Jonathan G. Schoenecker, Ph.D., M.D.

Assistant Professor
Faculty Appointments
Assistant Professor of Orthopaedic Surgery and Rehabilitation Assistant Professor of Pathology, Microbiology and ImmunologyAssistant Professor of PediatricsAssistant Professor of Pharmacology
M.D., MEDICINE-MD, Duke University, Durham, North CarolinaPh.D., PATHOLOGY, Duke University, Durham, North CarolinaB.A., Middlebury College, Middlebury, Vermont
Research Description
My research laboratory is dedicated to define the integrated role of coagulation and inflammation on orthopaedic related wound healing. My unique focus stems from my surgical training in musculoskeletal diseases in combination with my basic science training in coagulation and bone biology.

Our initial experiments have employed models of bone growth, tumor and wound healing to characterize and manipulate cell membrane associated coagulation receptors including tissue factor, thrombomodulin and protease activated receptors. Utilizing these same models, we are investigating how the currently used coagulation associated orthobiologics affect bone growth. Over the next 5-10 years I propose to develop novel coagulation based pharmaceuticals capable of manipulating fracture healing in osteoporotic bone or inhibiting bone based tumors and infections.

Clinically, we are developing new measures of coagulation to quantify hypercoaguability. Current clinical tests of coagulation are incapable of quantifying hypercoaguability. Instead, it can only be measured through surrogate markers such as the development of a DVT. These markers represent the end-stage complications of hypercoaguability and are impractical measures. Furthermore, because the extent and duration of orthopaedic and surgically related hypercoaguability has not been reported, it is unknown how long treatment of hypercoaguable plasma with anticoagulation is required. As a result, patients are treated in the post-surgical period with a “standard” dose of anticoagulant due to the absence of methods to inform accurate dosing or duration of therapy. This approach places patients at serious risk for developing complications either from i) under-treatment leaving the patient unprotected from hypercoaguability or ii) over-treatment, putting the patient at risk for hemorrhage, hematoma and complications of traumatic and surgical wound healing. Our preliminary data suggest that thrombin generation assays enable the sensitive detection orthopaedic and surgically related hypercoaguability. Therefore, clinically I propose that utilization of this assay will provide rational dose regiments for anticoagulant therapy for these patients. These studies have been initiated and will likely encompass the next 10 years of my clinical research program. Further, recent evidence suggests that many diseases treated by pediatric orthopaedic surgeons are secondary to a hypercoaguable state, such as; Legg-Calves-Perthes disease, osteosarcoma, osteomyelitis and cerebral palsy. We hope over the next five years to apply our novel clinical test to these diseases with the goal of diagnosing and treating the coagulation aspects of these diseases.
The strength of this research program is its uniqueness and clinical relevance. Coagulation research and its pharmaceutical application have already been identified by major cross-disciplinary clinical and research organizations for subject directed funding. The major innovation of this research is that it will i) provide a quantitative measure of hypercoaguability and ii) determine the critical threshold of hypercoaguability that is required for optimal skin and bone wound healing. These studies will have direct and immediate implications for patients undergoing orthopaedic surgery by defining optimal treatment strategies that prevent the complications of the hypercoaguable state, but permit wound healing. They will also allow potentially provide a novel understanding of the pathophysiology of many common diseases specific to pediatric orthopaedics.
Research Keywords
The role of Coagulation in Normal and Pathologic Orthopaedic Related Wounds.
Schoenecker J, Mignemi N, Stutz C, Liu Q, Edwards J, Lynch C, Holt G, Schwartz H, Mencio G, Hamm H. 2010 Young Investigator Award winner: Therapeutic aprotinin stimulates osteoblast proliferation but inhibits differentiation and bone matrix mineralization. Spine. 2010 Apr 4/20/2010; 35(9): 1008-16. PMID: 20407341, PII: 00007632-201004200-00014, DOI: 10.1097/BRS.0b013e3181d3cffe, ISSN: 1528-1159.

Schoenecker JG, Kim YJ, Ganz R. Treatment of traumatic separation of the proximal femoral epiphysis without development of osteonecrosis: a report of two cases. J Bone Joint Surg Am. 2010 Apr; 92(4): 973-7. PMID: 20360524, PII: 92/4/973, DOI: 10.2106/JBJS.I.00464, ISSN: 1535-1386.

Schoenecker JG, Johnson RK, Fields RC, Lesher AP, Domzalski T, Baig K, Lawson JH, Parker W. Relative purity of thrombin-based hemostatic agents used in surgery. J. Am. Coll. Surg. 2003 Oct; 197(4): 580-90. PMID: 14522327, PII: S1072-7515(03)00670-7, DOI: 10.1016/S1072-7515(03)00670-7, ISSN: 1072-7515.

Fields RC, Schoenecker JG, Hart JP, Hoffman MR, Pizzo SV, Lawson JH. Protease-activated receptor-2 signaling triggers dendritic cell development. Am. J. Pathol. 2003 Jun; 162(6): 1817-22. PMID: 12759239, PMCID: PMC1868121, PII: S0002-9440(10)64316-7, DOI: 10.1016/S0002-9440(10)64316-7, ISSN: 0002-9440.

Schoenecker JG, Johnson RK, Lesher AP, Day JD, Love SD, Hoffman MR, Ortel TL, Parker W, Lawson JH. Exposure of mice to topical bovine thrombin induces systemic autoimmunity. Am. J. Pathol. 2001 Nov; 159(5): 1957-69. PMID: 11696457, PMCID: PMC1867043, PII: S0002-9440(10)63043-X, DOI: 10.1016/S0002-9440(10)63043-X, ISSN: 0002-9440.

Schoenecker JG, Hauck RK, Mercer MC, Parker W, Lawson JH. Exposure to topical bovine thrombin during surgery elicits a response against the xenogeneic carbohydrate galactose alpha1-3galactose. J. Clin. Immunol. 2000 Nov; 20(6): 434-44. PMID: 11202233, ISSN: 0271-9142.

Cluss RG, Goel AS, Rehm HL, Schoenecker JG, Boothby JT. Coordinate synthesis and turnover of heat shock proteins in Borrelia burgdorferi: degradation of DnaK during recovery from heat shock. Infect. Immun. 1996 May; 64(5): 1736-43. PMID: 8613385, PMCID: PMC173986, ISSN: 0019-9567.