Can Implant Arthroplasty Become the Standard for Hallux Rigidus?

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Having practiced podiatric medicine for 47 years, and with a bachelor’s degree in biological sciences, I am very familiar with the scientific method. Specifically, I have designed and engineered great toe implants for 39 years. For these reasons, I feel I am uniquely qualified to share some observations on the role of great toe implants in the treatment of hallux rigidus.
 
Degenerative joint disease of the first metatarsophalangeal joint (MTPJ) affects 2.5% of all people over the age of 50 in the United States.¹ That extrapolates to 2.7 million people in the U.S. or 5.4 million people among the industrialized countries of the world. However, we as clinicians know this disease extends to other people not in this age group. Great toe joint disease is not less debilitating than joint disease of the ankle, hip, knee, or shoulder. The great toe is, in my opinion, the only affected joint not treated properly with implant replacement. There are joint implants for this disease, yet arthrodesis remains an accepted standard.
 
The question is why? In my experience, the designs and/or choice of materials used in these implants do not lead to the same confidence seen in other joints. This begets yet another question, why not? In my opinion, and looking at the literature, this is because the full extent of the disease that affects the great toe joint is not being addressed.
 
Most of us who study this important joint in efficient ambulation can agree that the sesamoids participate in motion and weight absorption. Esway and Conti previously acknowledged my work incorporating this concept into the first MTPJ implant, with a sesamoid articulation on the plantar condylar surface of the metatarsal head component.²
 
However, in my observation, concentrated effort seems to focus on the base of the proximal phalanx for hemi-joint replacement. This ignores the real movement and weight-bearing that exists at the metatarsal-sesamoid articulation. In my opinion, this is because replacement of the proximal phalanx is easy to accomplish and often erroneously identified as the structure most responsible for this deformity. I believe this comes from a lack of understanding of the function of the first metatarsal, its dynamic position, and movement. Others have hinged the metatarsal and phalanx together to create motion and stability, disregarding the triplanar motion of this joint. In this example, motion comes from “pistoning” the implant in bone, as hinged implants will piston. Surgeon designers, investigators, biomedical engineers and others have spent years investigating and ensuring that the implants do not move in bone. This unwanted movement, referred to as micromotion, can have a devastating impact on bone.³ This unwanted movement contributes to implant loosening and pain, but will also create a slow steady state inflammatory response and migration of inflammatory cells. The bone response to inflammation is to lay down a lining of fibrous tissue containing these inflammatory cells, releasing histamines, cytokines, nitric acid, and a multitude of inflammatory chemicals.⁴ Ultimately, bone will be compromised, and the implant material, depending on its durability, will be attacked. Thus, it is important to use and understand histopathology.
 
In order to succeed in any treatment course, one must fully understand the problem, then address the cause. A proposed implant design should undergo prototyping and lab testing for strength, endurance, and security in specimens of living bone. We have the robotic devices and machinery to accomplish these tasks, and failure to use them is unacceptable, in my opinion. According to Eckert, “You place an implant into a bone and there is movement between the bone and the implant, that movement is the micro motion. If the bone is real stiff the motion is less if the bone is real soft the relative motion is greater. (Depending upon the amount of force that is applied, the speed at which it is applied, etc.) When we talk about micro motion were generally talking about something that occurs during the healing phase of the bone to implant interface. Obviously the implant is not healed to the bone, but the bone does heal to the implant. The more motion that occurs early on during the healing process the less likely it is for the bone to heal to that implant because the motion that occurs at the interface exceeds some healing threshold of the bone.”⁵
 
Following that, a clinical evaluation is essential. Standardized data, collected at fixed intervals, and imaging should look for correlation between subjective and objective findings. In my experience, important metrics include complete blood count with differential, erythrocyte sedimentation rate, C-reactive protein, and defensins. These may be early warning signs that the implants are not secure or conversely, support that implants are secure and not eliciting that inflammatory response. Anecdotal testimonials should be avoided in deference to objective scientific data.
 
With respect to designing first metatarsophalangeal-sesamoid joints, we have known about the role of sesamoid participation in motion and weight-bearing of the great toe joint since at least 1984, evidenced by the works of Rzonca, Durrant, Camasta, and their respective teams, along with magnetic resonance imaging studies.^6–8
 
For arguments sake, let’s akin the first metatarsophalangeal-sesamoid joint to the knee. The metatarsal will serve and function as the femur. The sesamoids, not the phalanx will serve as the tibial plateau in absorbing weight and allowing range of motion of the femur/metatarsal.^8,9
 
The bulk of the sesamoids (especially diseased) can raise the height of the metatarsal, which in turn can dorsally jam the metatarsal and proximal phalanx. In my estimation, a rare exception is uncompensated forefoot and first metatarsal varus. One can see this addressed in 1984 by Rzonca and team.⁶
 
The time has come—and is perhaps overdue—to consider the needs of the patient and the requirements of the first metatatarsophalangeal-sesamoid articulation in the treatment of hallux rigidus.
 
I recall life before successful implant arthroplasty of the hip and knee. Arthrodesis was archaic and unkind. In the near past, I recall life before shoulder and ankle implant arthroplasty. I met both and I thank Dr. Neer (the shoulder)¹⁰ and Dr. Kofoed (the ankle)¹¹ for their dogged determination and good science. I believe we owe modern medicine a better look at the way we treat all degenerative joint diseases, especially that of the great toe joint. As a result, I believe future analysis and development of implants for this joint should particularly consider the role of the sesamoids in achieving the desired outcome.
 
Dr. Koenig is the Director of Island Podiatry Associates in Merritt Island, FL, and CEO of Good Vibrations Shoes. He discloses that he is the inventor of the Total Toe System by Biomet and its second generation UltraToe.
 
References
1. Ho B, Baumhauer J. Hallux rigidus. EFORT Open Rev. 2017 Mar 13;2(1):13-20. doi: 10.1302/2058-5241.2.160031. PMID: 28607766; PMCID: PMC5444234.
 2. Esway JE, Conti SF. Joint replacement in the hallux metatarsophalangeal joint. Foot Ankle Clin. 2005 Mar;10(1):97-115. doi: 10.1016/j.fcl.2004.09.002.
3. Berri S. Micromotion analysis in bone implants. Int J Engin Res Innovation. 2009; 2(1):17-21.
4. Kohli N, Stoddart JC, van Arkel RJ. The limit of tolerable micromotion for implant osseointegration: a systematic review. Sci Rep. 2021 May 24;11(1):10797. doi: 10.1038/s41598-021-90142-5. PMID: 34031476; PMCID: PMC8144379.
5. Eckert SE. Research Gate.
 6. Rzonca E, Levitz S, Lue B. Hallux equinus. The stages of hallux limitus and hallux rigidus. J Am Podiatry Assoc. 1984;74(8):390-393. doi: 10.7547/87507315-74-8-390.
7. Torshizy H, Hughes TH, Trudell D, Resnick D. Anatomic features of metatarsal heads that simulate erosive disease: cadaveric study using CT, radiography, and dissection with special emphasis on cross-sectional characterization of osseous anatomy. AJR Am J Roentgenol. 2008;190(3):W175-81. doi: 10.2214/AJR.07.2967.
8. Durrant MN, Siepert KK. Role of soft tissue structures as an etiology of hallux limitus. J Am Podiatr Med Assoc. 1993;83(4):173-80. doi: 10.7547/87507315-83-4-173.
9. Camasta CA. Hallux limitus and hallux rigidus. Clinical examination, radiographic findings, and natural history. Clin Podiatr Med Surg. 1996;13(3):423-48.
10. Frank JK, Siegert P, Plachel F, Heuberer PR, Huber S, Schanda JE. The evolution of reverse total shoulder arthroplasty-from the first steps to novel implant designs and surgical techniques. J Clin Med. 2022;11(6):1512. doi: 10.3390/jcm11061512.
11. Kofoed H. Concept and use of the Scandinavian Total Ankle Replacement. Foot Ankle Spec. 2009;2(2):89-94. doi:10.1177/1938640009331488

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