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Editorials Dental caries and periodontal disease The two universal diseases of teeth and their supporting tissues are initiated by a deposition of bacterial dental plaque on the teeth, near to the crevicular epithelium. Bacterial plaque may be considered to have three functional components: (1) cariogenic organisms, of which Streptococcus mutans, lactobacilli and actinomyces are most important (Gibbons & van Houte 1975); (2) organisms inducing gingivitis and periodontitis, such as veillonella, fusobacteria, bacteroides and actinomyces (Newman et al. 1976); and (3) adjuvant and tolerizing agents (Lehner et al. 1974, Lehner 1977). The most potent of the latter are lipopolysaccharides (Johnson et al. 1956), dextrans (Battisto & Pappas 1973, Howard et al. 1975) and levans (Miranda et al. 1972, Desaymard & Ivanyi 1976). The interaction of bacteria with the adjuvant and tolerizing agents in plaque may induce immune responses which could enhance or inhibit the development of caries and periodontal disease. Caries and periodontal disease were the subjects of an interdisciplinary symposium held at the Royal Society of Medicine on the borderland between caries and periodontal disease'. The microbiology of dental plaque has been comprehensively reviewed by Krasse (1977). It is now clear that some bacteria, such as Actinomyces viscosus and Strep. mutans, can induce in animals both caries and periodontal disease. Initial adherence of bacteria is associated with absorption of proteins and glycoprotein to the tooth surface and this may differ in the crevicular domain from that of the salivary domain. Specific adherence of bacteria may in addition be dependent on the formation of extracellular polysaccharides from sucrose and this favours colonization of Strep. mutans (Gibbons & van Houte 1975, Kilian & Rolla 1976). The attached bacteria will grow and produce microcolonies on the tooth surface and in the process they will aggregate other organisms. The apical advancement of plaque microorganisms has been 1 Section of Odontology, 28 February 1977; published December 1977 by Academic Press, London. Ed T Lehner
23MA
Q clearly defined with the aid of electron-microscopy (Schroeder 1977) and scanning electron microscopy (Newman 1977). Below the contact area of teeth, plaque is in the borderland between approximal caries and periodontal disease. The histopathology and fine structural features of the gingival sulcus have been described in considerable detail (Schroeder 1977). Maintenance of a healthy gingival sulcus is dependent on the proliferative rate of the junctional epithelium, the cellular and humoral immune responses and efficacy of the oral hygiene. The junctional epithelium appears to be a highly permeable tissue and enables a dual traffic of substances from the oral surface to the connective tissue (Listgarten 1972) and from the latter leukocytes and some proteins can pass into the oral cavity (Brill & Krasse 1958, Attstrom & Egelberg 1970, Attstrom et al. 1975). Pocket formation is the result of subgingival advancement of bacterial plaque which undermines and separates the junctional epithelium from the tooth surface. These changes are associated with humoral and cellular immune responses which may have a damaging effect on the junctional epithelium and related tissues. Detailed morphometric analysis of cells in the gingival sulcus has established the proportions of neutrophils, plasma cells, monocytes, lymphocytes and blast cells (Schroeder 1973). Plasma cells in the gingiva have been extensively investigated by Brandtzaeg (1974) who showed that IgG-producing cells predominate. IgAproducing cells are also present and the ratio of IgG to IgA might be significant, as IgA may have anti-inflammatory activity (Hall et al. 1971, Griffiss 1975, Van Epps & Williams 1976). Antibody activity to plaque bacteria has been reported in crevicular fluid (Wilton 1977) and antibody to IgG (rheumatoid factor) has been detected in gingival plasma cells (Brandtzaeg & Tolo 1977). Lymphocytes are particularly associated with the initial stages of gingivitis (Zachrisson 1968, Schroeder et al. 1973) and studies have begun to define T and B lymphocytes, as well as macrophages, in the gingiva (Walker 1977). However, the immune responses of peripheral blood lymphocytes to plaque antigens have been studied extensively in patients with perio-
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dontal disease (Ivanyi & Lehner 1970, Ivanyi et al. 1972, Horton et al. 1972). B cell mitogens, such as dextran, levan and lipopolysaccharides are found in dental plaque and the incidence and magnitude of the lymphoproliferative response is increased in periodontal disease (Ivanyi & Lehner 1974, Ivanyi 1977). These polysaccharides may also have an adjuvant effect, as was shown in vitro by exposure of lymphocytes to lipopolysaccharides or levan, before stimulating them with veillonella (Ivanyi 1976). Crevicular fluid appears to contain all the humoral and cellular components found in blood, though in smaller amounts or numbers. The principal cell is the polymorphonuclear leukocyte (PMNL), accounting for about 92 % of all the cells and its functional capacity has recently been established (Wilton et al. 1976, 1977a,b, Renggli 1977). Crevicular PMNL are viable and capable of phagocytosis and killing, though a strict comparison of their functions with those of peripheral blood PMNL has revealed a decreased ability of crevicular PMNL to phagocytose candida. This defect is due to blocked C3b, but not Fc receptors on the membrane of PMNL. Complement may be activated by the classical pathway by immune complexes, though these have not been adequately demonstrated in the gingiva. However, dental plaque (Allison et al. 1976) and plaque bacteria such as Strep. mutans, Actinomyces viscosus and lipopolysaccharides (Wilton 1977) can activate the alternative pathway. These mechanisms may prevent colonization or proliferation of some bacteria which are involved in both caries and periodontal disease. In addition to host immune factors, a variety of hydrolytic and proteolytic enzymes have been detected in crevicular fluid (Cimasoni 1977). The enzymes may originate from the bacteria or leukocytes, particularly PMNL and macrophages. Lysosomal enzymes can be released from macrophages (Page et al. 1973) and from PMNL (Taichman & McArthur 1976) in the presence of dental plaque or Strep. mutans. There is evidence to suggest that lysosomal enzymes could play a role in the pathogenesis of periodontitis by perpetuating the inflammatory reaction. The magnitude of the problem of periodontal disease and caries has been clearly outlined (Slack 1977). Among a number of preventive measures chlorhexidine mouthwash inhibits formation of dental plaque and may prevent gingivitis and caries (Loe & Rindom-Schiott 1970, Loe et al. 1972, 1976, Rindom-Schi6tt et al. 1976,Gjermo & Rolla 1970, 1971). The mode of action of chlorhexidine has not been fully elucidated but it is a strongly basic substance and, unlike most other antibacterial agents, up to 30 % is initially retained by the
mucous membrane, to be released into the mouth over a long period of time (Leach 1977). The realization that dental bacterial plaque is responsible for both caries and periodontal disease has led to a number of hypotheses concerning the effect of the host responses in protection and damage. The complexity of the effects of antibodies, complement, phagocytic cells and lymphocytes at present defies clear interpretation of the functions of these immune agents. However, a unified hypothesis has been postulated for caries and periodontal disease: under certain conditions dental plaque may induce a protective immune effect on dental caries but a damaging allergic effect on periodontal disease (Lehner 1977, p 129). The host immune responses to dental microorganisms have only relatively recently been the subject of scientific enquiries. There can be little doubt that important immunological responses are elicited by these organisms and it remains now to direct our investigations into prevention by immunological means of the two most common diseases in man. T Lehner Professor of Oral Immunology and Microbiology, Guy's Hospital, London
References Allison A C, Shorlemmer H U & Bitter-Suerman D (1976) Lancet ii, 1001 Attstrom R & Egelberg J (1970) Journal of Periodontal Research 5, 48 Attstrom R, Laurell A B, Larsson U & Sjoholm A (1975) Journal of Periodontal Research 10, 19 Battisto J R & Pappas F (1973) Journal of Experimental Medicine 138, 176 Brandtzaeg P (1974) Immunology 26, 1 101 Brandtzaeg P & Tolo K (1977) In: Lehner (1977); p 145 Brill N & Krasse B (1958) Acta Odontologica Scandinavica 16, 233 Cimasoni G (1977) In: Lehner (1977); p 13 Desaymard C & Ivanyi L (1976) Immunology 30, 647 Gibbons R J & van Houte J (1975) Annual Review of Medicine 26, 121 Gjermo P & Rolla G (1970) Scandinavian Journal of Dental Research 78, 464 Giermo P & Rolla G (1971) Scandinavian Journal of Dental Research 79, 126 Griffiss J M (I1975) Journal of Immunology 114, 1779 Hall W H, Manion R E & Zinneman H H (1971) Journal of Immunology 107, 41 Horton J E, Raisz L G, Simmons H A, Oppenheim J J & Mergenhagen S E (1972) Science 177, 793 Howard J G, Courtenay B M & Vicari G (I1975) Immunology 29, 61 1 Ivanyi L (1976) Clinical and Experimental Immunology 23, 385 Ivanyi L (1977) In: Lehner (I1977); p 199 Ivanyi L & Lehner T (1970) Archives of Oral Biology 15, 1089
Journal of the Royal Society of Medicine Volume 71 March 1978 Ivanyi L & Lehner T (1974) Clinical and Experimental Immunology 18, 347 Ivanyi L, Wilton J M A & Lehner T (1972) Immunology 22, 141 Johnson A G, Gaines S & Landy M (1956) Journal of Experimental Medicine 103, 225 Kilian M & Rolla G (1976) Infection and Immunity 14, 1022 Krasse B (1977) In: Lehner (1977); p 5 Leach S (1977) In: Lehner (1977); p 105 Lehner T ed (1977) The Borderland between Caries and Periodontal Disease. Academic Press, London; p 129 Lehner T, Wilton J M A, ChaHlacombe S J & Ivanyi L (1974) Clinical and Experimental Immunology 16, 481 Listgarten M A (1972) Oral Science Reviews 1, 3 Lde H & Rindom-Schiott C (1970) In: Dental Plaque. Ed. W D McHugh. Livingstone, Edinburgh; p 247 Loe H, Rindom-Schiott C, Glavind L & Karring T (1976) Journal ofPeriodontal Research 11, 135 Loe H, von der Fehr F R & Rindom-Schi6tt C (1972) Scandinavian Journal of Dental Research 80, 1 Miranda J J, Zola H & Howard J G (1972) Immunology 23, 843 Newman H N (1977) In: Lehner (1977); p 79 Newman M G, Socransky S S, Savitt E D, Propas D A & Crawford A (1976) Journal of Periodontology 47, 373 Page R C, Davies P & Allison A C (1973) Archives of Oral Biology 20, 1481 Renggli H H (1977) In: Lehner (1977); p 211 Rindom-Schiott C, Loe H & Briner W W (1976) Journal of Periodontal Research 11, 158 Schroeder H E (1973) Helvetica Odontologica Acta 17, 16 Schroeder H E (1977) In: Lehner (1977); p 43 Schroeder H E, Munzel-Pedrazzoli S & Page R (1973) Archives of Oral Biology 18, 899 Slack G L (1977) In: Lehner (1977); p 1 Taichman N S & McArthur W P (1976) Archives of Oral Biology 21, 257 Van Epps D E & Williams R C (1976) Journal ofExperimental Medicine 144, 1227 Walker D M (1977) In: Lehner (1977); p 185 Wilton J M A (1977) In: Lehner (1977); p 223 Wilton J M A, Renggli H H & Lehner T (1976) Journal of Periodontal Research 11, 262 Wilton J M A, Renggli H H & Lehner T (1977a) Clinical and Experimental Immunology 27, 127 Wilton J M A, Renggli H H & Lehner T (1 977b) Immunology 32, 955 Zachrisson B U (1968) Journal of Periodontal Research 3, 293
163
Development of rheumatology and rehabilitation services' Desmond Newton remarked in 1975 that one of the attractions of rheumatology is its continuing change. Since then the rate of change not only in rheumatology and rehabilitation but in the practice of medicine generally has increased to a level which to many is alarming. This particularly affects the hospitals but it is also apparent throughout the health and social service organizations. The health services in this country are in a turmoil. Reference to this unrest appears almost daily in the newspapers, in nearly every issue of the professional journals and even in departmental publications. The comments in the professional journals are more forthright and critical than they were in the pre-National Health Service storm in 1946-47. In reflecting on the current NHS difficulties and the setting up of the Royal Commission, one editorial went so far as to say: 'Governments faced with insoluble problems have been known to react by instructing a collection of eminent men and women to go away and knit a rice pudding, and there are those who believe that this was just what Sir Harold Wilson was up to last year. Professional outrage at that time was so high that we might have had no medical service at all and something had to be done.' (British Journal of Hospital Medicine 1976). It is now recognized that there is a crisis in health care in most developed countries. As Lock (1976) says: 'Even though the richest ones such as Sweden and the United States can still afford more EMIscanners, or more pacemakers, or more kidney transplants, we're all at the end of the road: the developments in medical technology have outstripped the money we've available to spend on health care.' The wants will always exceed the needs, which in turn can never be met by the available resources. The dust is now settling very slowly on the upheaval caused by the National Health Service reorganization, the Royal Commission under Sir Alec Merrison is taking evidence, and 1977 was World Rheumatism Year, so that it is opportune to examine progress in the practice of rheumatology and rehabilitation, to take stock of the current situation, and to examine the changing attitudes in the management of locomotor disease with reference to the future role of the specialty of rheumatology and rehabilitation. Perhaps the most important factor to influence the growth and importance of rheumatology and rehabilitation is the changed pattern of morbidity ' Based on Dr A K Tyler's Presidential Address to the Section of Rheumatology and Rehabilitation, 9 March 1977
0141-0768/78/0071-0163 'SOI.00 0
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Editorials Dental caries and periodontal disease The two universal diseases of teeth and their supporting tissues are initiated by a deposition of bacterial dental plaque on the teeth, near to the crevicular epithelium. Bacterial plaque may be considered to have three functional components: (1) cariogenic organisms, of which Streptococcus mutans, lactobacilli and actinomyces are most important (Gibbons & van Houte 1975); (2) organisms inducing gingivitis and periodontitis, such as veillonella, fusobacteria, bacteroides and actinomyces (Newman et al. 1976); and (3) adjuvant and tolerizing agents (Lehner et al. 1974, Lehner 1977). The most potent of the latter are lipopolysaccharides (Johnson et al. 1956), dextrans (Battisto & Pappas 1973, Howard et al. 1975) and levans (Miranda et al. 1972, Desaymard & Ivanyi 1976). The interaction of bacteria with the adjuvant and tolerizing agents in plaque may induce immune responses which could enhance or inhibit the development of caries and periodontal disease. Caries and periodontal disease were the subjects of an interdisciplinary symposium held at the Royal Society of Medicine on the borderland between caries and periodontal disease'. The microbiology of dental plaque has been comprehensively reviewed by Krasse (1977). It is now clear that some bacteria, such as Actinomyces viscosus and Strep. mutans, can induce in animals both caries and periodontal disease. Initial adherence of bacteria is associated with absorption of proteins and glycoprotein to the tooth surface and this may differ in the crevicular domain from that of the salivary domain. Specific adherence of bacteria may in addition be dependent on the formation of extracellular polysaccharides from sucrose and this favours colonization of Strep. mutans (Gibbons & van Houte 1975, Kilian & Rolla 1976). The attached bacteria will grow and produce microcolonies on the tooth surface and in the process they will aggregate other organisms. The apical advancement of plaque microorganisms has been 1 Section of Odontology, 28 February 1977; published December 1977 by Academic Press, London. Ed T Lehner
23MA
Q clearly defined with the aid of electron-microscopy (Schroeder 1977) and scanning electron microscopy (Newman 1977). Below the contact area of teeth, plaque is in the borderland between approximal caries and periodontal disease. The histopathology and fine structural features of the gingival sulcus have been described in considerable detail (Schroeder 1977). Maintenance of a healthy gingival sulcus is dependent on the proliferative rate of the junctional epithelium, the cellular and humoral immune responses and efficacy of the oral hygiene. The junctional epithelium appears to be a highly permeable tissue and enables a dual traffic of substances from the oral surface to the connective tissue (Listgarten 1972) and from the latter leukocytes and some proteins can pass into the oral cavity (Brill & Krasse 1958, Attstrom & Egelberg 1970, Attstrom et al. 1975). Pocket formation is the result of subgingival advancement of bacterial plaque which undermines and separates the junctional epithelium from the tooth surface. These changes are associated with humoral and cellular immune responses which may have a damaging effect on the junctional epithelium and related tissues. Detailed morphometric analysis of cells in the gingival sulcus has established the proportions of neutrophils, plasma cells, monocytes, lymphocytes and blast cells (Schroeder 1973). Plasma cells in the gingiva have been extensively investigated by Brandtzaeg (1974) who showed that IgG-producing cells predominate. IgAproducing cells are also present and the ratio of IgG to IgA might be significant, as IgA may have anti-inflammatory activity (Hall et al. 1971, Griffiss 1975, Van Epps & Williams 1976). Antibody activity to plaque bacteria has been reported in crevicular fluid (Wilton 1977) and antibody to IgG (rheumatoid factor) has been detected in gingival plasma cells (Brandtzaeg & Tolo 1977). Lymphocytes are particularly associated with the initial stages of gingivitis (Zachrisson 1968, Schroeder et al. 1973) and studies have begun to define T and B lymphocytes, as well as macrophages, in the gingiva (Walker 1977). However, the immune responses of peripheral blood lymphocytes to plaque antigens have been studied extensively in patients with perio-
162
Journal of the Royal Society of Medicine Volume 71 March 1978
dontal disease (Ivanyi & Lehner 1970, Ivanyi et al. 1972, Horton et al. 1972). B cell mitogens, such as dextran, levan and lipopolysaccharides are found in dental plaque and the incidence and magnitude of the lymphoproliferative response is increased in periodontal disease (Ivanyi & Lehner 1974, Ivanyi 1977). These polysaccharides may also have an adjuvant effect, as was shown in vitro by exposure of lymphocytes to lipopolysaccharides or levan, before stimulating them with veillonella (Ivanyi 1976). Crevicular fluid appears to contain all the humoral and cellular components found in blood, though in smaller amounts or numbers. The principal cell is the polymorphonuclear leukocyte (PMNL), accounting for about 92 % of all the cells and its functional capacity has recently been established (Wilton et al. 1976, 1977a,b, Renggli 1977). Crevicular PMNL are viable and capable of phagocytosis and killing, though a strict comparison of their functions with those of peripheral blood PMNL has revealed a decreased ability of crevicular PMNL to phagocytose candida. This defect is due to blocked C3b, but not Fc receptors on the membrane of PMNL. Complement may be activated by the classical pathway by immune complexes, though these have not been adequately demonstrated in the gingiva. However, dental plaque (Allison et al. 1976) and plaque bacteria such as Strep. mutans, Actinomyces viscosus and lipopolysaccharides (Wilton 1977) can activate the alternative pathway. These mechanisms may prevent colonization or proliferation of some bacteria which are involved in both caries and periodontal disease. In addition to host immune factors, a variety of hydrolytic and proteolytic enzymes have been detected in crevicular fluid (Cimasoni 1977). The enzymes may originate from the bacteria or leukocytes, particularly PMNL and macrophages. Lysosomal enzymes can be released from macrophages (Page et al. 1973) and from PMNL (Taichman & McArthur 1976) in the presence of dental plaque or Strep. mutans. There is evidence to suggest that lysosomal enzymes could play a role in the pathogenesis of periodontitis by perpetuating the inflammatory reaction. The magnitude of the problem of periodontal disease and caries has been clearly outlined (Slack 1977). Among a number of preventive measures chlorhexidine mouthwash inhibits formation of dental plaque and may prevent gingivitis and caries (Loe & Rindom-Schiott 1970, Loe et al. 1972, 1976, Rindom-Schi6tt et al. 1976,Gjermo & Rolla 1970, 1971). The mode of action of chlorhexidine has not been fully elucidated but it is a strongly basic substance and, unlike most other antibacterial agents, up to 30 % is initially retained by the
mucous membrane, to be released into the mouth over a long period of time (Leach 1977). The realization that dental bacterial plaque is responsible for both caries and periodontal disease has led to a number of hypotheses concerning the effect of the host responses in protection and damage. The complexity of the effects of antibodies, complement, phagocytic cells and lymphocytes at present defies clear interpretation of the functions of these immune agents. However, a unified hypothesis has been postulated for caries and periodontal disease: under certain conditions dental plaque may induce a protective immune effect on dental caries but a damaging allergic effect on periodontal disease (Lehner 1977, p 129). The host immune responses to dental microorganisms have only relatively recently been the subject of scientific enquiries. There can be little doubt that important immunological responses are elicited by these organisms and it remains now to direct our investigations into prevention by immunological means of the two most common diseases in man. T Lehner Professor of Oral Immunology and Microbiology, Guy's Hospital, London
References Allison A C, Shorlemmer H U & Bitter-Suerman D (1976) Lancet ii, 1001 Attstrom R & Egelberg J (1970) Journal of Periodontal Research 5, 48 Attstrom R, Laurell A B, Larsson U & Sjoholm A (1975) Journal of Periodontal Research 10, 19 Battisto J R & Pappas F (1973) Journal of Experimental Medicine 138, 176 Brandtzaeg P (1974) Immunology 26, 1 101 Brandtzaeg P & Tolo K (1977) In: Lehner (1977); p 145 Brill N & Krasse B (1958) Acta Odontologica Scandinavica 16, 233 Cimasoni G (1977) In: Lehner (1977); p 13 Desaymard C & Ivanyi L (1976) Immunology 30, 647 Gibbons R J & van Houte J (1975) Annual Review of Medicine 26, 121 Gjermo P & Rolla G (1970) Scandinavian Journal of Dental Research 78, 464 Giermo P & Rolla G (1971) Scandinavian Journal of Dental Research 79, 126 Griffiss J M (I1975) Journal of Immunology 114, 1779 Hall W H, Manion R E & Zinneman H H (1971) Journal of Immunology 107, 41 Horton J E, Raisz L G, Simmons H A, Oppenheim J J & Mergenhagen S E (1972) Science 177, 793 Howard J G, Courtenay B M & Vicari G (I1975) Immunology 29, 61 1 Ivanyi L (1976) Clinical and Experimental Immunology 23, 385 Ivanyi L (1977) In: Lehner (I1977); p 199 Ivanyi L & Lehner T (1970) Archives of Oral Biology 15, 1089
Journal of the Royal Society of Medicine Volume 71 March 1978 Ivanyi L & Lehner T (1974) Clinical and Experimental Immunology 18, 347 Ivanyi L, Wilton J M A & Lehner T (1972) Immunology 22, 141 Johnson A G, Gaines S & Landy M (1956) Journal of Experimental Medicine 103, 225 Kilian M & Rolla G (1976) Infection and Immunity 14, 1022 Krasse B (1977) In: Lehner (1977); p 5 Leach S (1977) In: Lehner (1977); p 105 Lehner T ed (1977) The Borderland between Caries and Periodontal Disease. Academic Press, London; p 129 Lehner T, Wilton J M A, ChaHlacombe S J & Ivanyi L (1974) Clinical and Experimental Immunology 16, 481 Listgarten M A (1972) Oral Science Reviews 1, 3 Lde H & Rindom-Schiott C (1970) In: Dental Plaque. Ed. W D McHugh. Livingstone, Edinburgh; p 247 Loe H, Rindom-Schiott C, Glavind L & Karring T (1976) Journal ofPeriodontal Research 11, 135 Loe H, von der Fehr F R & Rindom-Schi6tt C (1972) Scandinavian Journal of Dental Research 80, 1 Miranda J J, Zola H & Howard J G (1972) Immunology 23, 843 Newman H N (1977) In: Lehner (1977); p 79 Newman M G, Socransky S S, Savitt E D, Propas D A & Crawford A (1976) Journal of Periodontology 47, 373 Page R C, Davies P & Allison A C (1973) Archives of Oral Biology 20, 1481 Renggli H H (1977) In: Lehner (1977); p 211 Rindom-Schiott C, Loe H & Briner W W (1976) Journal of Periodontal Research 11, 158 Schroeder H E (1973) Helvetica Odontologica Acta 17, 16 Schroeder H E (1977) In: Lehner (1977); p 43 Schroeder H E, Munzel-Pedrazzoli S & Page R (1973) Archives of Oral Biology 18, 899 Slack G L (1977) In: Lehner (1977); p 1 Taichman N S & McArthur W P (1976) Archives of Oral Biology 21, 257 Van Epps D E & Williams R C (1976) Journal ofExperimental Medicine 144, 1227 Walker D M (1977) In: Lehner (1977); p 185 Wilton J M A (1977) In: Lehner (1977); p 223 Wilton J M A, Renggli H H & Lehner T (1976) Journal of Periodontal Research 11, 262 Wilton J M A, Renggli H H & Lehner T (1977a) Clinical and Experimental Immunology 27, 127 Wilton J M A, Renggli H H & Lehner T (1 977b) Immunology 32, 955 Zachrisson B U (1968) Journal of Periodontal Research 3, 293
163
Development of rheumatology and rehabilitation services' Desmond Newton remarked in 1975 that one of the attractions of rheumatology is its continuing change. Since then the rate of change not only in rheumatology and rehabilitation but in the practice of medicine generally has increased to a level which to many is alarming. This particularly affects the hospitals but it is also apparent throughout the health and social service organizations. The health services in this country are in a turmoil. Reference to this unrest appears almost daily in the newspapers, in nearly every issue of the professional journals and even in departmental publications. The comments in the professional journals are more forthright and critical than they were in the pre-National Health Service storm in 1946-47. In reflecting on the current NHS difficulties and the setting up of the Royal Commission, one editorial went so far as to say: 'Governments faced with insoluble problems have been known to react by instructing a collection of eminent men and women to go away and knit a rice pudding, and there are those who believe that this was just what Sir Harold Wilson was up to last year. Professional outrage at that time was so high that we might have had no medical service at all and something had to be done.' (British Journal of Hospital Medicine 1976). It is now recognized that there is a crisis in health care in most developed countries. As Lock (1976) says: 'Even though the richest ones such as Sweden and the United States can still afford more EMIscanners, or more pacemakers, or more kidney transplants, we're all at the end of the road: the developments in medical technology have outstripped the money we've available to spend on health care.' The wants will always exceed the needs, which in turn can never be met by the available resources. The dust is now settling very slowly on the upheaval caused by the National Health Service reorganization, the Royal Commission under Sir Alec Merrison is taking evidence, and 1977 was World Rheumatism Year, so that it is opportune to examine progress in the practice of rheumatology and rehabilitation, to take stock of the current situation, and to examine the changing attitudes in the management of locomotor disease with reference to the future role of the specialty of rheumatology and rehabilitation. Perhaps the most important factor to influence the growth and importance of rheumatology and rehabilitation is the changed pattern of morbidity ' Based on Dr A K Tyler's Presidential Address to the Section of Rheumatology and Rehabilitation, 9 March 1977
0141-0768/78/0071-0163 'SOI.00 0
