To the Editor:

I have read with interest the Instructional Course Lecture by McCarthy, et al. My attention was particularly drawn to the paragraphs on etiology of Acute Hematogenous Osteomyelitis and Figures 2 and 3. I would draw the readers attention to the title of the article, especially the words "Recent Advancements", and the description of “vascular loops” in relation to metaphyseal venous sinuses.

The concept of so-called vascular loops was introduced in 1921 by Teruo Hobo(1), and perpetuated by Joseph Trueta(2), who did not adduce any further evidence for their presence. My experimental studies were, in part, stimulated by the question of why children were more prone than adults to acute hematogenous osteomyelitis, and why the metaphysis of long bones was a common site of infection.

Hobo (1) believed that the blood flow slowed when metaphyseal vessels ‘turned back’ as hairpin loops towards the diaphysis to reach dilated venous sinusoids. Despite lack of evidence to support this theory, Hobo suggested that the sluggish flow predisposed to bacterial deposition. The idea was later restated and emphasized by Trueta(2) in 1959 who, again, had no experimental data about blood flow rates to confirm this theory.

Based on animal studies Ogden(3) stated that bacteria localize in the large sinusoidal veins in the zone of provisional ossification resulting in secondary (retrograde) thrombosis on the arterial side of the metaphyseal vessels. He referred to this region as one of relative rheological stasis, although providing no supporting evidence.

Recent electron microscopic studies on avian(4) and mammalian(5-8) subjects have confirmed that ingrowth of metaphyseal vascular plexuses occurs by extension of ‘vascular sprouts’ into chondrocytic lacunae and this produces temporary gaps in the endothelial walls of these vessels. We have demonstrated(9) escape of red cells and other blood elements through these gaps. In a similar way, passage of bacteria through the endothelial gaps during an episode of septicaemia is likely and the surrounding extravascular tissue would provide an environment relatively inaccessible to mononuclear phagocytes, hence promoting bacterial proliferation. Since it is this same region which supports the earliest bacterial deposits in avian osteomyelitis(10,11), the presumed explanation for bacterial deposition, namely sluggish blood flow, may not be entirely correct. Rather, the presence of gaps in the extending tips of growing metaphyseal vessels, regardless of blood flow rates, may also play a critical role in the initiation of stapylococcal osteomyelitis.

We(9) produced experimental evidence to support the view that staphylococci adhere to cartilage of the growth plate at the physeo- metaphyseal junction. Once established, the adherent colony divided and spread rapidly within the vascular tunnel towards the diaphysis and resembled a thrombus-like mass totally occluding the vascular tunnel within 24 hours.

It appears more likely that endothelial gaps present in rapidly growing metaphyseal vessels could account for the selective deposition of bacteria in this region. The rapid occlusion of a metaphyseal tunnel with bacteria, the diffusion of bacterial toxins across the cartilaginous matrix of the growth plate (physis), and the development of an inflammatory response within surrounding tunnels suggests that the patency of the vascular lumens in the region of the abscess is lost. Under these conditions antibiotic drugs may have limited access to the centre of the abscess where the majority of the bacteria are situated. The effect of an abscess on vessels has been studied experimentally12.

The authors of the article in The Journal do not appear to have accessed these more recent studies in the preparation of their article, nor reviewed summary chapters in monographs published in 1987 and 1994(13,14).

We have also done similar studies on the pathology of septic arthritis(15). In the section of the review article on etiology of septic arthritis, the authors have perpetuated the concept of spread from metaphysis around the growth plate. This implies that septic arthritis is always associated with a focus of osteomyelitis. They do acknowledge the possibility of a direct vascular route from the metaphysis to the epiphysis, and use the term “vessels cross the epiphysis”. I would direct the reader's attention to an error in terminology. The vessels are transphyseal, crossing the physis (growth plate) and linking metaphysis and epiphysis. Such transphyseal vessels do exist, although transiently, contrary to the often taught view that the physis is avascular(16,17).

I would be grateful if you would bring this information to the attention of the authors. Readers of The Journal should have the opportunity of being brought up to date, rather than have 80 year old theories, often repeated in textbooks, again put before them. It does not advance the science of orthopaedics.

Yours sincerely

SYDNEY NADE Clinical Professor, The University of Sydney Formerly Assistant Editor, Journal of Bone and Joint Surgery [British and European edition]

The list of references cited appears on the next page

1. Hobo T. [On the pathogenesis of acute hematogenous osteomyelitis]. Acta Sch Med Univ Kioto. 1921; 4: 1-29. German.

2. Trueta J. The three types of acute haematogenous osteomyelitis. A clinical and vascular study. J Bone Joint Surg Br. 1959; 49-B: 671-680.

3. Ogden JA. Pediatric osteomyelitis and septic arthritis. The pathology of neonatal disease. Yale J Biol Med. 1979; 52: 423-448.

4. Howlett CR. The fine structure of the proximal growth plate and metaphysis of the avian tibia; endochondral osteogenesis. J Anat. 1980; 130: 745-768.

5. Ham KN, Hurley JV, Ryan GB et al. Localisation of particulate carbon in metaphyseal vessels of growing rats. Aust J Exp Biol Med Sci. 1965; 43: 625-638.

6. Anderson CE, Parker J. Invasion and resorption in enchondral ossification. An electron microscope study. J Bone Joint Surg Am. 1966; 48 -A: 899-914.

7. Schenk RK, Wiener J, Spiro D. Fine structural aspects of vascular invasion of the tibial epiphyseal plate of growing rats. Acta Anat (Basel). 1968; 69: 1-17.

8. Kalayjian DB, Cooper RR. Osteogenesis of the epiphysis. A light and electron microscope study. Clin Orthop. 1972; 85: 242-256.

9. Speers D, Nade S. Ultrastructural studies of Staphylococcus aureus in experimental acute osteomyelitis. Infec Immun. 1985; 49: 443-446.

10. Emslie K, Nade S. Acute haematogenous staphylococcal osteomyelitis: A description of the natural history in an avian model. Am J Pathol. 1983; 110: 333-345.

11. Emslie K, Ozanne N, Nade S. Acute haematogenous osteomyelitis: An experimental model. J Pathol. 1983; 141: 157-167.

12. Emslie K, Fenner L, Nade S. Acute haematogenous osteomyelitis II: The effect of a metaphyseal sbscess on the surrounding blood supply. J Pathol. 1984; 142: 129-134.

13. Gillespie WJ, Nade S. Musculoskeletal Infections. 1987; Melbourne: Blackwell Scientific Publications.

14. Norden CW, Gillespie WJ, Nade S. Infections in Bones and Joints. 1994; Boston: Blackwell Scientific Publications.

15. Alderson M, Nade S. The natural history of acute septic arthritis in an avian model. J Orthop Res. 1987; 5; 26-273.

16. Alderson M, Emslie K, Speers D, Nade S. Transphyseal blood vessels exist in avian species. J Anat. 1986;146:217-224.

17. Alderson M, Speers D, Emslie K, Nade S. Acute haematogenous osteomyelitis and septic arthritis – a single disease. J Bone Joint Surg Br. 1986; 68-B: 268-274.