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The connective tissue, composed of cells, fibers and ground substance, plays a vital role in the processes of craniofacial development, growth, wound healing and disease. This article reviews current knowledge of connective tissue biology and relates it to certain clinical situations of relevance in oral surgery.
Connective tissue diseases (CTDs) frequently present with one or only a few symptoms, which does not allow prompt diagnosis. Raynaud's phenomenon is one of those symptoms. However, only a minority of patients who present with Raynaud's phenomenon develop a CTD. Prognostic factors for the future development of CTD in such patients are older age at presentation, more severe Raynaud's phenomenon, the presence of antinuclear antibodies, and abnormal patterns on nailfold capillary microscopy. Some patients have overlapping symptoms of various CTDs. Mixed connective tissue disease (MCTD) is the prototype of such an overlapping syndrome. However, during follow-up, most patients with MCTD develop a specific CTD, either scleroderma, systemic lupus erythematosus, rheumatoid arthritis, or combinations of those illnesses. Primary pulmonary hypertension is one of the leading causes of death in MCTD. Its treatment is insufficient, although continuous prostacyclin infusion may provide some relief. New therapies such as nitric oxide and combined heart-lung transplantation in an early stage should be explored. The autoimmune response to small nuclear ribonucleoproteins, which is highly characteristic for MCTD, interestingly shows cross-reactivity with retroviral antigens, and the cooccurrence of human T cell lymphotropic virus type I and HIV infection with MCTD has been reported. This suggests that those viruses, possibly by molecular mimicry, play a role in the induction of the disease. Fibrotic conditions related to silicone exposure still evoke much interest. However, most recent data do not substantiate a role for silicone gel breast implants in the development of autoimmune CTDs.
Ten patients with mixed connective tissue disease (MCTD) were examined for signs and symptoms in the masticatory system. The study included clinical, radiological, histological and immunohistochemical examinations. The status of the teeth and periodontium did not seem to differ from that found in the general Finnish population. All 10 patients showed clinical dysfunction, and 7 had additional radiographic changes of the temporomandibular joints. Sialopenia was observed in 7 patients, and histological examination revealed sialoadenitis with a focus score exceeding 1 in the labial salivary glands in 9 patients. Only 1 patient had clinically detectable mucosal lesions. However, in 5 of 6 patients with normal-appearing mucosa, histological examination revealed chronic inflammation. Three of the 10 patients had clinically atrophic and erythematous oral mucosa; histological examination again revealed chronic inflammation. The signs and symptoms appearing in the masticatory system of these 10 MCTD patients were many and varied and indicate the importance of closely examining all oral structures. As with other connective tissue diseases, MCTD should be treated on a multidisciplinary basis.
We forget too often that the primitive mesenchyme cells are at the origin of healthy microvessels, lymphatic canaliculi and the conjunctival interstitium. In our different disciplines we tend to study in isolation the terminal circulatory unit, the lymphatic system, and the conjunctival tissues. Why not refer from the outset to histangiopathy in clinical situations as common as varicose illness, certain post-thrombotic syndromes and, in its classic form, to histangiopathy of stasis? In varicose illness, the conjunctival component of the vein wall is quantitatively differentiated from the normal wall; it is responsible for histochemical anomalies, and the inhomogeneities encountered are determined by the variable conditions of mechanomorphosis. There are also those very specific immunological reactions which some people have made so bold as to deny and changes in the ultrastructure, especially lysosomal changes which are not necessarily irreversible. Since 1965, amongst the post-thrombotic syndromes, Mario Degni has, with the aid of anatomopathological sections, isolated a very specific situation following parietal inflammatory lesions not the affection of the wall and valvules; the treatment of this is especially singular because the conjunctiva play a major part here and "parietal lymphostasis" is absent. There are many microvasculoconjunctival connections in the histo-angiopathy of stasis which are to be met in macrophlebopathies; they are responsible for the various clinical, capillaroscopic and histological pictures. The part played by the derivative channels, the tissular canals and the lymphatic canaliculi is important. The part played by the conjunctiva is even more important because of its retroactive information regulation. In pathological cases it is a degradation of plastic polymers.
The 3rd Workshop on Heritable Disorders of Connective Tissue was held at the National Institutes of Health from 16th to 18th November, 2000. The Workshop was sponsored by the National Institute of Arthritis and Musculoskeletal and Skin Diseases, NIH Office of Rare Diseases, March of Dimes, Coalition for Heritable Disorders of Connective Tissue, and the Foundation for Basic Cutaneous Research. It was supported by specific grants R13 AR46912 (US Public Health Service) and 4-FY00-4511 (March of Dimes Birth Defects Foundation). The Workshop was divided into six sessions, featuring 29 invited presentations. In addition to the invited participants, more than eighty guests (scientists, NIH staff, and members of the Coalition for Heritable Disorders of Connective Tissue) attended.
Pleuro-pulmonary involvement is frequently encountered in connective tissue disease. The pathological changes due to connective tissue disease are multifold. They include pleural, interstitial and nodular manifestations as well as airway lesions and vascular changes. In clinical decision making it is important to differentiate between effects of the underlying connective tissue disease, complications due to treatment, such as opportunistic infections, toxic and idiosyncratic drug reactions, and unrelated primary pulmonary diseases. We describe 2 patients with a connective tissue disease and pleuro-pulmonary complications. The diagnostic procedures are discussed. The result of the open lung biopsy was consistent with the diagnosis of rheumatic disease and also Sjögren's disease in the first patient and excluded infection and vasculitis in the second patient. Whenever histological investigation is needed to establish and/or exclude a diagnosis of pulmonary involvement in connective tissue disease, the open lung biopsy remains the "gold standard". We therefore propose a flow-chart for use in the clinical approach to the patient with interstitial lung disease of unknown origin.
Connective tissue is ubiquitous and subject to alterations that result in changes in the extracellular matrix of vessels and tissues leading to the long-term complications of diabetes. This article reviews only those abnormalities of interstitial connective tissue involving skeleton, joints, skin, and periarticular tissues. Abnormalities in the skin and periarticular tissues result in syndromes limiting joint movement, including limited joint mobility, Dupuytren disease, flexor tenosynovitis, carpal tunnel syndrome, stiff-hand syndrome, and shoulder-hand reflex dystrophy. Of these, only limited joint mobility and stiff-hand syndrome occur exclusively in patients with diabetes. In all of these conditions, advanced glycation end products are thought to form as a result of nonenzymatic reaction of glucose with proteins, causing stiffening.
The association of congenital heart block with maternal connective tissue disease and autoimmunity has been recently reported. Two cases of heart block were diagnosed in utero at 23 and 24 weeks' gestation. Both mothers had extensive workups for connective tissue disease that were negative. Two-dimensional and Doppler echocardiography were performed in utero and both infants had left atrial isomerism, atrioventricular canal defects, and severe hydrops in addition to heart block. Review of the recent literature identifies a subset of congenital heart block in which the mothers have no evidence for connective tissue disease, and the fetus or neonate has complex cardiac malformations and hydrops. The common features in these babies are atrioventricular canal defects and isomerism. No reports of congenital heart disease among the children of mothers with connective tissue disease fit this description. Our recent experience and literature review emphasize the previously known association between congenital heart block and congenital heart disease. This association is especially important in light of the poor prognosis for this group of fetuses and neonates.
Described is a unique mixed intracerebral tumor composed of schwannoma, piloid astrocytoma, and angiomatous malformation. Review of conventional staining methods for distinguishing glial from connective tissue fibrils reveals that Mallory's phosphotungstic acid-hematoxylin (PTAH) method is less specific than is generally recognized. Knowledge of these pitfalls, combined with use of hematoxylin and eosin stains, and reticulum impregnations are currently most useful in making the distinction by light microscopy. Criteria for malignancy of schwannoma and other mesenchymal tumors should be based on number of mitotic figures and invasiveness rather than on pleomorphiam of cells. Prior knowledge of the location of the tumor may lead to diagnosing some schwannomas as other types of tumor.
OBJECTIVE: To evaluate the association of breast implants with connective-tissue diseases. DESIGN AND PARTICIPANTS: Retrospective cohort study of 395,543 female health professionals who completed mailed questionnaires for potential participation in the Women's Health Study. A total of 10,830 women reported breast implants and 11,805 reported connective-tissue diseases between 1962 and 1991. Cox proportional hazards regression models were used in analyses. MAIN OUTCOME MEASURE: Self-reported connective-tissue diseases. RESULTS: Compared with women who did not report breast implants, the relative risk (RR) of the combined end point of any connective-tissue disease among those who reported breast implants was 1.24 (95% confidence interval, 1.08 to 1.41, P = .0015). With respect to the individual diseases, the finding for other connective-tissue diseases (including mixed) was statistically significant (P = .017), the findings for rheumatoid arthritis, Sjogren's syndrome, dermatomyositis or polymyositis, or scleroderma were of borderline statistical significance (.05 < P < .10), and the finding for systemic lupus erythematosus was not statistically significant (P = .44). There were no clear trends in RR with increasing duration of breast implants. CONCLUSION: These self-reported data from female health professionals are compatible with prior reports from other cohort studies that exclude a large hazard, but do suggest small increased risks of connective-tissue diseases among women with breast implants. The very large sample size makes chance an unlikely explanation for the results, but bias due to differential overreporting of connective-tissue diseases or selective participation by affected women with breast implants remains a plausible alternative explanation. The major contribution of this and other observational analytic studies has been to exclude large risks of connective-tissue diseases following breast implants.
A survey of connective tissue in general and human cervical connective in particular is presented. It is concluded that about 90% of the human cervix consists of fibrous connective tissue which, according to the composition of the collagen and the proteoglycans, is very similar to that in skin and sclera. The high activity of collagenase probably gives the cervical connective tissue from pregnant women its potential to ripen following prostaglandin treatment. Electron microscopical examination has revealed an increased amount of amorphous substance after such treatment. This may be caused partly by degraded collagen fibers and partly by newly synthesized proteoglycans.
From histologically stained transparent 0.7-0.8 cm thick serial sections of adult female pelves transparent glass-plate reconstructions of the connective tissue septa system were prepared. The analysis of these reconstructions revealed a bilateral symmetry and an interindividual uniformity of the connective tissue system and the adipose tissue components lying in between. The connective tissue system separating different functional compartments in the retroperitoneal space in order to envelop the muscles, the bones, the vessels and the viscera, forms a substaining system interwoven with the connective tissue elements of the musculus levator ani and perforating the muscle, and continues into the connective tissue system in the fossa ischiorectalis upto the fascia perinei superficialis is reached. The fasciae of the pelvic muscles, the sacro-tuberal and sacro-spinal ligaments and the ligaments of the uterus appear to be completely involved in this system of connective tissue septa. The connective tissue system links the pelvic viscera up to the muscular and bony parts of the locomotive systems of the trunk and the legs, giving a rise to a functional entity. The formulation of the hypothesis of this entity raised new questions about the structure of the different connective tissue septa in the female pelvic region.
Liver connective tissue cells have been characterized as perisinusoidal myofibroblasts and hepatic lipocytes (Ito cells, fat-storing cells). A concept of a single mesenchymal cell population that may be modulated between these two phenotypes has been postulated. We have previously established a continuous murine cell line, GRX, obtained from fibrotic granulomatous lesions induced by schistosomal infection in mouse liver. This cell line is considered to represent liver myofibroblasts. In the present study we have induced the conversion of these cells into lipocyte (fat storing) phenotype by treatment with insulin and indomethacin. We have quantified the lipid synthesis and the increase of activity of involved enzymes during the induction of the fat-storing phenotype and described modifications of cell organization along this modulation of cell functions.
Reactions in the connective tissue metabolism are of considerable importance in the pathophysiological process of diseases. It is from this aspect that new findings in chronic liver diseases are reported in the present paper. A report is given on cellular and extracellular pathological changes in connective tissue functions. Diagnostic and pharmacological methods undergoing continued development for controlling and influencing liver fibrosis are discussed.
The cells of the connective tissues contain lysosomes with enzymes capable of degrading intercellular substances (collagen, elastin, proteoglycans) and release their enzymes in membrane-bound or in free form into their intercellular substance. In this way extracellularly located lysosomes (= matrix lysosomes) can be detected by morphological and enzymatic means as well as by their metal concentrating property. This function of such matrix-lysosomes is in connection with the two step-degradation of the connective tissue and is thought to be the main part for the fibrocytic fibrolysis, chondrocytic chondrolysis, osteocytic osteolysis and myocytic mediolyses in the vessel wall. The cells of the mesenchymal tissues thus control the turnover and transformation of their own ground substance. Inflammatory and immunologic processes are suggested to be superimposed on this lysosomal action. If the lysosomal enzyme system in the connective tissues and the vessel wall gets out of control, the consequences can be dangerous as e.g. in case of relapsing polychondritis and arterial aneurysms. In this enzyme system proteolytic activators as well as proteolytic decomposable inhibitors are present. The corresponding proteolytic processes are of lysosomal nature and are subordinated to other regulatory mechanisms.
Periostin is predominantly expressed in collagen-rich fibrous connective tissues that are subjected to constant mechanical stresses including: heart valves, tendons, perichondrium, cornea, and the periodontal ligament (PDL). Based on these data we hypothesize that periostin can regulate collagen I fibrillogenesis and thereby affect the biomechanical properties of connective tissues. Immunoprecipitation and immunogold transmission electron microscopy experiments demonstrate that periostin is capable of directly interacting with collagen I. To analyze the potential role of periostin in collagen I fibrillogenesis, gene targeted mice were generated. Transmission electron microscopy and morphometric analyses demonstrated reduced collagen fibril diameters in skin dermis of periostin knockout mice, an indication of aberrant collagen I fibrillogenesis. In addition, differential scanning calorimetry (DSC) demonstrated a lower collagen denaturing temperature in periostin knockout mice, reflecting a reduced level of collagen cross-linking. Functional biomechanical properties of periostin null skin specimens and atrioventricular (AV) valve explant experiments provided direct evidence of the role that periostin plays in regulating the viscoelastic properties of connective tissues. Collectively, these data demonstrate for the first time that periostin can regulate collagen I fibrillogenesis and thereby serves as an important mediator of the biomechanical properties of fibrous connective tissues.
From very thick 7-8 cm thick sections of adult female specimine parts of the connective tissue septa system were isolated and their relationships to muscles, viscera and vessels were studied histologically. Following the identification of an integrated system of pelvic connective tissue septa as described in previous articles biomechanical views were formulated. The consideration of these views led to new questions concerning the correlation of the structure of the connective tissue septa at different places in the entire pelvic region. The septa appeared to continue uninterrupted into the fascia and the perimysium of the muscles. The interrelationships of the connective tissue fibres, the adipose tissue and the vessels is described. The adventitia of the pelvic veins are firmly attached to the connective tissue septa. The groundsubstance of the adipose tissue appeared to contain hydrophilic acid mucopolysaccharides. The arteries were found close to the septa but not attached to them freely embedded in the adipose tissue. The connective tissue septa appeared to be built as multi-layered, "puff-pastry"-like arranged structures. The possible functional aspects of the interrelationships of the connective tissue septa system with the vascular system are discussed.
To assess the prognostic value of capillaroscopy findings for the development of connective tissue disease in children and adolescents with Raynaud phenomenon, we followed up a group of 250 (mean age 15 years) for 1 to 6 years after the first capillaroscopy was performed. Every 6 months they were screened for signs and symptoms of connective tissue disease. Analysis was performed on capillary changes registered 6 months before the development of connective tissue disease. Capillary changes were classified into three types: normal, nonspecific, and sclerodermatous. At the end of the follow-up period, 191 (76%) subjects had primary Raynaud phenomenon, 27 (10.8%) were diagnosed as having undifferentiated connective tissue disease, and 32 (12.8%) fulfilled the criteria for a diagnosis of a specific connective tissue disease. Systemic lupus erythematosus was found in nine (3.6%) patients, rheumatoid arthritis in 10 (4%) patients (six of them with juvenile onset rheumatoid arthritis), and scleroderma spectrum disorders in 13 (5.2%). The mean time for the evolution of Raynaud phenomenon into undifferentiated connective tissue disease or a form of the disease was 2 years. Most of the subjects with primary Raynaud phenomenon (173/191, 91%), undifferentiated connective tissue disease (22/27, 81%), juvenile onset rheumatoid arthritis/rheumatoid arthritis (7/10, 70%), and systemic lupus erythematosus (6/9, 67%) had normal capillary findings. Nonspecific capillary changes occurred in 3 of 10 (30%) patients with rheumatoid arthritis, 2 of 9 (22%) with systemic lupus erythematosus, 4 of 27 (15%) with undifferentiated connective tissue disease, and 18 of 191 (9%) with primary Raynaud phenomenon. Of all the subjects, only 10 (4%) showed sclerodermatous disease type capillary changes 6 months before the expression of a particular disease: eight (62%) of these developed scleroderma spectrum disorders, one expressed systemic lupus erythematosus, and one had undifferentiated connective tissue disease. We concluded that there were no specific capillary changes predictive for future development of systemic lupus erythematosus, juvenile onset rheumatoid arthritis/rheumatoid arthritis, and undifferentiated connective tissue disease in children and adolescents with Raynaud phenomenon. Most of our study subjects with Raynaud phenomenon who developed these diseases had normal capillary findings or nonspecific changes. Children and adolescents who developed scleroderma spectrum disorders showed a sclerodermatous type of capillary changes 6 months before the expression of the disease, indicating that this type of capillary changes in children and adolescents with Raynaud phenomenon highly correlated with further development of scleroderma spectrum disorders.