Pathological Healing Research Articles

Ileo-caecal lymphoid nodular hyperplasia non-specific ileo-colitis with regressive behavioural disorder and food intolerance: A case study.

A boy developed normally till age of 20 months. At 13 months had MMR immunisation. 2 weeks later had head banging & screaming at night. From 20 months he lost vocabulary and had behavioural regression with hyperactivity. He also developed chronic diarrhoea and weight loss with evidence of food intolerance. There was some response of both behavioural and gastrointestinal symptoms at age of 4 years to an elimination diet. He had extensive negative neurological investigations and was diagnosed within autistic spectrum. Aged 8 years 8 months, ileo-colonoscopy revealed ileo-caecal lymphoid nodular hyperplasia with aphthoid ulcer. There was mild chronic inflammation which was patchy throughout the ileo-colon with mild crypt distortion and occasional acute cryptitis but no granuloma. He was treated with enteral polymeric feeding (CT3211) for two months with relief of diarrhoea and improvement of behaviour. Repeat ileo-colonoscopy and biopsy after 2 months showed complete return to normal. Serum tumour necrosis factor α was 25.8pg/ml pre-treatment. Median interleukin-1 mRNA (transcripts/ug RNA) in the ileal mucosa pre-treatment was 5.19 × 105 and after 1000. Subsequent attempts to reintroduce food has revealed persistent food intolerance and behaviour deterioration after some foods. Oral mesalazine therapy has led to further behavioural improvement. This child has ileo-caecal lymphoid nodular hyperplasia with non-specific entero-colitis associated with a regressive behavioural disorder, chronic diarrhoea and food intolerance. Enteral nutrition lead to healing of the ileo-colonic pathology and improvement in behaviour. Further behavioural improvement occurred with oral mesaiazine. Does this child have Crohn's disease or a new syndrome?

A Mechanochemical Model for Adult Dermal Wound Contraction and the Permanence of the Contracted Tissue Displacement Profile

The healing of adult mammalian skin wounds involves a complex sequence of spatially and temporally coordinated processes. Wound contraction, by reducing the size of the injury, is an intrinsic component of full-thickness excisional dermal wound healing. The underlying biomechanics of wound contraction, however, are not fully understood, and little is known about the pathogenesis of severe medical conditions known as fibrocontractive diseases. The aim of this work is to investigate a deterministic mathematical model in order to obtain insight into the mechanistic relationships between wound contraction and associated normal and pathological healing processes. The model describes the essential roles of fibroblast and myofibroblast cells, a chemical growth factor and the extracellular matrix which includes type I collagen. The model results are qualitatively consistent with the biology of fibroplasia and wound contraction. It is shown that contracted state evolves during a (long) transient phase of healing known as proliferation, while collagen kinetics are fundamental to the considerably longer `remodeling' phase. Some quantitative results, notably on the evolution of wound contraction, compare favourably with experimental data. Application of the model to adult human dermal wound healingin vitro, with a greater understanding of the underlying biological mechanisms involved, may suggest strategies for controlling contraction and fibrocontractive diseases.

Sports Injury, Assessment and Rehabilitation

BASIC PRINCIPLES Sports Medicine and Sports Therapy. Principles of Treatment. Physical Modalities. Connective Tissue Healing and Classification of Ligament and Tendon Pathology. Muscle Injury: Classification and Healing. Bone: A Specialized Connective Tissue REGIONAL CONSIDERATIONS Selected Conditions of the Foot. Hell Pain and Problems of the Hindfoot. Ankle Region. Exercise-Induced Leg Pain. Internal Derangement and Other Selected Lesions of the Knee. Anterior Knee Pain and the Patellofemoral Pain Syndrome. Bursitis and Knee Extensor Mechanism in Pain Syndromes. Knee Ligament Injuries: Classification and Examination. Knee Ligament Injuries: Treatment. Soft Tissue Injuries of the Thigh. Problems of the Hip, Pelvis, And Sacroiliac Joint. Injuries to the Thorax, Abdominopelvic Viscera, And Genitourinary System. Injuries and Conditions of the Neck and Spine. Injuries to the Head and Face. The Shoulder Region. The Elbow Region. Forearm, Wrist and Hand. Running, Injury Patterns, And Prevention APPENDICES Banned and Restricted Doping Classes and Methods. Travel with Atheletes. Traveller's Diarrhea (Emporiatric Enteritis). Temperature Control: Heat-Induced Injury. Participation Health Screening. Selected Protocols and Standards for Fitness Testing Index

Types I and III procollagen extension peptides in serum respond to fracture in humans

Markers of types I and III collagen turnover were measured in serial blood samples in 16 patients with a Colles' fracture. The collagen markers were the carboxy-terminal extension peptide of type I procollagen (PICP) and the amino-terminal extension peptide of type III procollagen (PIIINP). Significant increases were found of PIIINP within 1 week and of PICP within 2 weeks. This sequential appearance of PIIINP and PICP was found to be in agreement with the appearance of types III and I collagen during early fracture healing as demonstrated in previous animal experimental studies. PICP had levelled off after 9 months, whereas PIIINP remained elevated. Osteocalcin, a serum marker of osteoblast activity, increased within 1 week and levelled off after 9 months. Correlations between the change in osteocalcin and those in PICP and PIIINP, respectively, were weak. These new biochemical markers may prove relevant as non-invasive markers of normal and pathological fracture healing in humans.

The time course of 99Tc m-Sn-polyphosphate scintimetry of normally healing tibial fractures in man

In 38 fractures of the human tibia showing radiological consolidation within 6 months, the amount of callus formed was assessed monthly by scintimetry following intravenous administration of 99Tc m-Sn-poIyphosphate. The results of the scintimetry were expressed as a ratio (as radioactivity over the fracture divided by that over the contralateral area of the normal leg). The error of the scintimetric ratio within the period of measurements (20–60 minutes after the injection of isotope) was ± 5 per cent. More isotope accumulated around the fracture in all patients. The scintimetric time course of transverse as well as longitudinal fractures showed a peak value (scintimetric ratio 3.6 ± 0.6 s.d.) in the fourth to fifth week, whatever the primary treatment, and was of the same magnitude in the two types of fracture. A secondary increase of the scintimetric ratio was found in 70 per cent of the fractures following the start of weight bearing. Infection of a fracture induced a higher scintimetric ratio than that of an uninfected fracture. Re-fractures showed exceptionally high scintimetric ratios in the second to fourth week (twice the values of primary fractures), but the ratios decreased rapidly. Scintimetry is a non-invasive, quantitative method of estimating the formation of callus. In this study the scintimetric time course of healing fractures of the tibia was determined. The results are to serve as a basic study of the method's suitability in early diagnosis of pathological healing.

Parathyroid pathology: its relation to choice of operation for hyperparathydroidism.

AbstractMultichannel autoanalyzers have diagnosed many unsuspected, largely asymptomatic cases of primary hyperparathyroidism. The age of onset of the disease and its rate of progression are not well understood. Surgical restoration of the eucalcemic state is associated with the healing of bone pathology, but many patients are not relieved of hypertensive or renal disease, and sometimes these problems continue to develop in the postoperative period, resulting in continued morbidity and mortality despite “successful” surgery. Conflicting opinions regarding the differentiation between parathyroid adenomas, hyperplasia, and normal glands appear to be resolving as newer data, both retrospective and prospective, reemphasize the pathologic importance of the clinically enlarged or abnormal glands. Parathyroid surgery for renal osteodystrophy of secondary hyperparathyroidism and for persisting hypercalcemia of tertiary hyperparathyroidism may be modified by autotransplantation. Carcinoma of the parathyroid glands is rare, but operative findings merit review. A variety of surgical approaches have been proposed. The surest method for restoring normal calcium levels with minimal permanent hypocalcemia is identification of 4 parathyroid glands and removal of those which are grossly abnormal. For patients with multiple endocrine adenomatosis or familial hyperparathyroidism, subtotal parathyroidectomy is preferred. Additional surgical guidelines are reviewed and the development of a parathyroid registry to ensure closer follow‐up is suggested.

Osteomalacia Due to 1α,25-Dihydroxycholecalciferol Deficiency

Oncogenic osteomalacia is a syndrome in which unexplained osteomalacia remits after resection of a coexisting mesenchymal tumor. We have investigated the mechanism by which a giant cell tumor of bone caused biopsy-proved osteomalacia in a 42-yr-old woman. The biochemical abnormalities were: hypophosphatemia; decreased renal tubular maximum for the reabsorption of phosphate per liter of glomerular filtrate; negative calcium and phosphorus balance; hyperaminoaciduria; and subnormal calcemic response to exogenously administered parathyroid hormone. Malabsorption, hypophosphatasia, fluorosis, and acidosis were excluded as causes of the osteomalacia. Serum 25-hydroxycholecalciferol was normal (27+/-1 ng/ml). However, the serum concentration of 1alpha,25-dihydroxycholecalciferol was low (1.6+/-0.1 ng/100 ml). Oral administration of physiological amounts of 1alpha,25-dihydroxycholecalciferol resulted in resolution of the biochemical abnormalities of the syndrome and healing of the bone pathology. We suggest that tumor-induced inhibition of 1alpha,25-dihydroxycholecalciferol synthesis caused the osteomalacia. The causal role of the tumor was proved by demonstrating that resection was accompanied by roentgenographic evidence of bone healing and maintenance of normal serum phosphorus; renal tubular maximum for the reabsorption of phosphate; calcium and phosphorus balance; aminoaciduria; and calcemic response to exogenous parathyroid hormone.

Pathologic fracture of tibial tubercle in osteitis deformans

A case of pathologic fracture of the tibial tubercle is presented. The patella tendon was sutured back to the pathologic bone and healing occurred without further incident in eight weeks.