‘HOT PULP’ SYNDROME Sir, It is a truism to state that clinical dentistry has made spectacular advances in the last decades, but one problem which remains and sporadically threatens the profession’s public credibility is the so-called ‘hot pulp’ syndrome: the tooth which steadfastly resists anaesthesia. Cases where even superficial enamel cannot be prepared without excruciating pain arise only irregularly but are of the greatest frustration not only to the patient but also to dentists who see themselves as caring and proficient. Experienced clinicians have observed that achieving anaesthesia in these situations is not merely a matter of injecting more accurately or extensively; invariably all the accessory signs of anaesthesia are present and adjacent teeth may be prepared without difficulty. Techniques such as the placement of sedative dressings or injecting intraosseously into the interproximal cool area usually produce no improvement. When relief of pain and a pulpectomy is required, anaesthesia is only attained after injecting directly into the pulp canals. The mechanism of this resistance is poorly understood. The ‘hot pulp’ is usually described as being hyperaemic. However, pulps with inflammatory conditions exhibit increased blood supplies and yet resistance to anaesthesia is seen only rarely. It has

been suggested that pH changes in the periapical and surrounding tissues are responsible as the action of anaesthetic solutions is inhibited in acidic environments. Similarly, this explanation must be questioned: the anaesthetizing of mandibular molars requires a block technique whereby anaesthetic solution is deposited adjacent to the inferior alveolar, and occasionally the long buccal and mental nerves, at some distance removed from the tooth in question. It would appear that our understanding of sensory pathways is not sufficient to explain this phenomenon. Perhaps just as conhsing is the lack of an obvious clinical pattern. Teeth that resist anaesthesia are usually painful but a certain percentage are symptom-free and exhibit minimal caries. The ‘hot pulp’ syndrome represents a gap in our knowledge and is an area where research into aetiology and treatment is urgently needed. Until we can overcome this problem we cannot claim to consistently practise pain-free dentistry. MARKKNAPP 45 Toorak Road, South Yarra, Victoria, 3141. 18 May 1992.

DENTURE STOMATITIS Sir, I read with interest the review article by Jeganathan and Lin on denture stomatitits which appeared in a recent issue of your Journal (Aust Dent J 1992; 37:107-14).As an oral microbiologist interested in oral candida infections for over a decade, I wish to point out a few misconceptions and omissions which have crept into the latter review. With regard to the laboratory diagnosis of candida-induced denture stomatitis, swabs and Australian Dental Journal 1992:37:4.

smears from the palate as well as the fitting surface of the denture are essential requirements.’.2 The swabs are cultured on Sabouraud’s agar and observed for candidal growth whilst the smears are fured and stained either by periodic acid Schiff (PAS) or Gram reagent. The authors have overlooked the importance of swabbing these surfaces as, in my experience, candidal growth is observed (from cultured swabs) on many occasions when the 31 9

organisms are not seen in smears. Further, the authors correctly describe imprint and replica cultures as techniques available to investigate the condition. However, in my opinion, foam pads used for these special techniques are not routinely available to the general practitioner (as they are research rather than diagnostic techniques) and hence simple bacteriological swabs together with smears, as above, should suffice for a laboratory diagnosis of candida-induced denture stomatitis. Perhaps it is noteworthy at this juncture that newer techniques such as the oral rinse technique has immense potential in the diagnosis of oral candid~sis.~ In the section on the management of denture stomatitis the authors describe that candidaemia consequent to denture stomatitis may be a serious risk to those with valvular heart disease. However, there are no reports to substantiate this assertion and I fail to see how the presence of candida in the oral cavity of, especially, edentulous individuals may lead to candidal endocarditis, bearing in mind that the candida species are commensals in the gastro-intestinal t r a ~ t . ~ These criticisms apart, I welcome the authors

emphaisis on the importance of oral and denture hygiene in the prevention and management of this condition. A fact which all practitioners should be cognizant of.

References 1. Sarnaranayake LP, MacFarlane TW. Oral candidosis. London: Wright Butterworth, 1990:213-35. 2. MacFarlane TW, Sarnaranayake LP. Clinical oral microbiology. London: Wright Butterworth, 1989: 129-33. 3. Sarnaranayake LP, MacFarlane TW, Larney PJ, Ferguson MM. A comparison of oral rinse and imprint sampling techniques for detection of yeasts, coliform and Staphylococcus uureus in the oral cavity. J Oral Path 1986;15:386-8. 4. Odds FC. Candida and candidosis. 2nd edn. London: Bailliere Tindall, 1988. L. P. SAMARANAYAKE, Reader in Oral Microbiology, University of Hong Kong. Oral Biology Unit, University of Hong Kong, Prince Philip Dental Hospital, 34 Hospital Road, Sai Ying Pun, Hong Kong. 12 June 1992.

DENTURE STOMATITIS Sir, We thank you for forwarding the letter by Dr L. P. Samaranayake. As practising clinicians, we have described some microbiological investigations which we are familiar with and which we use in our hospital fairly routinely. We are in agreement with Dr Samaranayake that swab culture and oral rinse techniques have immense potential in the diagnosis of oral candidosis. However, we would like to highlight that in the section of ‘Microscopic examination’ we have indeed stated that scrapings should be taken from the palatal mucosa and the fitting surface of the denture and, therefore, we have not overlooked the importance of these surfaces. With regards to candidaemia, we do agree that it is not encountered routinely. Candidal endocarditis have been reported in the literature.’,’ Whilst candida species are commensals in the gastrointestinal tract, in patients with cardiac abnormalities, this endogenous microbe assumes pathogenetic significance.* Any focus of infection is a potential risk to patients with cardiac abnorm320

ality.’ Therefore, it is our contention that candidal endocarditis cannot be discounted totally. Finally, we would like to assure Dr Samaranayake that there were no misconceptions, rather differences in opinion. However, we take great pleasure in thanking Dr Samaranayake for his valuable comments and input on the laboratory aspects.

References 1. Andriole VT, Kravetz HM, Roberts WC, Utz JP. Candida

endocarditis. Am J Med 1962;32:251-85. 2. Robbins LS, Angel1 M, Kumar V. Basic pathology. Tokyo: WB Saunders, 1981:306-7.

S. JEGANATHAN. CHEWCHONGLIN. Department of Restorative Dentistry, National University of Singapore. Faulty of Dentistry, National University of Singapore, National University Hospital, Lower Kent Ridge Road, Singapore 05 1 1. 1 July 1992. Australian Dental Journal 1992;37:4.