, sex, type of fracture, complications, surgical method, preoperative walking ability, preoperative ADL, dementia, osteoporosis treatment, and preoperative wait (days) was obtained from the patients’ clinical records.

Factors affecting postoperative walking ability were examined. On logistic regression analysis, age, bone and joint disease, and dementia were significant factors for failure to walk after hip fracture surgery.

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Collagen Mutant Mouse Models Provide an Important Tool to Study Osteoarthritis

Mutations in the human type II (COL2A1) collagen gene appear to be the basis for many skeletal disorders such as spondyloepiphyseal dysplasia [1], achondrogenesis, Kniest, and Stickler syndrome. Several of these conditions include early-onset osteoarthritis in addition to the chondrodysplasia phenotype.

Other collagen genes are also involved etiologically in the chondrodysplasias, e.g., an autosomal dominant form of Stickler syndrome, characterized by mild spondyloepiphyseal dysplasia (SED) and early-onset osteoarthritis, results from a mutation involving the COL11A2 gene that encodes the α2 (XI) chain of the quantitatively minor fibrillar type XI collagen.

Multiple epiphyseal dysplasia in humans involving flattening of the epiphyses, shortening of endochondral bones, and early-onset osteoarthritis has been linked to a mutation in type IX collagen, and mice made transgenic for α1 (IX) mutation have been shown to develop osteoarthritis and intervertebral disc degeneration prematurely. The Disproportionate micromelia (Dmm) mouse has a mutation that causes lethal dwarfism in the homozygote and mild dwarfism in the heterozygote.

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Treatment by Quacks Still An Issue of Concern

It was not all about writing a research paper or a case report. This time it was writing our experience regarding mismanagement of simple injuries or fractures by quacks. Lots of patients frequently come to our orthopaedic OPD with complaints of deformities stiffness of joint, non union of fractures or an ugly swelling.

It is not uncommon to see patient left handicapped by a quack after a simple fracture. Not only do these quacks treat injuries but they also put their hands on other orthopaedic ailments like rheumatoid arthritis. Most of time history is same.History of trauma sustaining injury to limbs and often injury is of 5 to 6 months old.

Usually the patients are form lower socioeconomic group.The so called different treatment tactics by these quacks keeps on puzzling you and make your work even difficult. The outcome is now further complicated if these cases reach late, after initially getting treatment from “Quacks” in the form of massage and traditional manipulations.

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